Final Digestive Disorders Flashcards
(157 cards)
1
Q
Location that defines lower GI bleeding
A
Originates in site distant to ligament of Treitz
2
Q
Etiology of lower GI bleeding
A
Erosive or inflammatory → diverticulosis
Vascular → hemorrhoids
Tumors → angiodysplasia
Traumatic or iatrogenic
Other → anal fissures
3
Q
Presence of multiple colonic diverticula without infection
A
Diverticulosis
4
Q
Most common cause of brisk hematochezia
A
Diverticulosis
5
Q
Risk factors for diverticulosis
A
Fiber poor diet
High meat diet
Obesity
Smoking
Physical inactivity
6
Q
Pathogenesis of diverticulosis (2 types)
A
Traction → due to pulling forces of an adjacent inflammatory site (true diverticula)
Pulsion → high pressures created during strained bowel movement (pseudodiverticula)
7
Q
Where are pseudodiverticula most commonly found
A
Left and sigmoid colon
8
Q
Clinical features of diverticulosis
A
Asymptomatic
Constipation
Vague abdominal discomfort after meals
9
Q
Diagnosis of diverticulosis
A
Incidentally through colonoscopy or CT scan
10
Q
Most common cause of lower GI bleeding
A
Diverticular hemorrhage
11
Q
Risk factors of diverticular hemorrhage
A
Older age
Ischemic heart
Obesity
Chronic renal insufficiency
Aspirin and NSAID
12
Q
Where are most of diverticular hemorrhages commonly found
A
Right colon
13
Q
Clinical differences between right and left colon diverticular hemorrhages
A
Left colon → bright red hematochezia
Right colon → dark/maroon hematochezia
14
Q
Diagnosis for diverticular hemorrhage
A
Colonoscopy
15
Q
Treatment of diverticular hemorrhage
A
Resuscitation with IV fluids and endoscopic therapy
16
Q
Complications of diverticular hemorrhage
A
Bleeding due to weakening or breaking of blood vessels near a diverticula
17
Q
Infection of diverticula
A
Acute diverticulitis
18
Q
Pathophysiology of acute diverticulitis
A
High pressure in the lumen → food impactions → micro perforations in the diverticula
19
Q
Clinical features of acute diverticulitis
A
LLQ abdominal pain and low grade fever
Change in bowel habits altering constipation and diarrhea
20
Q
Treatment for acute diverticulitis
A
Antibiotics
21
Q
Most common congenital anomaly of GI tract
A
Meckels diverticulum
22
Q
Pathophysiology of Meckels diverticulum
A
Incomplete obliteration of omphalomesenteric duct → true diverticulum
23
Q
Treatment of Meckels diverticulum
A
Surgery
24
Q
Risk factors associated with angiodysplasia
A
End stage kidney disease
Von willebrand disease
Aortic stenosis
25
Clinical features of angiodysplasia
Chronic bleeding
26
Diagnosis of angiodysplasia
Endoscopy and colonoscopy
27
2nd most common cause of diverticulosis
Angiodysplasia
28
Where is angiodysplasia most commonly found
Right colon
29
Clinical features of angiodysplasia
Mostly asymptomatic
30
Diagnosis for angiodysplasia
Incidentally during colonoscopy
31
Treatment for angiodysplasia
Endoscopic obliteration of affected vessels (not necessary for asymptomatic px)
32
Dilated submucosal vascular cushions within the anal canal that can be asymptomatic or manifest as painless masses, pruritus, or intermittent scant hematochezia
Hemorrhoids
33
Difference between internal and external hemorrhoids
Internal hemorrhoids → above pectinate line; painless
External hemorrhoids → below pectinate line; painful
34
Risk factors for hemorrhoids
Older age
Pregnancy
Pelvic tumors
Prolonged sitting
Straining
Chronic constipation
35
Clinical features associated with thrombosed hemorrhoids
Perianal pruritus, fecal soilage, pain
36
Initial treatment for hemorrhoids
Adequate fluid intake and high fiber diet
37
Treatment for hemorrhoids when initial treatment fails
Band ligation and sclerotherapy
Hemorrhoidectomy for stage 4
38
Hemorrhoids grading classification
Grade I → prominent vasculature with engorgement but no prolapse
Grade II → hemorrhoidal tissue prolapses only with straining but spontaneously reduces
Grade III → hemorrhoidal tissue prolapses beyond the dentate line with straining and can only be reduced manually
