GASTROINTESTINAL- Pathology Flashcards

1
Q

Normaly how is the prognosis of salivary gland tumors?

A

Generally benign

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2
Q

Which glands are often affected by cancer?

A

Parotid glands

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3
Q

Salivary gland tumors

A

Pleomorphic adenoma
Warthin tumor
Mucoepidermic carcinoma

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4
Q

Most common salivary gland tumor

A

Pleomorphic adenoma

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5
Q

How is Pleomorphic adenoma consider?

A

Benign mixed tumor

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6
Q

How is pleomorphic adenoma presented?

A

As a painless, mobile mass

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7
Q

Histological characteristics of Pleomorphic adenoma

A

Chondromyxoid stroma and epithelium

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8
Q

Which is the expected evolution of Pleomorphic adenoma?

A

Recurs if incompletely excised or ruptured intraoperatively

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9
Q

What is Warthin tumor?

A

Papillary cystadenoma lymohomatosum

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10
Q

How is Warthin tumor classified?

A

Benign cystic tumor with germinal centers

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11
Q

Most common malignant tumor of Salivary glands

A

Mucoepidermoid carcinoma

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12
Q

Which are the components of Mucoepidermoid carcinoma?

A

Mucinous and squamous components

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13
Q

How is mucoepidermoid carcinoma manifested?

A

Painless, slow growing mass

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14
Q

What is Achalasia?

A

Failure of relaxation of LES due to loss of myenteric (Auerbach) plexus

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15
Q

Main Characteristics of Achalasia

A

High LES opening pressure and uncordinated peristalsis

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16
Q

Findings of Achalasia

A

Progressive dysphagia to solids and liquids

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17
Q

How is dysphagia when caused by obstructive processes?

A

Dysphagia to solids only

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18
Q

Which imaging study helps to diagnose Achalasia? and what does it shows?

A

Barium swallow shows dilated esophagus with an area of distal stenosis

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19
Q

With which disease is Achalasia related to?

A

Associated with ↑ risk of esophageal squamous cell carcinoma

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20
Q

What does Achalasia means?

A

A- chalasia= absence of relaxation

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21
Q

Finding of Achalasia in barium swallow

A

Bird’s beak

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22
Q

Which is the most common cause of secondary achalasia?

A

Chagas disease

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23
Q

Which is the most common cause of secondary achalasia?

A

Chagas disease

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24
Q

What is Boerhaave syndrome?

