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e-Mental Script
1
Contents
Clinical Manifestations
1 Dysphagia PCD 1 Harrison’s
2 UGIB GCD 1 Harrison’s
3 LGIB GCD 2 Harrison’s
4 Dyspepsia Lecture 1 Sleisenger
5 Constipation Lecture 2 Harrison’s
6 Chronic Diarrhea Lecture 2 Harrison’s
Disease Script
UGIB
Peptic Ulcer Disease GCD 1 Harrison’s
Gastric Cancer GCD 1 Harrison’s
LGIB
Colorectal CA GCD 2 Harrison’s
Chronic Diarrhea
Inflammatory Bowel Disease PCD 2 Harrison’s
Malabsorption Syndrome PCD 2 Harrison’s
Irritable Bowel Syndrome PCD 2 Harrison’s
2
CLINICAL MANIFESTATIONS
Approach to Diagnosis?
3
PCD 1
Dysphagia
Harrison’s pp.
oropharynx striated
Oropharyngeal dysphagia
Clinical drooling
Manifestations difficulty swallowing
food retention in pharynx
d/t poor tongue/pharyngeal propulsion or
obstruction of the UES)
Causes Iatrogenic* Muscular Iatrogenic – surgery & radiation (esp. in head & neck CA)
Neurologic* Infectious Neurogenic – from CVA, PD, amyotrophic lateral sclerosis
Structural* Metabolic – *major source of morbidity related to
aspiration & malnutrition
Zenker’s diverticulum
Cricopharyngeal bar lateralization of pharyngeal dysphagia
Neoplasia = structural/ neurogenic lesion selectively targeting
ipsilateral brainstem nuclei since medullary nuclei
directly innervate the oropharynx
Diagnosis Functional brain imaging Structural
: asymmetry in the cortical representation of pharynx Zenker’s diverticulum
= dysphagia d/t unilateral cortical CVA - regurgitation of food debris
- aspiration
Rapid-sequence fluoroscopy - halitosis
: asymmetry in the cortical representation of pharynx - stenosis of CP → diminished opening of UES →
= dysphagia d/t unilateral cortical CVA increased hypopharyngeal pressure during
swallowing … Killian’s dehiscence
Cricopharyngeal bar
Neoplasia
Esophageal dysphagia
Clinical In GERD patients without stricture *altered esophageal sensation, reduced esophageal mural
Manifestations Achalasia: absent peristalsis + failure of deglutive LES distensibility
relaxation
Diagnosis
4
GCD 1
UGIB
5
GCD 2
LGIB
6
Lec 1
Dyspepsia
“sinisikmura”, “kinakabag”, “nabubunsol”, mabigat ang tiyan”, “impatso”, “di natunawan”
Sleisenger pp. ?-190
DYSPEPSIA
Alarm Symptoms - ??? : demographic data, nature & frequency, chronicity, relat
-
Laboratory Tests
Factors to consider in work-up:
-
History & PE - esp. comorbidities, drugs
ORGANIC DYSPEPSIA
High Risk ≥50 – 60 yrs old
NSAID use
Alarm symptoms
Management Low Risk for organic dyspepsia: High Risk for organic dyspepsia
1. Test for H. pylori then treat. prompt Endoscopy
2. Empiric anti-sec drug: PPI
Prokinetic Drug
3. Endoscopy followed by
targeted medical treatment
FUNCTIONAL DYSPEPSIA
Pathophysiology impaired gastric accommodation (40%) impaired gastric accommodation
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Lec 1: DYSPEPSIA
Table 1-1. Rome IV Criteria for Functional Dyspepsia, Postprandial Distress Syndrome, and Epigastric Pain Syndrome,
Rome IV Criteria
Criteria fulfilled for the previous 3 months
with symptom onset at least 6 months prior to diagnosis
functional ≥1 of these: organic dyspepsia (no criteria but see causes)
dyspepsia Bothersome postprandial fullness
Bothersome early satiation
Bothersome epigastric pain
Bothersome epigastric burning
No evidence of structural disease (including at upper
GI endoscopy -EGD) that is likely to explain the
symptoms
PDS ≥1 of these at least 3 days a week: EPS ≥1 of these at least 1 day a week:
Bothersome postprandial fullness Bothersome postprandial fullness
Bothersome early satiation Bothersome early satiation
No evidence of structural disease (including at EGD) No evidence of structural disease (including at EGD)
Supportive Criteria: Supportive Criteria:
Postprandial epigastric pain or burning, epigastric Pain may be induced by ingestion of a meal, relieved
bloating, excessive belching, and nausea can also by ingestion of a meal, or may occur while fasting