Grade IV → prolapsed tissue are evident that cannot be reduced manually
39
Clinical features of lower GI bleeding
Anemia
Acute hemorrhage: hypovolemia
Hematochezia
40
Diagnosis for occult bleeding
FOBT and complete blood count
41
Diagnosis for intermittent hematochezia
Digital rectal examination or sigmoidoscopy: px <40 w/o underlying features of malignancy
Colonoscopy: px with red flag symptoms
42
Age onset of inflammatory bowel syndrome
20-39 years old
43
Associated conditions to inflammatory bowel syndrome
Somatic pain syndromes
Psychiatric disorders
GI disorders
44
Most common pathophysiological findings in inflammatory bowel syndrome
Altered GI motility
Visceral hypersensitivity/hyperalgesia
Altered permeability of GI mucosa
Psychosocial aspects
45
GI clinical features of inflammatory bowel sx
Chronic abdominal pain and changes in bowel habits
46
Extraintestinal clinical features of inflammatory bowel sx
Generalized somatic symptoms
Disturbed sexual function
Dysmenorrhea
Increased urinary frequency and urgency
47
Classification of inflammatory bowel sx
IBS-D → diarrhea is predominant symptoms
IBS-C → constipation is predominant symptom
IBS-M → mixed diarrhea and constipation
IBS-U → criteria for IBS are met but bowel movements cannot be categorized into above subgroups
48
Diagnosis criteria used for inflammatory bowel syndrome
Rome IV criteria
49
Rome IV criteria
Timing → >6 months since onset of symptoms
Symptoms → Recurrent abdominal pain (>1 day per week during previous 3 months) + 2 of the following:
*Abdominal pain related to defecation
*Change in stool frequency
*Change in appearance of stool
50
Differential diagnosis for inflammatory bowel sx
Crohn, CUCI, colorectal cancer
51
Red flag symptoms of inflammatory bowel sx
Nighttime diarrhea and abdominal pain, fever, bloody stools, weight loss, and acute onset of symptoms
52
Non pharmacological treatment for inflammatory bowel sx
Low FODMAP diet → diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols
53
Pharmacological therapy for inflammatory bowel sx
Diarrhea → loperamide, rifaximin
Constipation → polyethylene glycol (PEG)
Abdominal pain → antispasmodics (dicyclomine) and tricyclic antidepressants
54
Difference between malabsorption and maldigestion
Malabsorption → impaired absorption of nutrients due to functional or structural alterations of intestinal mucosa
Maldigestion → impaired breakdown of food in intestinal lumen
55
Etiology of malabsorption
Mucosal damage
Small intestinal bacterial overgrowth
Short bowel sx
Hormonally active tumors
Maldigestion
56
Variants of malabsorption
Carbohydrate malabsorption
Exocrine pancreatic insufficiency
Short bowel syndrome
Patients without functional colon
57
General clinical symptoms of malabsorption
Chronic diarrhea
Steatorrhea, weight loss, fatigue, abdominal distention, flatulence
58
Clinical features of specific nutritional deficiencies
Vitamin D → osteoporosis
Vitamin B12 → fatigue, pallor, peripheral neuropathy
Zinc → alopecia, diarrhea, periorificial and/or acral dermatitis
Iron deficiency → fatigue, pallor
Protein deficiency → edema, cachexia
Electrolyte deficiency → Hypokalemia and hypocalcemia
59
Indirect marker of vitamin A deficiency
B-carotene
60
Evaluation of steatorrhea: screening and gold standard test
Screening test → sudan III stain
Gold standard test → 72 hrs fecal fat test
61
Evaluation of exocrine pancreatic insufficiency
Fecal elastase 1
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Test to assess absorptive function of upper small intestine
D-xylose absorption test
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How is the D-xylose absorption test performed
Overnight fasting → 25 g D-xylose administered orally, urine collected over 5 hrs and blood sample after 1 hr
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What do low levels of the D-xylose absorption test indicate
Damage to duodenal/jejunal mucosa or small intestine bacterial overgrowth