A

Transmural, usually distal esophageal rupture due to violent retching

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25
Which is the treatment for Boerhaave syndrome?
Surgical emergency
26
In which patients is more common to see Eosinophilic esophagitis?
Atopic patients
27
What is the detonant of Eosinophilic esophagitis?
Food allergens → dysphagia, heartburn, strictures
28
How is the benefict of GERD therapy in Eosinophilic esophagitis?
Unresponsive to GERD therapy
29
What is associated to esophageal strictures?
Lye ingestion and acid reflux
30
What are the Esophageal varices? what cause them?
Painless bleeding of dilated submucosal veins in lower 1/3 of esophagus secondary to portal hypertension
31
Which are agents associated to Esophagitis?
Reflux Infection in immunocompromised Chemical ingestion
32
Most common causing agents of Esophatitis in immunodepressed
Candida- white pseudomembrane HSV-1: punched out ulcers CMV: linear ulcers
33
How is gastroesophageal reflux disease manifested?
Commonly presents as heartburn and regurgitation upon lying down Nocturnal cough and dyspnea, adult onset asthma
34
What is affected in gastroesophageal reflux disease?
Decrease in LES tone
35
Mucosal lacerations at the gastroesphageal junction due to severe vomiting
Mallory Weiss syndrome
36
What does Mallory Weiss syndrome leads to?
Hematemesis
37
In which patients is more often to see Mallory Weiss syndrome?
In alcoholics and bulimics
38
In which patients is more often to see Mallory Weiss syndrome?
In alcoholics and bulimics
39
Characteristics of Plummer Vinson syndrome
Triad of dysphagia, Iron deficicency anemia, and Glossitis
40
Why is the reason of dysphagia in Plummer Vinson syndrome?
Due to esophageal webs
41
Which is the result of Sclerodermal esophageal dysmotility?
Esophageal smooth muscle atrophy → ↓ LES pressure and dysmotility → acid reflux and dysphagia → stricture, Barret esophagus and aspiration
42
When do we see Sclerodermal esophageal dysmotility?
CREST syndrome
43
What is Barret esophagus?
Glandular Metaplasia
44
What changes of epithelium is seen in Barret esophagus?
Replacement of nonkeratinized (stratified) squamous epithelium with intestinal epithelium (nonciliated columnar with Goblet cells) in distal esophagus
45
Main reason of Barret esophagus
Chronic acid Reflux (GERD)
46
With which diseases is Barret esophagus associated?
Esophagitis, esophageal ulcers, and increased risk of esophageal adenocarcinoma
47
Where is squamocolumnar junction found?
SCJ of Z line of esophagus
48
Where is squamocolumnar junction found?
SCJ of Z line of esophagus
49
Types of Esophageal cancer
Squamous cell carcinoma | Adenocarcinoma
50
How is the evolution of symptoms ans signs in Esophageal cancer?
Typically Presents with progressive dysphagia (first solids, then liquids) and weight loss
51
How is the prognosis of esophageal cancer?
Poor prognosis
52
Risk factors for Esophageal cancer
``` AABCDEFFGH Achalasia Alcohol Barret esophagus Cigarettes Civerticula (eg Zenker) Esophageal web Familial Fat (obesity) GERD Hot liquids ```
53
Which risk factors are related to Adenocarcinoma of Esophagus?
Barret esophagus Cigarettes Fat (obesity) GERD
54
Risk factors related to Squamus cell carcinoma of esophagus
``` Alcohol Cigartte Diverticula Esophageal web Hot liquids ```
55
World wide which is the most common type of esophageal cancer?
Squamous cell
56
In United states which is the most common type of esophageal cancer?
Adenocarcinoma
57
Where does Squamous cell carcinoma of Esophagus affects more?
Upper 2/3
58
Where does Adenocarcinoma of Esophagus affects more?
Lower 1/3
59
Erosive Gastritis
Acute Gastritis
60
In acute gastritis what causes inflmmation?
Disruption of mucosal barrier
61
Reasons of Acute Gastritis
``` Stress NSAIDs Alcohol Uremia Burns Brain injury ```
62
Reasons of Acute Gastritis
``` Stress NSAIDs Alcohol Uremia Burns Brain injury ```
63
How do NSAIDs cause Acute Gastritis?
↓ PGE2 → ↓ gastric mucosa protection
64
What causes Curling Ulcer?
↓ plasma volume → sloughing of gastric mucosa
65
How does a brain injury causes Acute Gastritis?
↑ vagal stimulation → ↑ ACh → ↑ H+ production
66
What is the Cushing Ulcer?
↑ vagal stimulation → ↑ ACh → ↑ H+ production
67
In which patients is more common to see Erosive gastritis?
Especially common among alcoholics and patients taking daily NSAIDs
68
Which patients are propense to acute Gastritis which take daily NSAIDs?
Patiens with Rheumatoid Arthritis
69
Also known as nonerosive gastritis
Chronic gastritis
70
How is Chronic gastritis classified?
Type A | Type B
71
Where does Type A chronic Gastritis affect?
Fundus/body
72
Where does Type B chronic Gastritis affect?
Antrum
73
What is the cause of Type A chronic Gastritis?
Autoimmune | Autoantibodies to parietal cells
74
What could be the results of type A chronic gastritis?
pernicious Anemia and Achrolrhydia
75
Most common type of Chronic gastritis
Type B
76
What causes type B chronic Gastritis?
By H. pylori infection
77
What risks are increased with type B Chronic Gastritis?
↑ risk of MALT lymphoma and gastric adenocarcinoma
78
What is Menetrier disease?
Gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucous cells
79
How risky is Menetrier disease?
Precancerous
80
In which disease rugae of stomach are so hypertrophied that they look like brain gyri
Menetrier disease
81
Most common type of Gastric cancer
Almost always Adenocarcinoma
82
How is the prognosis of Gastric cancer?
Early agressive local spread and node/liver metastases
83
Which is the often finding of Gastric cancer?
Acantosis nigricans
84
Pathological variants of Stomach cancer
Intestinal | Diffuse
85
What causes Intestinal variant of Stomach cancer?
Associated with H. pylori infection, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, chronic gastritis
86
What has dietary nitrosamines?
Smoked foods
87
Where does Intestinal variant of Stomach cancer affect more?
Lesser curvature
88
Macroscopically how does Intestinal variant of Stomach cancer looks like?
Ulcer with raised margins
89
Is diffuse Stomach cancer associated to H. pylori?
No
90
Histological findings of Diffuse stomach cancer
Signet ring cells
91
Characteristic of Diffuse Stomach cancer
Stomach wall grossly thickened and leathery (linitis plastica)
92
When do we see linitis plastica?
In diffuse Stomach cancer
93
What is Linitis plastica?
Stomach wall grossly thickened and leathery
94
What is Virchow node?
Involvement of left supracavicular node by metastasis from stomach
95
What is Krukenberg tumor?
Bilateral metastases to ovaries
96
Histological findings of Krukenberg tumor
Abundant mucus, signet ring cells
97
What is Sister Mary Joseph nodule?
Subcutaneous periumbilical metastasis
98
This peptic ulcer pain decreases with meals
Duodenal ulcer
99
Which peptic ulcer loses weight?
Gastric ulcer
100
How is the pain in Gastric ulcer?
Can be greated with meals
101
In how many cases of Gastric Ulcer is H. pylori infection involved?
70%
102
In how many cases of Duodenal Ulcer is H. pylori infection involved?
In almost 100%
103
What is the mechanism of cause of Gastric ulcer?
↓ mucosal protection against gastric acid
104
How is Duodenal ulcer formed?
↓ mucosal protection or ↑ gastric secretion
105
Other causes for Gastric ulcer
NSAIDs
106
Another cause related to Duodenal ulcer
Zollinger Ellison syndrome
107
Which peptic ulcer is related with increased risk of carcinoma?
Gastric ulcer
108
How risky can Duodenal ulcer be related to carcinoma?