be present
Postprandial epigastric bloating, belching, and
Vomiting warrants consideration of another disorder nausea can also be present
Heartburn is not a symptom of dyspepsia but often Persistent vomiting likely suggests another disorder
may coexist with PDS
Heartburn is not a symptom of dyspepsia but may
Symptoms that are relieved by evacuation of feces or often coexist with EPS
gas should generally not be considered part of the
The pain does not fulfill criteria for biliary pain
dyspepsia symptom complex
Symptoms that are relieved by evacuation of feces or
Other individual digestive symptoms or groups of
gas generally should not be considered part of the
symptoms (e.g., from GERD or IBS) may coexist
dyspepsia symptom complex
with PDS
Other digestive symptoms (such as GERD and IBS)
may coexist with EPS
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Table 1-2. Organic Causes of Dyspepsia
ORGANIC DYSPEPSIA: Causes
Luminal GI Tract Medications Pancreaticobiliary Disorders Systemic Conditions
Chronic gastric volvulus Acarbose Biliary pain: cholelithiasis, Adrenal insufficiency
Chronic gastric or intestinal Aspirin, other NSAIDs (including choledocholithiasis, SOD Diabetes mellitus
ischemia COX-2 selective agents) Chronic pancreatitis Heart failure
Food intolerance Colchicine Pancreatic neoplasms Hyperparathyroidism
Gastric infections (CMV, fungus, Digitalis preparations Intra-abdominal malignancy
tuberculosis, syphilis) Estrogens Myocardial ischemia
Gastric or esophageal neoplasms Ethanol Pregnancy
Gastroesophageal reflux Glucocorticoids Renal insufficiency
Gastroparesis (diabetes mellitus, Iron, potassium chloride Thyroid disease
postvagotomy, scleroderma, Levodopa
chronic intestinal pseudo- Narcotics
obstruction, postviral, idiopathic) Niacin, gemfibrozil
IBS Nitrates
Infiltrative gastric disorders Orlistat
(Ménétrier disease, Crohn Quinidine
disease, eosinophilic Sildenafil
gastroenteritis, sarcoidosis, Theophylline
amyloidosis)
Parasites (Giardia lamblia,
Strongyloides stercoralisrom)
PUD
Figure 1-2. Algorithm for the management of patients with dyspepsia. <insert reference>
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Lec 2
Constipation
Harrison’s pp. 268 - 270
Sleisenger pp. 250-295
Alarm Symptoms Change in bowel habits : demographic data, nature & frequency, chronicity, relat
Unexplained IDA
Recent sudden onset of sysmptoms
10
Treatment Treat if secondart
Non-Pharmacologic:
Reassurance
Lifestyle change
Psycho
Pah
Pharmacologic:
Bulk forming Laxatives
Emollient Laxatives
Saline Laxatives
Saline Cathartics
Hyperosmotic Laxatives (pediatric)
Castor oil (unpleasant)
Lactulose (best place to start)
Sorbitol
Stimulant Laxatives
Stimulant Laxatives (Senna)
5HT4 (Prucalopride)
Polyethylene Glycol (one of the best, needs 4L)
Cl Channel Activator
Guanylate cyclase-c (Linacloide)
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Lec 2: CONSTIPATION
Defecation
12
PCD 2
Chronic Diarrhea
Harrison’s pp. 263-
CHRONIC DIARRHEA
SECRETORY derangements in fluid & electrolyte transport - watery, large-volume fecal outputs Medications
- typically painless Bowel Resection
- persists with fasting
Mucosal Disease
Entero
OSMOTIC
STEATORRHEAL
INFLAMMATORY
DYSMOTILITY
FACTITIAL
IATROGENIC
1
Etiology derangements in fluid and electrolyte transport across the enterocolonic
mucosa
Clinical Features - Because there is no malabsorbed solute,
Stool osmolality is accounted
Why is DRE as an overall screening limited?
~50% of patients with documented colorectal CAs have a (-) FOBT,
consistent with intermittent bleeding pattern of these tumors
In random cohorts of asymptomatic persons, 2-4% have (+) FOBT
stools:
o colorectal CA is found only in <10% of these (+) individuals
∴ early detection of localized, superficial CAs in asymptomatic individuals
will increase surgical cure rate
Why Proctosigmoidoscopy?