65
Treatment for malabsorption
Identify and treat underlying disease
Optimize diet → calorie and protein enriched
66
Complication of malabsorption
Protein-losing enteropathy
67
Age onset of Crohn disease
15-35 years and 55-70 years
68
Population with highest prevalence of Crohn disease
Northern Europe and Ashkenazi Jews
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Cause of Crohn disease (suspected pathophysiology)
Immune dysregulation and dysbiosis, which promotes chronic inflammation
70
Genetic predisposition for Crohn disease
NOD2 gene, HLAB27 association
71
Primary modifiable risk factor for Crohn disease
Tobacco smoke
72
Pathophysiology of the inflammation of Crohn disease
Dysregulation of IL-23 Th17 signalling → unrestrained Th17 cell function → inflammation → local tissue damage
73
Pathophysiology of fistula and abscess formation found in Crohn disease
Intestinal aphthous ulcers → transmural fissures and inflammation of intestinal walls → adherence of other organs or skin → penetration of tissue → micro perforation and abscess formation → macroperforation into these strictures → fistula formation
74
Clinical features of Crohn disease
Episodic acute flares and periods of remission
Chronic diarrhea
Abdominal pain → RLQ
75
Where is Crohn disease most commonly found
Terminal ileum and colon
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Initial diagnostic method for all px with suspected with Crohn disease
Ileocolonoscopy
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Hallmark of endoscopic findings with Crohn disease
Discontinuous areas of inflammation, cobblestone appearance of affected mucosa, and mucosal ulcerations
78
Type of imaging preferred and findings in Crohn disease
**Cross-sectional imaging**
Edematous thickening of intestinal wall
Creeping fat
Complications
79
Antibodies that predominate in Crohn disease
High anti-saccharomyces cerevisiae antibodies (ASCA)
80
Antibodies that predominate in ulcerative colitis
pANCA
81
Lab studies to monitor disease activity in Crohn disease
Fecal calprotectin and fecal lactoferrin
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Pathology findings for Crohn disease
Transmural inflammation
Noncaseating granulomas
Creeping fat
Hypertrophic lymph nodes
83
Pharmacotherapy for Crohn disease
Induction phase → Glucocorticoids & biologics
Maintenance phase → Biologics & immunomodulators
84
Characteristics of surgical treatment in Crohn disease
Surgery can lead to remission but is not curative
85
Vaccinations recommended in px with Crohn disease
Pneumococcal vaccine and yearly influenza vaccine
86
Age prevalence of ulcerative colitis
15-35 years old
87
Genetic predisposition for ulcerative colitis
HLA-B27
88
Risk factors for ulcerative colitis
Increased fat intake
Oral contraceptive use
89
Protective factors for ulcerative colitis
Appendectomy
Smoking
90
Montreal classification for extent of ulcerative colitis
Ulcerative proctitis (E1): Limited to rectum
Left-sided ulcerative colitis (E2): Limited to colon distal to splenic flexure
Extensive ulcerative colitis (E3): Extends proximal to splenic flexure
91
Pathophysiology for the dysregulation of intestinal epithelium in ulcerative colitis
Secretion proinflammatory cytokines and chemokines
Differentiation naive CD4 cells to Th2
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Pathophysiology of the dysregulaton of immune system in ulcerative colitis
Autoantibodies (pANCA) against cells of intestinal epithelium
Th2-cell mediated response
93
Pattern of involvement in ulcerative colitis
Ascending inflammation that begins in rectum (always) and spreads continuously proximally throughout colon
94
Clinical features of ulcerative colitis
Bloody diarrhea
Fecal urgency
Abdominal pain and cramps
Tenesmus
95
Most common extraintestinal feature of ulcerative colitis
Skeletal → osteoarthritis, ankylosing spondylitis, sacroiliitis
96