Ganerally benign
109
In which group of age is Gastric ulcer more often?
Older patients
110
Histological findings in Duodenal ulcer
Hypertrophy of Brunner glands
111
Possible ulcer complications
Hemorrhage | Perforation
112
Which peptic ulcer can complicate with hemorrhage?
Gastric, duodenal | posterior> anterior
113
How is hemorrhage produced by gastric ulcer?
Ruptured gastric ulcer on the lesser curvature of the stomach → bleeding form left gastric artery
114
How is hemorrhage produced by duodenal ulcer?
An ulcer of the posterior wall of the duodenum → bleeding from gastroduodenal artery
115
Which peptic ulcer can complicate with perforation?
Duodenal ulcer | anterior> posterior
116
What could be the finding on perforation of duodenal ulcer?
May see free air under diaphragm
117
Clinical findings in perforation of duodenal ulcer
With refered pain to the shoulder
118
Malabsorption syndromes
``` These Will Cause Devastating Absorption Problems Tropical sprue Whipple disease Celiac sprue Disaccharidase deficiency Abetalopoproteinemia Pancreatic insufficiency ```
119
Which are the complications of Malabsorption syndromes?
Diarrhea, steatorrhea, weight loss, weakness, and vitamin and mineral deficiencies
120
Which Malabsorption syndrome has similar findings to Celiac sprue?
Tropical sprue
121
What is the difference of treating Tropical sprue and celiac sprue?
Tropical sprue Responds to antibiotics
122
What is the cause of Tropical sprue?
Cause is unknown, but seen in residents of ot recent visitors to tropics
123
Who causes Whipple disease?
Infection with Tropheryma whipplei (gram positive)
124
Findings in Whipple disease
PAS+ foamy macrophages in intestinal lamina propria, mesenteric nodes
125
Which clinical findings could be found in Whipple disease?
Cardiac symptoms, Arthralgias, and Neurologic symptoms are common
126
Which group of age is more affected by Whipple disease?
Most often occurs in Older men
127
What is the cause of Celiac sprue?
Autoimmune mediated intolerace of gliadin (wheat) leading to malabsorption and steatorrhea
128
What factors are associated to Celiac sprue?
HLA-DQ2 HLA-DQ8 northern descent
129
Main findings of Celiac sprue
Anti endomysial, anti tissue transglutaminase, and anti gliadin antibodies
130
Histological findings of Celiac sprue
Blunting of villi and lymphocytes in the lamina propria
131
Pathophysiology of Celiac sprue
↓ mucosal absorption that primarily affects distal duodenum and/or proximal jejunum
132
What is used in diagnosis of Celiac sprue?
Serum levels of tissue transglutaminase antibodies
133
Which dermatologic finding is associated to Celiac sprue?
Dermatitis herpetiformis
134
What risk does Celiac sprue has?
Moderately ↑ risk for malignancy (eg. T cell lymphoma)
135
What is the treatment for Celiac sprue?
Gluten free diet
136
Most common disaccharidase deficiency
Lactase deficiency- ---> Milk intolerance
137
Characteristics of villi in Lactase deficiency
Normal villi
138
How is the diarrhea in disaccharidase deficiency?
Osmotic diarrhea
139
What is the explanation of self limited lactase deficiency can occur following injury (eg. viral diarrhea)?
Since lactase is located at tips of intestinal villi, self limited lactase deficiency can occur following injury
140
How is lactose tolerance test done?
Administration of lactose produces symptoms, and Blucose rises
141
Pathophysiology of Abetalipoproteinemia
↓ synthesis of apolipoprotein B → inability to generate chylomicrons →↓ secretion of cholesterol, VLDL into bloodstream → fat accumulation in enterocytes
142
How is abetalipoproteinemia presented?
Presents in early childhood with failure to thrive, steatorrhea, acanthocytosis, ataxia, night blindness
143
Causes of pancreatic insufficiency
Due to cystic fibrosis, obstructing cancer, and chronic pancreatitis
144
What does pancreatic insufficiency causes?
Malabsorption of fat and fat soluble vitamins (Vitamins A, D, E, K)
145
What is found in stools in Pancreatic insuficiency?
↑ neutral fat in stool
146
What test helps in diagnosing Pancreatic insufficiency?
D xylose absorption test
147
How is D-xylose absorption test in Pancreatic insuficiency?
Normal urinary excretion in pancreatic insufficiency | ↓ excretion with intestinal mucosa defects or bacterial overgrowth
148
Name inflammatory bowel diseases
Chron Disease | Ulcerative Colitis
149
Possible etiology of Crohn disease
Disordered response to intestinal bacteria
150
Possible etiology of Crohn disease
Disordered response to intestinal bacteria
151
Ulcerative possible etiology
Autoimmune
152
Where can Crohn disease be localized?
Any portion of GI tract, ussually termina ileum and colon
153
How are the lesion known in Crohn Disease?
Skip lesions, rectal sparing
154
How are the lesions in Ulcerative Colitis?
Colitis= Colon inflammation | Continouns colonic lesions, always with rectal involvement
155
Gross morphology on Crohn Disease
Transmural inflammation → Fistulas Cobblestone mucosa, creeping fat, bowel wall thickening Linear ulcers Fissures
156
What imaging study helps in diagnosis of Crohn disease? What could be found?
"Sting sign" on barium swallow X ray
157
Gross findings in Ulcerative colitis
Mucosal and submucosal inflammation only Friable mucosal pseudopolyps with freely hanging mesentery Loss of Haustra
158
What is seen in imaging studies in Ulcerative Colitis?
"Lead pipe" aperance on imaging
159
Microscopic findings of Crohn disease
Noncaseating granulomas and lymphoid aggregates
160
Who mediates inflammatory response in Crohn disease?
Th1 mediated
161
Microscopic findings of Ulcerative Colitis
Crypt abscesses and ulcer, bleeding, no granulomas
162
Who mediates inflammatory response in Ulcerative Colitis?
Th2 mediated
163
Complications of Crohn disease
Strictures (leading to obstruction), fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer, gallstones
164
Complications of Ulcerative Colitis
Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma
165
When is worst the prognosis of Colorectal Cancer related to Ulcerative Colitis?
With right sided colitis or pancolitis
166
Intestinal manifestations of Crohn disease
Diarrhea that may or may not be bloody
167
Intestinal manifestation of Ulcerative Colitis
Bloody Diarrhea
168
Extraintestinal manifestations of Crohn disease
Migratory polyathritis, erythema nodosum, ankylosing spondylitis, pyoderma gangrenosum, aphthous ulcers, uveitis, kidney stones
169
Extraintestinal manifestations of Ulcerative Colitis
Pyoderma gangrenosum, erythema nodosum, prymary sclerosing cholangitis, ankylosing spondylitis, apthous ulcers, uveitis
170
Treatment for Crohn disease
Corticosteroids, azathioprine, methotrexate, infliximab, adalimumab
171
Treatment for Ulcerative Colitis
ASA preparations (sulfasalazine), 6- mercaptopurine, ifliximab, colectomy
172
How is Irritable Bowel syndrome is suspected?
Recurrent abdominal pain associated with > 2 of the following: - Pain improves with defecation - Change in stool frequency - Change in apperance of stool
173
Which are the structural abnormalities seen in irritable Bowel syndrome?
No structural abnormalities
174
In which patients is more common to see irritbale Bowel syndrome?
In middle aged women
175
Which are the posible symptoms of Irritable Bowel syndrome?
Diarrhea, constipation, or alternating symptoms
176
Pathophysiology of Irritable Bowel syndrome
Multifaceted
177
How is Irritable bowel syndrome treated?
Treat symptoms
178
Which is the possible cause of Appendicitis in adults?