60% of early lesions are located in the rectosigmoid
but the proportion of CAs arising in the rectum has been decreasing with
more corresponding increase in CAs arising in the proximal descending
colon
-
2 DIARRHEA
Definition X
3 DIARRHEA
Definition X
4 DIARRHEA
Definition X
13
14
DISEASE ILLNESS SCRIPT
15
Esophageal Cancer
16
GERD and Benign Peptic Ulcer
17
Peptic Ulcer Disease
18
Gastric Cancer
19
20
IBD
COLORECTAL CANCER
Epidemiology
Risk Factors/Causes
Clinical
Presentation
Pathology
Pathophysiology
21
Duodenal Ulcer
- common in the 1st portion of duodenum (95%), with ~90%
located within 3 cm of the pylorus
- ≤1cm in diameter (giant ulcer 3-6 cm)
Sharply demarcated sometimes reaching the muscularis
propria
- base: consists of a zone of eosinophilic necrosis with
surrounding fibrosis
- rare to be malignant
Treatment
Prognosis
Surveillance
22
Malabsorption Syndrome
COLORECTAL CANCER
Epidemiology
Risk Factors/Causes
Clinical
Presentation
Pathology
Pathophysiology
23
Duodenal Ulcer
- common in the 1st portion of duodenum (95%), with ~90%
located within 3 cm of the pylorus
- ≤1cm in diameter (giant ulcer 3-6 cm)
Sharply demarcated sometimes reaching the muscularis
propria
- base: consists of a zone of eosinophilic necrosis with
surrounding fibrosis
- rare to be malignant
Treatment
Prognosis
Surveillance
24
Irritable Bowel Syndrome
IBS
Definition abdominal pain or discomfort and altered bowel habits in the absence
of detectable structural abnormalities
Epidemiology - female
-
Pathology - ng
Pathophysiology
25
Recommendations: Other Screening Strategies but not really recommended::
American Cancer Society and the Stool Guiac Screening
National Comprehensive Cancer Network: - annual screening shows significant reduction in
asymptomatic individuals aged 50 above with NO personal or mortality rate from colorectal CA
family history of polyps & colorectal CA - but benefit emerged after >13 years of follow-up
annual FOBT + flexible sigmoidoscopy every 5 years making the benefit expensive to achieve because all
or positive tests (mostly a false +) were followed by
colonoscopy
colonoscopy every 10 years + flexible sigmoidoscopy
every 5 years Stool Testing: fecal DNA
Air Contrast Barium Enema
- used before the advent of fiberoptic endoscopy
- cumbersome, inconvenient to patients
Imaging: virtual colonography(e.g. CT)
- equivalent sensitivity with colonoscopy
- does not require degree of level of expertise as
fiberoptic endoscopy
- requires the same cathartic preparation
- diagnostic but not therapeutic (because pxs with
suspicious findings will still undergo subsequent
endoscopic procedure for polypectomy or biopsy
- less sensitive compared to endoscopy
Prognosis
Surveillance
26
Colorectal Cancer
COLORECTAL CANCER
Epidemiology
Risk Factors/Causes
Clinical
Presentation
Pathology
Pathophysiology
27
Duodenal Ulcer
- common in the 1st portion of duodenum (95%), with ~90%
located within 3 cm of the pylorus
- ≤1cm in diameter (giant ulcer 3-6 cm)
Sharply demarcated sometimes reaching the muscularis
propria
- base: consists of a zone of eosinophilic necrosis with
surrounding fibrosis
- rare to be malignant
Treatment
Prognosis
Surveillance
28
Disease Illness Script:
Disease
Secretory
COLORECTAL CANCER
Epidemiology
Risk Factors/Causes
Clinical
Presentation
Pathology
Pathophysiology
29
Recommendations: Other Screening Strategies but not really recommended::
American Cancer Society and the Stool Guiac Screening
National Comprehensive Cancer Network: - annual screening shows significant reduction in
asymptomatic individuals aged 50 above with NO personal or mortality rate from colorectal CA
family history of polyps & colorectal CA - but benefit emerged after >13 years of follow-up
annual FOBT + flexible sigmoidoscopy every 5 years making the benefit expensive to achieve because all
or positive tests (mostly a false +) were followed by
colonoscopy
colonoscopy every 10 years + flexible sigmoidoscopy
every 5 years Stool Testing: fecal DNA
Air Contrast Barium Enema
- used before the advent of fiberoptic endoscopy
- cumbersome, inconvenient to patients
Imaging: virtual colonography(e.g. CT)
- equivalent sensitivity with colonoscopy
- does not require degree of level of expertise as
fiberoptic endoscopy
- requires the same cathartic preparation
- diagnostic but not therapeutic (because pxs with
suspicious findings will still undergo subsequent
endoscopic procedure for polypectomy or biopsy
- less sensitive compared to endoscopy
Prognosis
Surveillance
30