Inflammation of terminal ileum in context of CUCI
Backwash ileitis
97
Recommended method for diagnosis and disease monitoring ulcerative colitis
Ileocolonoscopy
98
X ray finding in ulcerative colitis
Loss of colonic austra (lead pipe appearance)
99
Pathology of ulcerative colitis
Early stages → Granulocyte infiltration limited to mucosa and submucosa, crypt abscesses
Chronic stages → Lymphocyte infiltration, mucosal atrophy, altered crypt architecture
100
Pharmacological therapy for ulcerative colitis
Systemic corticosteroids for induction of remission
Azathioprine in combination with anti-TNF therapy
101
Surgical procedure used for ulcerative colitis
Restorative proctocolectomy with an ileal pouch-anal anastomosis (IPAA or J pouch)
102
Peak age incidence of colorectal cancer
65 and 74 years of age
103
3 main pathological pathways of colorectal cancer
Chromosomal instability pathway
Microsatellite instability pathway
Hypermethylation phenotype pathway
104
Mutations found in the chromosomal pathway of colorectal cancer
APC gene mutation
KRAS gene mutation
TP53 and DCC gene mutation
105
How does the microsatellite instability pathway occur in colorectal cancer
Methylation or mutations in mismatch repair genes (MLH1 and MSH2)
106
How does the hypermethylation phenotype pathway occur in colorectal cancer
Global hypermethylation of CpG islands
Associated with BRAF mutations
107
Type of polyps associated with the hypermethylation phenotype pathway for the development of colorectal cancer
Serrated polyps
108
Pathogens that are a risk factor for colorectal cancer
Streptococcus bovis and Clostridium septicum
109
Lifestyle and diet factors that are a risk factor for colorectal cancer
Smoking and alcohol consumption
Obesity
Processed meat, high fat and low fiber
110
Protective factors for colorectal cancer
Long term use of aspirin and other NSAIDS
Physical activity
Diet rich in fiber and vegetables and lower in meat
111
When should iron deficiency anemia raise suspicion for colorectal cancer
Men >50 years old and postmenopausal women
112
Clinical features of right-sided colon carcinoma
Occult bleeding or melena
Manifestations of iron deficiency anemia
Diarrhea
113
Clinical features of left sided colon carcinoma
Changes in bowel habits
Blood-streaked stools
Colicky abdominal pain
114
Clinical features of rectal carcinoma
Hematochezia
Low stool caliber (pencil-shaped)
Rectal pain, tenesmus, flatulence
Fecal incontinence
115
Most common site of metastasis for colorectal cancer
Liver
116
Red flag features for colorectal cancer
Melena and hematochezia
Altered bowel habits
Unexplained weight loss
Unexplained iron deficiency anemia
117
Gold standard test for colorectal cancer
Complete colonoscopy
118
Alternative to dx method in px who decline or cannot undergo a complete colonoscopy
Double contrast barium enema
119
Double contrast barium enema finding in colorectal cancer
Napkin ring sign→ sharply defined circumferential narrowing of bowel caused by stenosing CRC
120
Prognostic marker of colorectal cancer
Carcinoembryonic antigen (CEA)
121
Curative treatment for colorectal cancer
Surgery for colorectal cancer
122
What is the use of palliative surgery
Prevent or treat complications of colorectal cancer
123
Chemotherapy regimens for colorectal cancer
FOLFOX → folinic acid (leucovorin) + 5-fluorouracil + oxaliplatin
FOLFIRI → folinic acid (leucovorin) + 5-fluorouracil + irinotecan
CAPOX → capecitabine + oxaliplatin
124
Standard tx modality in most cases of rectal cancer
Radiation therapy
125
Pathology of right sided and left sided colon carcinoma
Right sided colon carcinomas → mostly exophytic mass
Left sided colon carcinomas → mostly infiltrating mass
126
Complication of colorectal cancer (besides death lol)
Peritoneal carcinomatosis
127
Gold standard for screening of colorectal cancer
>45 years of age → complete colonoscopy every 10 years
128
Main cause of primary constipation
IBS
129
Type of constipation due to mechanical disorder or medication