Inflammation due to obstruction by fecalith
179
Possible cause of Appendicitis in children
Lymphoid hyperplasia
180
How is the progression of pain in Appendicitis?
Initial difusse periumbilical pain migrates to McBurney point
181
Where is McBurney point?
1/3 the distance from anterior superior iliac spine to umbilicus
182
Common symptoms seen in Appendicitis
Nausea, fever
183
Possible risk of Appendicitis
May perforate → peritonitis
184
Other possible findings in Appendicitis
May see psoas, obturador, Rovsing signs
185
Differential diagnosis of Appendicitis in elderly
Diverticulitis
186
What helps to rule out ectopic preganancy from Apendicits?
β-hCG
187
Treatment for Appendicitis?
Appendectomy
188
What is Diverticulum?
Blind pounch protrunding from the alimentary tract that communicates with lumen of the gut
189
Structures that might present with diverticulum
Esophagus, Stomach, duodenum, Colon
190
How is possible a Diverticulum?
They are acquired
191
Why are Diverticulum called false?
In that they lack or have and attenuated muscularis externa
192
Where are Diverticulum most often found?
Sigmoid colon
193
What is a True Diverticulum?
All 3 gut wall layers outpuch
194
Example of True diverticulum
Meckel
195
This diverticulum only presents with mucosa and submucosa outpuch
Flase diverticulum or pseudodiverticulum
196
Where does Flase diverticulum especially occurs?
Where vasa recta perforate muscularis externa
197
What is Diverticulosis?
Many false diverticula of the colon
198
Common site of apperance of Diverticulosis
Sigmid colon
199
How common is Diverticulosis?
Common (in 50% of >60 years old)
200
Which is the reason Diverticulosis is formed?
Caused ↑ intraluminal pressure and focalweakness in colonic wall
201
Which factor is associated to Diverticulosis?
Low fiber diets
202
Clinical findings of Diverticulosis
Often asymptomatic or associated with vague discomfort | A common cause of hematochezia
203
Complications of Diverticulosis
Include Diverticulitis, fistulas
204
What is Diverticulitis?
Inflammation of Divericula
205
Classical manifestation of Diverticulitis
LLQ pain, fever, leukocytosis
206
Possible complications of Diverticulitis
``` May perforate → peritonitis, abscess formation, or bowek stenosis Colovesical fistula (fistula with bladder) ```
207
Treatment for Diverticulosis?
Antibiotics
208
What findings can we see in Colovesical fistula?
Pneumatura
209
Lift sided apendicitis
Diverticulitis
210
Pharyngoesophageal flase diverticulum
Zenker diverticulum
211
Pathophysilogy of Zenker diverticulum
Herniation of mucosal tissue at KIllian triangle between the thyropharingeal and cricopharyngeal parts of tje inferior pharyngeal constrictor
212
Presenting symptoms of Zenker diverticulum
Dysphagia, obstruction, foul breath from trapped food particles (halitosis)
213
Who are more propense to Zenker Diverticulum?
Elderly males
214
Which imaging studie helps to diagnose Zenker diverticulum?
Barium swallow shows content filling flase diverticulim
215
Example of false Diverticulum
Zenker Diverticulum
216
Example of True diverticulum
Mekel diverticulum
217
Explanation of Mekel diverticulum
Persistence of Vitelline duct
218
What can Mekel diverticulum may contain?
Ectopic acid secreting gastric mucosa and/or pancreatic tissue
219
Most common congenital anomaly of GI tract
Mekel diverticulum
220
Complications of Meckel diverticulum
Melena, RLQ pain, intussusception, volvulus, or obstruction near the terminal ileum
221
With which disease Meckel diverticulum has contrast?
Omphalomesenteric cyst
222
What is Omphalomesenteric cyst?
Cystic dilation of vitelline duct
223
How is Meckel diverticulum diagnose?
Pertechnetate study for uptake by ectopic gastric mucosa
224
Which are the five 2's rule in Meckel diverticulum?
2 inches long 2 feet from ileocecal valve 2% of population Commonly presents in first 2 years of life May have 2 types of epithelia (gastric/ pancreatic)
225
What is Intussusception?
"Telescoping" of 1 bowel segment into distal segment
226
Where is the most common site of Intussusception?
Ileocecal junction
227
Presentation of Intussusception
Compromised blood supply → intermittent abdominal pain often with "currant jelly" stools
228
How common is Intussusception in adults?
Unsual in adults
229
When can we see Intussusception in adults?
Associated with intraluminal mass or tumor that acts as lead point that is pulled into the lumen
230
In whom is more common to see Intussusception?
Majority of cases occur in children
231
What might be the causes of Intussusception in children?
Idiopathic; may be associated with recent enteric or respiratory viral infection
232
How is Intussusception consider?
Abdominal emergency in early childhood
233
What is Volvulus?
Twisting of portion of bowel around its mesentery
234
What could be the results of volvulus?
Can lead to obstruction and infarction
235
Where can Volvulus occur?
Throughout the GI tract
236
Which is the most common volvulus in infants and children?
Midgut volvulus
237
Which is the most common volvulus in eldery?
Sigmoid volvulus
238
Which is the most common volvulus in eldery?
Sigmoid volvulus
239
What is Hirschsprung disease?
Congenital megacolon characterized by lack of ganglion cells/ enteric nervous plexuses (Auerbach and Meissner plexuses) in segment of intestinal biopsy
240
Which is the cause of Hirschsprung disease?
Due to failure of Neural crest cell migration
241
What gene mutation is associated to Hischsprung disease?
RET gene
242
How is Hischsprung disease presented?
Presents with bilious emesis, abdominal distension, and failure to pass meconium in the first 48 hours of life, ultimately manifesting as chronic constipation
243
In imaging studies what is seen in Hirschsprung disease? Why?
Dilated portion of the colon proximal to the aganglionic segment, resulting in a "transition zone"
244
Can Hischsprung disease involve rectum?
Yes
245
Which disease has increased risk of Hirschsprung disease?
Down syndrome
246
How is Hirschsprun disease diagnosis made?
Rectal suction biopsy
247
Which is the treaatment for Hirschsprung disease?
Resection
248
What are intestinal adhesions?
Fibrous band of scar tissue
249
When are adhesions formed?
Commonly formed after surgery
250
Most common cause of bowel obstruction
Adhesion
251
What else can be seen in Adhesion?
Can have well demarcated necrotic zones
252
Tortous dilation of vessels in GI tract
Angiodysplasia
253
Clinical finding of angiodysplasia
Hematochezia
254
Where is more often found angiodysplasia?
Cecum, terminal ileum and ascending colon
255
In which patiens is more common angiodysplasia?
In older patients
256
How is angiodysplasia confirmed?
By angiography
257
What does Duodenal atresia causes?
Early bilious vomiting with proximal stomach distention
258
What is seen in Duodenal atresia in Imamging studies?
"Double bubble" on X-ray
259
Why is proximal stomach distention seen in Duodenal atresia?
Because of failure of small bowel recanalization
260
Which disease is associated to Duodenal atresia?
Down syndrome
261
What is Ileus?
Intestinal hipomotility without obstruction
262
Findings of Ileus
Constipation and Decreased Flatulus; distened/ tympanic abdomen with ↓ bowel sounds
263
Which factor are associated to Ileus?
Abdominal surgeries, opiates, hypokalemia, and sepsis
264
Reduction in intestinal blood flow causes ischemia
Ischemic colitis
265
Clinical findings of Ischemic colitis
Pain after eating → weight loss
266
