Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hayders Phase 2A > GI > Flashcards

GI Flashcards

1
Q

what is some anti reflux physiological mechanism

A

Lower oesophageal sphincter formed by the diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is oesophagitis

A

Inflammation of the oesophagus due to reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

diagnosis of GORD

A

usually a clinical diagnoses and sees its improved by PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Investigations for GORD

A

first line is PPI trial, if symptoms persist past this time then further investigation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Further investigations for GORD

A

Barium swallow- if dysphagia
endoscopy, can show oesophagitis (erosive ulcers) or barrett’s oesophagus
ambulatory PH monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Triggers of GORD and foods to avoid

A

Caffeine, chocolate, spicy food, alcohol, citrus, fizzy drinks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

surgical management of GORD

A

endoscopic nissen fundoplication, operation to treat Hiatus hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

complications of GORD

A

if prolonged can cause oesophagitis
Barrett’s oesophagus
oesophageal ulcers, perforation hemorrhage or strictures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how is GORD classified

A

Los angeles GORD classification

categories ulcerations and erosions as mucosal breaks. 1 to 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

diagnoses of barrett’s oesophagus

A

Endoscopy with biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

risk factors for barrett’s oesophagus

A

Age, white men
prolonged GORD
Smoker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

management of barrett’s oesophagus

A

PPI + surveillance
plus Radiofrequency ablations and endoscopic mucosal resection
Potential esophagectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where does UCs affect

A

only affects the colon unless ileocecal valve is incompetent or backwash ileitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is it known as when crohn’s affects the entirety of the GI tract

A

Total colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe UC lesions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe Crohns macroscopic appearance

A

small bowel is thickened and has ulcers and fissures that give rise to cobble stone appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe UC macroscopic appearance

A

mucosa appears reddened and inflamed

Erythematous appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe Crohns Biposy result

A 
Transmural inflammation 
patchy inflammation 
Granulomatous present in 50%
goblet cells present 
Crypt abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe UC biopsy result

A 
Affects only serosa
continuous inflammation 
Goblet cell depletion 
and crypt abscess 
Granulomas are rare to see
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Symptoms of Crohn’s disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Symptoms of UC

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Biochemisty, bloods and serology in Crohns disease

A

Normocytic anemia, can have iron deficency
ESR CRP and WCC elevated
PANCA antibody -ve
ASCA +ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Biochemistry Bloods and serology in UC

A

Iron deficeny anemia
ESR and CRP elevated
PANCA antibody present
ASCA -Ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Investigations in Inflammatory Bowel disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Crohn’s Management

conservative and non disease modifying treatment

A

Symptomatic treatment, control diarrhoea (antidiarrhoeal agenst Imodium) control abd pain (analgesics)
stop smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Crohn’s management

Disease and pharmacological

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Crohn’s management

surgery option

A

resection of extremely inflamed areas

treat complications like strictures of fissures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

UC Management

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is a 5 ASA and method of action

A

anti inflammatory only in bowel, because it gets activated when in the lower PH of bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

UC complications

A 
Colon cancer 
bowel perforation 
toxic dilation
 hemorrhage 
ankylosing spondylitis (not a complication but can can occur concurrently)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

CD Complications

A 
stenosis strictures
fistulas 
abscess forming 
cancer in ileocaecal 
malabsorption 
perforation 
obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

risk factors to inflammatory bowel disease

A

Family history age groups 20-40 and 60 plus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the gene associated with UC

A

HLA - B27

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the prevalence of coeliac disease

A

1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is coeliac disease

A

Inflammation in the small intestine due to autoimmune response triggered by Gliadin in Gluten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Coeliac disease pathophysiology

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Presentation of coeliac disease

A 
suspect in weight loss + diarrhoea 
Abdominal distension - Bloating 
Anemia - iron deficiency 
Depression 
Gas
failure to thrive in children 
dermatitis herpetiformis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is skin change associated with coeliac disease

A

dermatitis herpetiformis ( pretty much specific to Coeliac disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

diseases associated with coeliac disease

A

Other autoimmune disorders
Type 1 DM
Thyroid disease
IBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Complications of coeliac disease

A 
Iron deficiency anemia 
lactose intolerance 
osteoporosis - since less mineral and ca absorption 
T cell Lymphoma 
Increased risk of malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Investigations of Coeliac disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the histology of coeliac disease show

A

this is shown by duodenal biopsy
villous atrophy and crypt hyperplasia
flattened villi and longer crypts

53
Q

Management of coeliac disease

A

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
Q

what are commonest causes of malabsorption

A

Coeliac disease
chronic pancreatitis
Crohn’s disease

55
Q

other causes of malabsorption

A

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
Q

Presentation of malabsorption

A

diarrhoea
weight loss
lethargy
steatorrhea
(anything from crohn’s coeliac or infection, pain,
distention, anemia nausea and vomiting, malaise)