Secondary constipation
130
Metabolic causes for secondary constipation
Hypokalemia
Hypothyroidism
Diabetes mellitus
131
Mechanism of altered stool consistency pathophysiology
External factors like lack of exercise or inadequate fluid and fiber intake (primary) / internal factors like changes within colon or rectum (secondary) → slow passage stool → prolonged absorption water by bowel → dry, hard stool → sensation of incomplete and irregular bowel emptying → constipation
132
Mechanism of altered bowel motility pathophysiology
Alteration bowel innervation → ineffective peristalsis → difficult passage of stool regardless of stool consistency → sensation of incomplete and irregular bowel emptying
133
Approach to management for constipation when there are no abnormal findings or red flags
Obtain CBC to evaluate anemia
134
Approach to management for constipation when there are abnormal findings or red flags
Red flags → colonoscopy to evaluate colorectal malignancy
Suspected secondary constipation → identify and treat underlying cause
135
Red flags for constipation
Blood in stool
Rectal bleeding
Rectal tenesmo
Clinically significant unintentional weight loss
Unexplained iron deficiency anemia
Jaundice
Obstructive symptoms
Px >50 years old w/o previous screening for CRC
Abdominal or rectal mass
Sudden change bowel habits
Family history
136
Rome IV diagnostic criteria for constipation
Onset >6 months
Presence +2 symptoms in at least 25% bowel movements for over 3 months
*Passage spontaneous stool <3 times/week
*Passage hard or lumpy stool
*Sensation anorectal obstruction
*Sensation incomplete evacuation
*Straining during attempts to defecate
*Manual aid to evacuate stool
137
Characteristics of anorectal function testing and colon transit studies
Anorectal function testing → evaluate for defecatory disorders
Colon transit studies → differentiate between normal transit constipation and slow transit constipation
138
1st line treatment for constipation
Non pharmacological measures (high fiber diet, increased fluid intake, exercise) and/or trial of bulk-forming laxatives
139
2nd line treatment for constipation
Stepwise pharmacotherapy with laxatives
Begin with osmotic laxative
If symptoms persist, add short course of stimulant laxative
140
Preferred osmotic and stimulant laxatives for constipation
Polyethylene glycol and lactulose → osmotic
Bisacodyl and sodium picosulfate → stimulant
141
Group of drugs that improve colonic transit time by increasing intestinal secretion of water, bicarbonate and chloride
Intestinal secretagogues
142
Examples of intestinal secretagogues
Linaclotide → peptide agonist of guanylate cyclase-C
Lubiprostone → prostaglandin derivative that activates chloride channels
143
Contraindication for intestinal secretagogues
Pregnancy
144
Abdominal X ray findings in fecal impaction
Dilated bowel loops
Fecal shadows in colon and rectum
Air-fluid levels may be visible
145
Most common cause of hereditary polyposis
Lynch syndrome
146
Second most common cause of hereditary polyposis
Familial adenomatous polyposis
147
Mutations in Lynch syndrome
Mismatch repair genes mutations → MLH1 and MSH2
148
Management of Lynch syndrome
Colonoscopy every 1-2 years starting at age 25
149
Mutation in familial adenomatous polyposis
APC gene mutation
150
Average age onset in which polyps start to appear in FAP
10-12 years old
151
Risk of no proper management of FAP
Will progress to colon cancer by late thirties
152
Screening for FAP
Starting at 10-15 years old annually
153
Treatment for FAP
Prophylactic colectomy in late teens or earlier if symptoms present
154
Similar presentation of FAP but at a later age and with lesser polyps
Attenuated familial adenomatous polyposis
155
Surveillance of attenuated familial adenomatous polyposis
Every 2 years starting at age 18-20
156
Predominant type of polyps in Peutz-Jeghers syndrome
Hamartomatous polyps
157
Gene mutation in Peutz-Jeghers syndrome
STK11 gene