Where is commonly to see inschemic colitis?
Splenic flexure and distal colon
267
Who are mainly affected by ischemic colitis?
Elderly
268
When is meconium ileus seen?
In cystic fibrosis
269
What happens in meconium ileus?
Moconium plug obstructs intestine, preventing stool passage at birth
270
Necrosis of intestinal mucosa and possilbe perforation
Necrotizing enterocolitis
271
What is mainly affected by Necrotizing enterocolitis?
Colon is usually involved, but can involve entire GI tract
272
Who are mainly affected by Necrotizing enterocolitis?
In neonates, more common in preemies (↓ immunity)
273
What are Colonic polyps?
Masses protruding into gut lumen
274
What apperance do colonic polyps have?
Sawtooth apperance
275
Which are the most common Colonic polyps?
90% are non neoplastic
276
Where are more common to see Colonic polyps?
Rectosigmoid
277
How are Colonic polyps classified?
Tubular | Villous
278
Colonic polyps types
Adenomatous Hyperplastic Juvenile Hamartomatous
279
How are adenomatous polyps consider?
Precancerous
280
With which characteristics is adenomatous polyp associated with malignant risk?
↑ size, villous hystology | ↑ epithelial dysplasia
281
Precursor to Colorectal cancer
Adenomatous polyps
282
Which characteristic of Adenomatous polyps has increased tendency to be malignant?
The more villous the polyp, the more likely it is to be malignant (Villous= Villainous)
283
Polyp symptoms
Often asymptomatic, lower GI bleed, partia; obstruction, secretopry diarrhea (villous adenomas)
284
Most common non neoplastic polyp in colon
Hyperplastic
285
Where are Hyperplastic polyps more often found?
> 50% found in rectosigmoid colon
286
Characteristic of Juvenile polyps
Mostly sporadic lesions in children
287
Where areJuvenile polyps commonly found ?
80% in Rectum
288
When do Juvenile polyps have increased risk for Adenocarcinoma?
Multiple Juvenile polyps in GI tract
289
What is the Juvenile Polyposis syndrome?
Multiple Juvenile polyps in GI tract
290
What cancer is associated to Juvenile Polyposis syndrome?
Adenocarcinoma
291
How risky is having a single Juvenile polyp?
No malignant potential
292
Which kind of polyps do Peutz Jeghers syndrome has?
Hammartomatous
293
Inheritance mode of Peutz Jeghers syndrome
Autosomal dominant
294
Findings of Peutz Jeghers syndrome
Multiple nonmalignant hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, genitalia
295
What is associated to Peutz Jeghers syndrome?
Increase risk of Colorectal cancer and other malignancies
296
What is associated to Peutz Jeghers syndrome?
Increase risk of Colorectal cancer and other malignancies
297
Which group of age is more propense to be affected by Colorectal Cancer?
> 50 years old
298
Which percentage of patients with colorectal cancer have a family history?
25%
299
Syndromes associated to Colorectal cancer
Familial adenomatous polyposis (FAP) Gardner syndrome Turcot syndrome Hereditary nonpolyposis colorectal cancer (HNPCC/Lynch syndrome)
300
Inheritance mode of Familial Adenomatous polyposis
Autosomal dominant
301
Which gene is affected in Familial adenomatous polyposis?
APC gene on chromosome 5q. 2 hit hypothesis
302
Which percentage of Familial adenomatous polyposis progress to Colorectal cancer?
100%
303
How do you stop Familial adenomatous polyposis progresses to Colorectal Cancer?
Colon resection
304
How many polyps arise in Familial adenomatous polyposis?
Thousans of polyps arise starting at a young age
305
Which structures are involved in Familial adenomatous polyposis?
Pancolonic, always involve rectum
306
Findings of Gardener Sydrome
Familial adenomatous polyposis+ osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium
307
What does Turcot syndrome includes?
Familial adenomatous polyposis+ malignant CNS tumor
308
How else is Hereditary nonpolyposis colorectal cancer known?
Lynch syndrome
309
Mode of inheritance of Hereditary nonpolyposis colorectal cancer
Autosomal dominant mutation of mutation of DNA mismatch repair genes
310
Which percentage of Hereditary nonpolyposis colorectal cancer progresses to Colorectal Cancer?
80%
311
Which structure is always involved in Hereditary nonpolyposis colorectal cancer ?
Proximal colon
312
Additional risk factors for Colorectal cancer
``` Inflammatory bowel disease Tobaco use Large villous adenomas Juvenile polyposis syndrome Peutz Jeghers syndrome ```
313
In order, which structures suffer more colorectal cancer?
Rectosigmoid> ascending> descending
314
Findings of Colorectal cancer in Ascending colon
Exophytic mass Iron deficiency anemia Weight loss
315
Presentation of Colorectal cancer in descending colon
Infiltrating mass, partial obstruction, colicky pain, hematochezia
316
Rare presentation of Colorectal cancer
Presents as Streptococcus bocis bacteremia
317
Mnemonic of side presentation of Colorectal cancer
Right side bleeds | Left obstructs
318
When do you suspect of Colorectal cancer?
Iron deficiency anemia in males (especially > 50 years old) and postmenopausal females raises suspicion
319
When and how do you screen patiens from Colorectal cancer?
> 50 years old with colonoscopy or stool occult blood test
320
What imaging study made us suspect of Colorectal cancer? and What might be seen?
"Apple core" lesions seen on barium enema x ray
321
Good for monitoring recurrence of Colorectal cancer, not useful for screening
CEA tumor marker
322
What utility does CEA tumor marker has in Colorectal cancer?
Good for monitoring recurrence, not useful for screening
323
Which are the 2 molecular pathways that lead to Colorectal cancer?
Microsatelite instability pathway | APC/ β catenin pathway
324
How common is Microsatelite instability pathway causing Colorectal cancer?
15%
325
How common is APC/ β catenin pathway causing Colorectal cancer?
85%
326
Which is genetic cause of Microsatelite instability pathway in Colorectal cancer?
Mismatch repair gene mutations
327
Which Colorectal cancer is related to Microsatelite instability pathway?
Sporadic and HNPCC syndrome
328
Characteristic of Microsatelite instability pathway
Mutations accumulate, but not defined morphologic correlates
329
Chromosomalinstability of Colon cancer
APC/ β catenin pathway
330
What is the result of APC/ β catenin pathway in Colon cancer?
Sporadic cancer
331
Order of gene events
AK-53 | Loss of APC → K-RAS mutation → Loss of gene suppresor gene (p53, DCC)
332
From a normal colon to Colon at risk, what is affected?
Loss of APC
333
Celular changes of Colon ephitelia when loss of APC
Decreassed intercellular adhesion and increased proliferation
334
From colon at risk to Adenoma, which gene is affected?
K-RAS mutation
335
What happens when K-RAS mutation?
Unregulated intracellular signal transduction
336
What is affected form the conversion from adenoma to Carcinoma?
Loss of tumor supressor gene (p53, DCC) | Increased Tumorogenesis
337
Effects of portal hypertension
``` Esophageal varices Melena Splenomegaly Caput medusae, ascites Portal hypertensive gastropathy Anorectal varices ```
338
How is Melena produced in Portal hypertension?
Esophageal varices→ Melena | Peptic ulcer → Melena
339
Clinical findings of Esophageal varices
Melena | Hematemesis
340
Effects of liver cell failure
``` Hepatic encephalopathy Scleral icterus Fetor hepaticus (breath smells musty) Spider nevi Gynecomastia Jaundice Testicular atrophy Liver "flap"= asterixis (coarse hand tremor) Bledding tendency (↓ clotting factors, ↑ prothrombin time) Anemia Ankle edema ```
341