57
Q

signs of malabsorption

A

anemia ( iron, B12, Folate)
bleeding disorder easy bruising ( vit K)
oedema (protein)
Osteoporosis (vit D and Ca)

58
Q

tests for malabsorption

A 
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
Q

Common pathogen that lead to malabsorption and how is it treated

A 
Giardia Lamblia (Extensive surface parisitation) diagnosed by biopsy 
Treat with tetracycline
60
Q

What is irritanble bowel syndrome

A

a group of abdominal syndromes where no other cause is found

61
Q

main causes/RF of IBS

A 
Depression and anxiety 
psycological stress and trauma 
GI infection 
eating disorer 
physical or sexual abuse 
Female
62
Q

IBS prevalence and age of onset

A

10-20%

usually under 40 Y O

63
Q

clinical features of IBS

A

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
Q

Diagnostic criterias of IBS

A

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
Q

further Investigations of IBS

A 
Duodenal biopsy -ve
Stool cultures -ve 
ESR and CRP -ve 
endoscopy normal 
colonoscopy normal 
absence of EMA anti TTG IgA
ERCP etc
66
Q

Management of IBS

A

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
Q

what is the differential for haematemesis

A

Upper GI Bleed. think peptic ulcer is commonest cause
GO Varices
mallory weiss tear

68
Q

Natural defences of stomach against acid

A

Alkaline mucus
tight junctions
replacement of damaged cells
Feedback loops

69
Q

Causes of peptic ulcers

A

NSAIDs, - inhibit prostaglandins which make mucus
Bile salts due to duodenal gastro reflux, Bile salts strip away mucus layer
H-Pylori

70
Q

how does H pylori cause Peptic ulcers

A

secretes Urease, which becomes ammonia then ammonium which causes inflammation and destroys mucosal defence
H pylori is precursor for Gastritis and Peptic ulcers

71
Q

Risk factors for peptic ulcers

A 
H pylori infection 
Smoking 
NSAIDs
Duodenal reflux 
Delayed gastric emptying 
Stress
72
Q

Presentation of peptic ulcers

A

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
Q

Red Flags that for dyspepsia that make you think to exclude malignancy before thinking peptic ulcers

A 
ALARM Symptoms 
Anemia - iron deficient 
Loss of weight 
Anorexia 
Recent onset
Malena / Haematemesis
Swallowing difficult
74
Q

Differential diagnosis for dyspepsia

A 
oesophagitis/ GORD 
Duodenal or gastric ulcer
Gastric malignancy (ALARM signs)
Duodenitis
Gastritis
non ulcer dyspepsia
75
Q

duodenal ulcers presentation

A

Epigastric pain before meals or night
relieved by eating or drinking milk
pain can be localised by finger
Epigastric tenderness

76
Q

Investigations and management of dyspepsia

A

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
Q

Investigations for H. Pylori

A

Non Invasive C 13 Urea Breath test

78
Q

Treatment for H. Pylori

A

Triple therapy
1 PPI- Lansoprazole, Omeprazole
2 antibiotics- Amoxicillin and clarithromycin

79
Q

Complications of peptic ulcers

A

Hemorrhage and bleed
perforation
malignancy and gastric outlet obstruction (projectile vomiting)

80
Q

What is H pylori

A

Gram -ve Curved bacteria present in around 50% f population but asymptomatic

81
Q

What can H Pylori cause

A

Gastritis
Peptic ulcers, gastric or duodenal
Gastric cancer

82
Q

what is zollinger ellison syndrome

A

Gastrin secreting tumour or hyperplasia in pancreatic islets causing recurrent peptic ulcers

83
Q

what is gastritis

A

Inflammation of the gastric mucosa, essentially pre peptic ulcer stage
Describes the redness seen on endoscope

84
Q

Causes of gastritis

A

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
Q

Treatment of gastritis

A

Treat Underlying disease,

H pylori triple therapy

86
Q

what are different types of intestinal obstruction

A

firstly small bowel (60^, commonest) or large bowel

can have Volvulus
Adhesions
Intussusception (Telescoping)

87
Q

causes of small bowel Obstruction

A

Adhesions (commonest) often post surgery
Inguinal Hernia
Crohn’s
malignancy

in Children
Appendicitis
volvulus
Intussusception

88
Q

Pathophysiology of SBO and complications

A

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
Q

what is adhesive obstruction

A

Extra luminal obstruction, usually post surgery, talc from gloves becomes silicon and binds parts of bowel together

90
Q

what type of obstruction of crohn’s disease

A

Intramural obstruction

91
Q

What is a volvulus

A

Type of SBO extra luminal, occurs when bowel twists around itself in mesentery causing obstruction and can lead to ischemia