Why is it possible to see a patient feminized in liver cell failure?
Due to ↑ estrogen
342
What happens during cirrhosis?
Diffuse fibrosis and nodular regeneration destroys normal architecture of liver
343
What risk is increased with Cirrhosis?
Hepatocellular carcinoma
344
Etiologies of Cirrhosis
Alcohol Viral hepatitis Biliary disease Hemochromatosis
345
How many cases of Cirrhosis are related to Alcohol?
60-70%
346
Benefit of Portosytemic shunts
Partially alleviate portal hypertension: Esophageal varices Caput medusae
347
Benefit of Portosytemic shunts
Partially alleviate portal hypertension: Esophageal varices Caput medusae
348
Major diagnostic use for Alkaline phosphatase
Obstructive hepatobiliary disease Hepatocellular carcinoma Bone disease
349
When are aminotransferases (AST and ALT) elevated?
``` Viral hepatitis (ALT> AST) Alcoholic hepatitis (AST> ALT) ```
350
Wehn do we see Amylase elevated?
Acute pancreatitis, mumps
351
Serum marker decreased in Wilson disease
Ceruloplasmin
352
γ glutamil transpeptidase (GGT) is elevated in these situations
Increased in various liver and biliary diseases (just as ALP can), but not in bone disease; asociated with alcohol with alcohol use
353
Serum marker in acute pancreatitis (most specific)
Lipase
354
What is Reye syndrome?
Rare, often fatal childhood encephalopathy
355
Findings in Reye syndrome
``` Mitochondrial abnormalities Fatty liver (microvesicular fatty change) Hypoglycemia Vomiting Hepatomegaly Coma ```
356
When do we see Reye syndrome?
Associated with viral infection (especially VZV and influenza B) that has been treated with aspirin
357
Which is the patophysiology of Reye syndrome?
Aspirin metabolites ↓ β oxidation by reversible inhibition of mithocondrial enzyme
358
What precautions are made in order to avoid Reye syndrome?
Avoid aspirin in children
359
When is necesary to use aspirin in children?
In those with Kawasaki disease
360
Phases of Alcoholic liver disease
Hepatic steatosis Alcoholic hepatitis Alcoholic hepatitis
361
How is the progression of Hepatic steatosis?
Reversible with moderate alcohol intake
362
Hystological findings in Hepatic Steatosis
Macrovesicular fatty change that may be reversible with alcohol cessation
363
What is needed to get Alcoholic Hepatitis?
Requires sustained, long term consuption
364
Hystologic findings of Alcoholic hepatitis
Swollen and necrotic hepatocytes with neutrophilic infiltration Mallory bodies are present
365
What are Mallory bodies?
intracytoplasmatic eosinophilic inclusiones in hepatocytes
366
What is increased in Alcoholic hepatotitis?
AST> ALT (ratio usually >1.5)
367
How is Alcoholic cirrhosis consider?
Final and irreversible form
368
Gross findings of Alcoholic cirrhosis
Micronodular, irregular shrunken liver with "hobnail" aperance
369
Microscopic findings in alcoholic cirrhosis
Scleoris around central vein (zone III)
370
Manifestation of Alcoholic cirrhosis
Of chronic liver diasease: | eg. jaundice, hypoalbuminemia
371
Pathophysiology of Non alcoholic fatty liver disease
Metabolic syndrome (insulin resistance) → fatty infiltration of hepatocytes → cellular "ballooning" and eventual necrosis
372
What could be the results of Non alcoholic fatty liver disease?
Cirrhosis | Hepatocellular carcinoma
373
Which labs are modified in Non alcoholic fatty liver disease?
ALT > AST
374
Pathophysiology of Hepatic encephalopathy
Cirrhosis → portosystemic shunts → ↓ NH3 metabolism → neuropsychiatric dysfunction
375
How could Hepatic encephalopathy be manifested?
Spectrum from disorientation/asterixis (mild) to difficult arousal or coma (severe)
376
Which are the triggers of Hepatic encephalopathy?
↑ NH3 production | ↓ NH3 removal
377
Which situations have ↑ NH3 production?
Dietary protein GI bleed Constipation Infection
378
Which situations have ↓ NH3 removal?
Renal failure Diuretics Post-TIPS
379
Which is the treatment for Hepatic encephalopathy?
Lactulose (↑ NH4+ generation), low protein diet, and rifaxim (kills intestinal bacteria)
380
Most common primary malignant tumor of the liver in adults
Hepatocellular carcinoma
381
Alternative name for Hepatocellular carcinoma
Hepatoma
382
Diseases associated to Hepatocellular carcinoma
``` Hepatitis B and C Wilson disease Hemochromatosis α1 antitrypsin deficiency Alcoholic cirrhosis Carcinogens ```
383
Examples of Carcinogens related to Hepatocellular carcinoma
Aflatoxins from Aspergillus
384
What can Hepatocelular Carcinoma lead to?
Budd Chiari syndrome
385
Other liver tumors
Cavernous hemangioma Hepatic adenoma Angiosarcoma
386
How is Cavernous hemangioma classified?
Common, benign liver tumor
387
When does Cavernous hemangioma commonly occurs?
At age 30-50 years
388
What is contraindicated in Cavernous hemangioma if suspected? Why?
Biopsy, because of risk of hemorrhage
389
How is Hepatic adenoma classified?
Rare benign liver tumor
390
What is related to Hepatic adenoma?
To oral contraceptive or anabolic steroid use
391
How is the progression of Hepatic adenoma?
May regress spontaneously or rupture (abdominal pain and shock)
392
Malignant tumor of endothelial origin in liver
Angiosarcoma
393
Which factors are associated to Angiosarcoma?
Exposure to Arsenic, vinyl chloride
394
Reason of Nutmeg liver
Due to backup of blood into liver
395
Causes of Nutmeg liver
By right sided heart failure and Budd Chiari syndrome
396
Which is the apperance of Nutmeg liver?
Mottled like nutmeg
397
If the Nutmeg liver persists, what is the risk?
Centrilobular congestion and necrosis can result in cardiac cirrhosis
398
Pathophysiology of Budd Chiari syndrome
Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease
399
Signos of Congestive liver disease
Hepatomegaly Ascites Abdominal pain Eventual liver failure
400
Findings of Budd Chiari syndrome
May develop varices and have visible abdominal and back veins Absence of JVD
401
Which disease are associated to Budd Chiari syndrome?
Hypercoagulabel states Polycythemia vera Pregnancy Hepatocelular carcinoma
402
Which disease are associated to Budd Chiari syndrome?
Hypercoagulabel states Polycythemia vera Pregnancy Hepatocelular carcinoma
403
Pathophysiology of α1 antitrypsin deficiency
Misfolded gene product protein aggregates in hepatocellular ER→ cirrhosis with PAS + globules in liver
404
Genetic characterisitic of α1 antitrypsin deficiency
Codominant trait
405
What other disease is associated to α1 antitrypsin deficiency?
Panacinar emphysema
406
Pathophysiology of Panacinar emphysema
In lungs, ↓ α1 antitrypsin deficiency → uninhibited elastase in alveoli→ ↓ elastic tissue → panacinar emphysema
407
What is Jaundice?
Abnormal yellowing of the skin and/ or sclera due to bilirubin deposition
408
When does jaundice occurs?
At high levels of Bilirubin (>2.5 mg/dL) in the blood secondary to ↑ production or defective metabolism
409
How is Urine Urobilinogen in unconjugated (indirect) hyperbilirubinemia?
410
Diseases that have unconjugated hyperbilirubinema
Hemolytic physiologic (newborns), Crigler Najjar, Gilbert syndrome
411
How is Urine Urobilinogen in conjugated (direct) hyperbilirubinemia?
412
Diseases that present with unconjugated hyperbilirubinema
Biliary tract obstruction Biliary tract disease Excretion defect
413
Examples of biliary tract obstruction
Gallstones, pancreatic liver cancer, liver fluke
414
Examples of Biliary tract disease
Primary sclerosing cholangitis, Primary biliary cirrhosis
415
Excretion defects
Dubin- Johnson syndrome, Rotor syndrome
416
How is Urine urobilinogen in Mixed (direct and indirect) hyperbilirubinemia?
Normal/ ↑
417
Diseases that present with Mixed (direct and indirect) hyperbilirubinemia
Hepatitis | Cirrhosis
418
Explanation of physiologic neonatal jaundice leading to kernicterus
At birth, immature UDP- glucoronosyltransferase → Unconjugated hyperbilirubinemia → jaundice/ kernicterus
419
Which is the treatment for physiologic neonatal jaundice
Phototherapy
420
How does phototherapy helps treating physiologic neonatal jaundice
Converts unconjugated bilirubin to water soluble form
421
How does phototherapy helps treating physiologic neonatal jaundice
Converts unconjugated bilirubin to water soluble form
422
Pathophysiology of Gilbert syndrome
Mildly ↓ UDP- glucoronyltransferanse conjugation activity→ ↓ bilirubin uptake by hepatocytes
423
Clinical findings of Gilbert syndrome
Asymptomatic or mild jaundice
424
Labs found in Gilbert syndrome
Elevated unconjugated bilirubin without overt hemolysis
425
When is bilirubin during Gilbert syndrome?
With fasting and stress
426
How common is Gilbert syndrome?
Very common. clinical consequences
427
Pathophysiology of Crigler Najjar syndrome
Absent UPD glucoronosyltransferase
428
How is the prognosis of Crigler Najjar syndrome?
Presents early in life; patients die within a few years
429
Clinical findings in Crigler Najjar syndrome
Jaundice, Kernicterus (bilirubin depositions in brain)
430
Which labs are affected in Crigler Najjar syndrome?
↑ unconjugated bilirubin
431
Treatment for Crigler Najjar syndrome?
Plasmapheresis, Phototherapy
432
Which Crigler Najjar syndrome type is less severe?
Type II
433
Which drug helps in Crigler Najjar syndrome type II?
Phenobarbital, Which ↑ liver enzyme synthesis
434
Pathophysiology of Dubin Johnson syndorme
Conjugated hyperbilirubinemia due to defective liver excretion
435
How is the liver in Dubin Jonhson syndrome?
Grossly black
436
How is Dubin Johnson sindrome consider?
Benign
437
Which disease is similar to Dubin Johnson syndrome? What is the difference?
Rotor syndrome is similar but even milder and does not cause black liver
438
Where is Space of Disease ubicated?
Between endothelial cell and Hepatocyte
439
What circulates in Hepatic sinusoid?
Circulating bilirubin, comes from hemoglobin
440
From the bilirubin uptake in hepatocytes what is formed?
Unconjugated bilirubin
441
Which enzyme is needed for bilirubin conjugation?
Glucuronyl transferase
442
Characteristic of Conjugated bilirubin
Bilirubin diglucorinida, water soluble
443
Once Conjugated Bilirubin is formed what happens next?
Intracellular transport, and then to Bile flow
444
What is the problem in Gilbert syndrome?
With bilirubin uptake
445
What kind of hyperbilirubinemia is Gilbert syndrome?
Unconjugated hyperbilirubinemia
446
What is the problem in Crigler Najjar syndrome?
With bilirubin conjugation
447
What kind of hyperbilirubinemia in Crigler Najjar syndrome?
Unconjugated hyperbilirubinemia
448
What problem is seen in Dublin Johnson syndrome?
With excretion of conjugated bilirubin
449
What kind of hyperbilirubinemia is Dublin Johnson?
Conjugated hyperbilirubinemia
450
What kind of hyperbilirubinemia is Rotor syndrome?
Mild conjugated hyperbilirubinemia
451
Alternative name for Wilson disease
Hepatolenticular degeneration
452
Pathophysiology of Wilson disease
Inadequate hepatic cooper excretion and failure of cooper to enter circulation as ceruloplasmin
453
What is the result of Wilson disease?
Leads to cooper accumulation
454
Where does cooper accumulates primarily in Wilson disease?
Liver, brain, cornea, kidneys and joints
455
Characteristics of Wilson disease
Cooper is Hella BAD ↓ Ceruloplasmin, Cirrhosis, Corneal deposits, Cooper accumulation, Carcinoma (hepatocellular) Hemolytic anemia Basal ganglia degeneration (parkinsonian symptoms) Asterixis Dementia, dyskinesia, dysarthria
456
What is the treatment for Wilson disease?
Penicillamine or trientine
457
Mode of inheritance of Wilson disease
Autosomal recessive inheritance
458
Which chromosome is related to Wilson disease?
Chromosome 13
459
How is Cooper normally excreted?
Excreted into bile by hepatocyte cooper transporting ATPase
460
Which gene is related to cooper transporting ATPase ?
ATP7B gene
461
Kayser Fleisher ring
Golden brown corneal ring (Corneal cooper deposits)
462
Deposition of hemosiderin (iron)
Hemosiderosis
463
Disease caused by iron deposition (hemosiderin)
Hemochromatosis
464
How else is Hemochromatosis known?
Bronze diabetes
465
Classic triad of Hemochromatosis
Micronodular Cirhosis Diabetes Mellitus Skin pigmentation
466
Classic triad of Hemochromatosis
Micronodular Cirhosis Diabetes Mellitus Skin pigmentation
467
What could be the complications of Hemochromatosis?
Congestive Heart failure Testicular atrophy Increased risk of Hepatocelular Carcinoma
468
How can Hemochromatosis be acquired?
Primary | Secondary
469
How is primary hemochromatosis acquired?
Autosomal recessive
470
How is secondary hemochromatosis acquired?
To chronic transfusion therapy (eg. β-thalassemia major)
471
Lab alterations in hemochromatosis
↑ ferritin, ↑ iron, ↓ TIBC (Total Iron Binding Capacity)→ ↑ tranferrin saturation
472
How much total iron can the body reach?
50g
473
Which levels of iron in the human body can be detected with metal detectors at airports?
50g
474
Genes that cause Primary hemochromatosis
Due to C282Y or H63D mutation on HFE gene | Associated with HLA-A3
475
What factor in women slows the progression of hemochromatosis?
Iron loss through menstruation
476
Which is the treatment for hereditary hemochromatosis?
Repeated phlebotomy, deferasirox, deferoxamine
477
Which is the treatment for hereditary hemochromatosis?
Repeated phlebotomy, deferasirox, deferoxamine
478
Main biliary tract diseases
Secondary biliary cirrhosis Primary biliary cirrhosis Primary sclerosng cholangitis
479
Pathophysiology of Secondary biliary crirhosis
Extrahepatic biliary obstruction→ ↑ pressure in intrahepatic ducts → injury/fibrosis and bile stasis
480
Examples of extraheptaic biliary obstructions
Gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head
481
How is the Presentation of all biliary tract diseases?
Pruritus, jaundice, dark urine, light stools, hepatosplenomegaly
482
Labs found in all biliary tract diseases
↑ conjugated bilirrubin, ↑ cholesterol, ↑ ALP
483
What complicates Secondary biliary cirhosis?
By ascending cholangitis
484
Pathophysiology of Primary biliary cirrhosis
Auroimmune reaction → lymphocytic infiltrate + granulomas → destruction of infralobular bile ducts
485
Which other special labs are alterated in Primary biliary cirrhosis?
↑ serum mitochondrial antibodies, including IgM
486
Which diseases are associated to primary biliary cirrhosis?
Other autoimmune conditions (eg. CREST, Sjogren syndrome, rheumatoid arthritis, celiac disease)
487
Pathophysiology of primary sclerosing cholangitis
Unknown cause of concentric "onion skin" bile duct fibrosis → alternating strictures and dilation with beading of intra ans extra hepatic bile ducts on ERCP
488
What special lab is found in primary sclerosing cholangitis?
Hypergammaglobulinemia (IgM)
489
Pathology associated to Primary sclerosing cholangitis
Ulcerative colitis
490
What can Primary sclerosing cholangitis lead to?
Secondary cirrhosis and cholangiocarcinoma
491
What can Primary sclerosing cholangitis lead to?
Secondary cirrhosis and cholangiocarcinoma
492
Reasons that cause Gallstone?
↑ cholesterol and/or bilirubin, ↓ bile salts, and gallblader stasis
493
Types of stones in cholelithiasis
Cholesterol stones | Pigemented stones
494
80% of stones in cholelithiasis
Cholesterol stones
495
Which percentage of Cholesterol stones are identified in Gallstones?
80%
496
In image studies how are cholesterol stones seen?
Radiolucent with 10-20% opaque due to calcifications
497
Which factors are associated to Cholesterol stones?
Obesity, Chron disease, cystic fibrosis, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss , Native american origins
498
In image studies how are pigmented stones seen?
``` Black= radiopaque, hemolysis Brown= radiolucent, infection ```
499
Causes of pigemented stones in Cholelithiasis
Seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection
500
Possible Consequences of Cholelithiasis
Most common cholecystitis, also ascending cholangitis, acute pancreatitis, bile statis
501
Which factors are associated to Cholesterol stones?
Obesity, Crohn disease, cystic fibrosis, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss , Native american origins
502
Possible Consequences of Cholelithiasis
Most common cholecystitis, also ascending cholangitis, acute pancreatitis, bile statis
503
Possible and common effect of Cholelithiasis
Biliary colic
504
What is Biliary colic?
Neurohormonal activation triggers contraction of the gallbladder, forcing a stone into the cystic duct
505
In which patients is possible to see painless biliary colic?
Diabetics
506
What activates neurohormonal biliary colic?
by CCK after a fatty meal
507
What other risk does cholelitiasis has?
Can cause fistula between gallbladder and small intestine, leading to air in the biliary tree
508
What is gallstone ileus?
When gallstone obstruct ileocecal valve
509
How is Cholelithiasis diagnose?
Ultrasound
510
Treatment for Cholelithiasis
Cholecystectomy if symptomatic
511
Name the 4 F's risk factors for cholelithiasis
Female Fat Fertile (pregnant) Forty
512
Charcot triad of cholangitis
Jaundice Fever RUQ pain
513
Acute or chronic inflammation of gallbladder
Cholecystitis
514
Pathophysiology of Cholecystitis
Usually from cholelithiasis; most commonly blocking the cystic duct → secondary infection
515
Possible complications of Cholecystitis
Rarely ischemia or primary infection
516
Primary infection related to cholecystitis
CMV
517
Which sign helps in the diagnosis of Cholecystitis?
Murphy sign
518
In what consists Murphy sign?
Inspiratory arrest on RUQ palapation to pain due to pain
519
When does ALP increases during Cholecystitis?
If bile duct becomes involved (eg. ascending cholangitis)
520
How is cholecystitis diagnose?
With ultrasound or HIDA (hepatobiliary iminodiacetic acid)
521
What is porcelain gallbladder?
Calcified gallbladder due to chronic cholecystitis
522
How is porcelain gallbladder found?
Usually found uncudentally on imaging
523
What is the treatment for porcelain gallbladder?
Prophylactic cholecystectomy
524
Why is recommended prophylactic cholecystectomy in porcelain gallbladder?
Due to high rates of gallbladder carcinoma
525
What happens in acute pancreatitis?
Autodigestion of pancreas by pancreatic enzymes
526
Causes of acute pancreatitis
``` Gallstones Ethanol Trauma Steroids Mumps Autoimmune disease Scorpion sting Hypercalcemia/ Hypertriglyceridemia ERCP Drugs idipathic ```
527
Which Triglycerides levels are consider to cause risk of Acute pancreatitis?
> 1000 mg/ dL
528
Example of drug that can cause acute pancreatitis
Sulfa drugs
529
Clinical presentation of Acute pancreatitis
Epigastric abdominal pain radiating to back, anorexia, nausea
530
Labs that help in the diagnosis of acute pancreatitis? Which one is more specific?
Amylase, lipase (more specific)
531
What can Acute pancreatitis lead to?
DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst formation , hemorrhage, infection, and multiorgan failure
532
Explanation of hypocalcemia due to acute pancreatitis
Ca2+ collects in pancreatic cakcium soap deposits
533
Possible complication of Acute pancreatitis
Pancreatic pseudocyst
534
Characteristics of pancreatic pseudocyst
Lined by granulation tissue, not epithelium; can rupture and hemorrhage
535
What happens in chronic pancreatitis?
Chronic onflammation, athrophy, calcification of the pancreas
536
Major causes of Chronic pancreatitis
Alcohol abuse and idiopathic
537
What can Chronic pancreatits lead to?
Pancreatic insufficiency
538
Findings of pancreatic insufficiency
Steatorrhea, fat soluble vitamin deficiency, diabetes mellitus
539
What could be the final result of Pancreatic insuffiency?
Increase risk of pancreatic adenocarcinoma
540
How is amylase and lypase in Chronic pancreatitis?
May or may not be elevated (almost always elevated in acute pancreatitis)
541
Which image study helps in diagnosis of Porcelain gallbladder? what is seen?
X ray of the abdomen shows calcified gallblader wall
542
What image study helps in acute pancreatitis diagnosis? What is seen?
Axial CT shows acute exudative pancreatitis with extensive fluid collections surrounding the pancreas
543
What is seen in CT in chronic pancreatitis?
Near complete atrophy of the pancreas with residual coarse calfication
544
What is seen in CT in chronic pancreatitis?
Near complete atrophy of the pancreas with residual coarse calfication
545
How is the prognosis of Pancreatic adenocarcinoma?
Averages 1 year
546
How is Pancreatic adenocarcinoma consider?
Very agressive tumor arising from pancreatic ducts
547
Histologic findings in Pancreatic adenocarcinoma
Disorganized glandular structure with cellular infiltration
548
From where does pancreatic adenocarcinoma arise from?
From pancreatic ducts
549
When is commonly found pancreatic adenocarcinoma?
Already metastasized at presentation
550
Where is more common to see pancreatic adenocarcinoma? What does it cause?
Pancreatic head (causing obstructive jaundice)
551
Which tumor markers are associated to pancreatic adenocarcinoma?
Ca-19-9 tumor marker (also CEA, less specific)
552
Risk factors for pancreatic adenocarcinoma
``` Tobacco use Chronic pancreatitis Diabetes Age > 50 years Jewish and african american males ```
553
When does chronic pancreatitis increases the risk of pancreatic adenocarcinoma?
Especially > 20 years
554
How does Pancreatic adenocarcinoma often presents?
Abdominal pain radiating to back Weight loss Migratory thrombophlebitis Obstructive jaundice with palpable, nontender galbladder
555
What explains weight loss in Pancreatic adenocarcinoma?
Due to malabsorption and anorexia
556
Characteristics of Migratory thrombophlebitis
Redness and tenderness on palpation of extremities
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What is Trousseau syndrome?
Redness and tenderness on palpation of extremities | Seen in migratory thrombophlebitis
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What is Courvoisier sign?
Obstructive jaundice with palpable, nontender gallblader
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Which is the treatment for Pancreatic adenocarcinoma?
Whipple procedure, chemotherapy, radiation therapy
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How could Pancreatic adenocarcinoma be seen in CT scan?
Large lobulated low density mass in the head if the pancreas
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Possible signs found in Pancreatic adenocarcinoma
Trousseau syndrome | Courvoisier sign
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Possible signs found in Pancreatic adenocarcinoma
Trousseau syndrome | Courvoisier sign