92
Q

what are examples of Intramural obstructions

A

Crohn’s or Diverticular disease

93
Q

what is mechanical obstruction

A

obstructions in SBO

volvulus, Hernia Adhesion

94
Q

Presentation of small bowel obstruction

A 
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
Q

Diagnosis of SBO

A

CT- Gold standard
`Abd X ray
FBC shows WBC elevated and electrolyte imbalance due to dehydration
Other is laparotomy Laparoscopy

96
Q

Treatment of SBO

A 
Analgesia + antiemetics 
Antibiotics, ampicillin + Gentamicin 
Bowel Decompression:
Fluid resuscitation 
Surgery, Laparotomy to remove obstruction
97
Q

causes of LBO

A

commonly malignancy 90%
volvulus
Benign structures ( diverticular disease, ischemia)
Hirschsprung disease

98
Q

Indication of bowel perforation

A

Persistent tachycardia
Fever
Abdominal pain and tenderness, rebound tenderness and Guarding

99
Q

pathophysiology of LBO

A

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
Q

Presentation of LBO

A 
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
Q

Investigations in LBO

A 
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
Q

Treatment of LBO

A

supportive measures: Antibiotics Gentamicin
IV fluids
potentially transfusion
Surgery emergency Laparotomy

103
Q

What is Hirschsprung’s disease

A

Balloon Man disease
congenital disease where no innervation of the colon so dilation and no peristalsis
this causes obstruction

104
Q

What is diverticulitis

A

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
Q

Presentation of diverticulitis

A

Severe pain in Left iliac fossa
Constipation and fever
Abdominal tenderness and potentially a mass

106
Q

Investigations and management of diverticular disease

A

Ultrasound or CT of abdomen will show diverticular disease

Fluid and antibiotics amoxicillin or metronidazole
Surgery if perforated

107
Q

appendicitis pathophysiology and causes

A

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
Q

Clinical features of Appendicitis

A

Vague abdominal Pain that will develop into localized severe R Iliac fossa pain
Tenderness, rebound
guarding

Nausea vomiting diarrhoea anorexia

109
Q

Investigations of Appendicitis

A

WCC ESR and CRP all elevated
Ultrasound is diagnostic
Can do CT if unclear

110
Q

Management of appendicitis

A

Laparoscopic surgery to do appendectomy

IV antibiotics, Cefoxitin

111
Q

Differential diagnosis of Appendicitis

A 
Gynaecological causes Ectopic or Ovarian Torsion 
Testicular Torsion 
Colic, Renal Or biliary 
Crohn's
Intussusception
112
Q

Causes of localised peritonitis

A

Any inflammation, Appendicitis, Cholecystitis

113
Q

causes of Generalised Peritonitis

A

Infection or perforated
appendix, gallbladder gangrene and perforation and Bowel perforation
Perforated Ulcer

114
Q

Features of localised peritonitis

A

Secondary to inflammation

Slower onset and symptoms are that of underlying condition. tenderness, rebound tenderness guarding

115
Q

Features of generalised Peritonitis

A 
Sudden Onset 
Acute severe abdominal pain 
collapse and shock 
can lead to septicemia 
rebound tenderness and guarding 
pain made worse by moving
116
Q

Investigations for peritonitis

A

CXR, checks for air under diaphragm Serum Amylase- check acute pancreatitis
Ultrasound CT - Diagnostic

117
Q

Management of peritonitis

A

surgically treated
NG tube
Iv Fluid
antibiotics- Metronidazole

118
Q

What is spontaneous bacterial peritonitis

A

when there is an infection in ascites: often e coli, kelbestia or enterococci

119
Q

causes of bowel ischemia

A

most commonly, Thrombosis or thromboemboli
other occlusive causes is volvulus, tumour, intussusception, herno

and hypovolemic causes like spesis or reduced Co after MI

120
Q

where is ischemic colitis most likely to occur

A

Always in large bowel

commonly in Splenic flexure or L colon

121
Q

Where is mesenteric colitis likely to occur

A

Small bowel

122
Q

Mesenteric colitis presentation

A

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
Q

Ischemic colitis presentation

A 
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
Q

Investigations of Ischemic colitis

A

Ultrasound or CT to exclude perforation
AXR

later can do Barium enema
colonoscopy + Biopsy

125
Q

Investigations of mesenteric colitis

A 
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
Q

what is gold standard to exclude perforation

A

CT

127
Q

Management of ischemic colitis

A

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
Q

how to identify stricture formations

A

Barium enema

129
Q

Management of Mesenteric colitis

A

fluid plus antibiotics
gentamicin plus metronidazole
IV heparin
Surgery to remove necrotic bowel

monitor for signs of sepsis

Hayders Phase 2A (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions