Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

USMLE > GI > Flashcards

GI Flashcards

1
Q

Foregut develops into

A

Pharynx to duodenum

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

Midgut develops into…

A

duodenum to transverse colon

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

Hindgut develops into…

A

Distal transverse colon to the rectum

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

Developmental Defect of Anterior Abdominal Wall Due to Failure of
Rostal Fold Closure:
Lateral Fold Closure:
Caudal Fold Closure:

A

Rostal Fold Closure: Sternal Defects
Lateral Fold Closure: Omphalocele, Gastroschisis
Caudal Fold Closure: Bladder Exstrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q 
Duodenal atresia 
What is it?
Genetics?
Presentation 
XR
A

Failure to Recanalize
Trisomy 21 (Down Syndrome)
Early bilious vomiting with proximal stomach distention
“Double Bubble” on XR

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

Jejunal, Ilial, or Colonic Atresia

What causes them?

A

Vascular accident (apple peel atresia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Timing of midgut development

A

6th week: Midgut Herniates through umbilical ring

10th week: Returns to abdominal cavity and rotates around SMA

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

Gastroschisis
What is it?
Peritoneum?

A

Extrusion of the abdominal contents through the abdominal folds; not covered by peritoneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Omphalocele
What is it?
Peritoneum?

A

Persistance of herniation of abdominal contents into umbilical cord; covered by peritoneum

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

Most common Tracheoesophageal anomaly?

A

Esophageal atresia with distal tracheoesophageal fistula (85%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q 
Esophageal atresia with distal tracheoesophageal fistula
Presentation
XR
Cyanosis?
Clinical test?
A

Drooling, choking, vomiting with first feeding
Air in stomach visible on XR (TEF allows air into stomach)
Cyanosis secondary to laryngospasms (to avoid reflux-related aspiration)
Clinical test: failure to pass NG tube into stomach

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

H type Tracheoesophageal anomaly

A

Fistula alone

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

CXR in pure atresia type Tracheoesophageal anomaly?

A

In pure atresia (esophageal atresia only) CXR shows gasless abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q 
Congenital Pyloric Stenosis
What causes it?
Presentation?
Physical exam?
Treatment
Occurrence?
More often in...
A 
Hypertrophy of pylorus 
Nonbilious projectile vomiting at 2 weeks of age
Palpable olive mass in epigastric region
Surgical incision
Occurs 1/600 live births
More often in first born males
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pancreas Derived from

A

Foregut

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

Ventral Pancreatic bud contributes to

A

Pancreatic head and main pancreatic duct

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

Uncinate process of pancreas formed by the

A

Ventral bud alone

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

Dorsal pancreatic bud becomes

A

Body, tail, isthmus and accessory pancreatic duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Annular Pancreas
What is it?
What may it cause?

A

Ventral pancreatic bud abnormally encircles 2nd part of duodenum
May cause duodenal narrowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pancreas divisum

A

Ventral and dorsal parts of pancreas fail to fuse at 8 weeks

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

Where does the spleen arise from?
What kind of tissue is this?
Where does it get its blood supply from?

A

Arises in mesentery of stomach
Mesodermal tissue
Supplied by foregut (celiac artery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Do retroperitoneal structures have a mesentery?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Injuries to retroperitoneal structures can cause

A

Blood or gas accumulation in the retroperitoneal space

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

List of Retroperitoneal Structures

A 
"SAD PUCKER"
Suprarenal gland (adrenal)
Aorta and IVC
Duodenum (2nd and 3rd parts)
Pancreas (except the tail)
Ureters
Colon (descending and ascending)
Kidneys
Esophagus (lower 2/3)
Rectum (lower 2/3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Falciform Ligament
Connects
Structures Contained
Derivative of

A

Connects liver to abdominal wall
Contains ligamentum teres hepatis (from fetal umbilical vein)
Derivative of ventral mesentery

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

Hepatoduodenal Ligament
Connects
Structures Contained

A

Connects liver to duodenum

Contains portal triad

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

Portal Triad

A

Hepatic Artery, Portal Vein, Common Bild Duct

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

Omental Foramen
Name
What is it?
What is inside of it?

A

Epiploic Foramen of Winslow
Connects Greater and Lesser Sacs
Hepatoduodenal Ligament is inside of it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pringle Maneuver

A

Compression of Hepatoduodenal ligament in omental foramen to control bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q 
Gastrohepatic Ligament
Connects?
Structures contained?
Separates?
Surgery?
A

Connects Liver to lesser curvature of the Stomach
Contains gastric arteries
Separates greater and lesser sacs on the Right
May be cut during surgery to access lesser sac

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

Gastrocolic Ligament
Connects?
Structures contained?
Part of?

A

Connects greater curvature of stomach to transverse colon
Contains gastroepiploic arteries
Part of greater omentum

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

Gastrosplenic Ligament
Connects?
Structures contained?
Function?

A

Connects greater curvature of stomach to the spleen
Contains short gastrics and Left gastroepiploic vessels
Separates greater and lesser sacs on the left

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

Splenorenal Ligament
Connects?
Structures contained?

A

Connects Spleen to Posterior Abdominal Wall

Splenic artery and vein. Tail of pancreas

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

Layers of Gut Wall

A

From Inside to Outside: “MSMS”

Mucosa, Submucosa, Muscularis Externa, Serosa (when intraperitoneal)/Adventitial (when retroperitoneal)

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

Layers of Gut Mucosa and function of each layer

A

Epithelium (absorption), Lamina Propria (support), Muscularis Mucosa (motility)

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

What is included inside the submucosa?

A

Submucosal Nerve Plexus (Meissner’s)

Glands

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

What is included inside the Muscularis externa?

A

Myenteric Nerve Plexus (Auerbach’s)

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

Ulcers extend into

A

submucosa, inner or outer muscular layers

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

Erosions extend into

A

Mucosa only

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

Frequency of basal electric rhythm?
Stomach
Duodenum
Ileum

A

Stomach: 3 waves/min
Duodenum: 12 waves/min
Ileum: 8-9 waves/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Histology of the Esophagus

A

Non-Keratinized Stratified Squamous Epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Histology of the Stomach

A

Gastric Glands

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

Histology of the Duodenum

A

Villi and Microvilli
Brunner’s Glands (in submucosa)
Crypts of Lieberkuhn

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

Histology of the Jejunum

A

Plicae Circulares

Crypts of Lieberkuhn

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

Histology of the Ileum

A

Peyer’s Patches (lamina propria, submucosa)
Plicae Circulares (proximal ileum)
Crypts of Lieberkuhn
Largest # of goblet cells in SI

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

Histology of the Colon

A

Crypts by no villi

Numerous goblet cells

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

Branches of the abdominal Aorta that supply GI structures branch in which direction?

A

Anteriorly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Branches of the abdominal Aorta that supply non-GI structures branch in which direction?

A

Laterally

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

SMA Syndrome

A

Transverse portion (3rd part) of Duodenum entrapped between SMA and Aorta –> Intestinal Obstruction

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

Level of Celiac Trunk

A

T12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Level of SMA

A

L1

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

Level of Left Renal Artery

A

L1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Level of IMA

A

L3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Bifurcation of Abdominal Aorta occurs at what level?

A

L4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q 
Foregut
Artery
Parasympathetic Innervation
Vertebral Level
Structure supplied
A

Celiac
Vagus
T12/L1
Stomach to proximal duodenum, Liver, Gallbladder, Pancreas, Spleen (mesoderm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q 
Midgut
Artery
Parasympathetic Innervation
Vertebral Level
Structure supplied
A

SMA
Vagus
L1
Distal duodenum to proximal 2/3 of transverse colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q 
Hindgut 
Artery
Parasympathetic Innervation
Vertebral Level
Structure supplied
A

IMA
Pelvic
L3
Distal 1/3 of transverse colon to upper portion of rectum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Splenic flexure

A

Bend between transverse and descending colon

Watershed region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Branches of Celiac Trunk

A

Common Hepatic, Splenic, Left Gastric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Strong anastomoses in stomach blood supply

A

L and R Gastroepiploics

L and R Gastrics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Poor anastomoses in stomach blood supply

A

Short Gastrics (if splenic artery is blocked)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Collateral circulation if abdominal aorta is blocked?

A

Internal Thoracic (mammary) –> Superior epigastric ↔ Inferior epigastric –> External iliac
Celiac Trunk –> Superior pancreaticoduodenal ↔ Inferior pancreaticoduodenal – SMA
SMA –> Middle Colic ↔ Left Colic –> IMA
IMA –> Superior Rectal ↔ Middle and Inferior Rectal –> Internal Iliac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Portosystemc Anastomoses

A

L Gastric Vein ↔ Esophageal Vein –> Azygos
Paraumbilical Vein ↔ Superficial and Inferior Epigastric (below umbilicus) and Superior Epigastric and Lateral Thoracic (above umbilicus)
Superior Rectal ↔ Middle and Inferior Rectal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

SMV and IMV drain into

A

Portal Vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Varices of Portal HTN

A

Varices of “Gut, Butt, and Caput”

Esophageal varices, Internal hemorrhoids, Caput medusae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Surgical treatment of Portal HTN

A

“TIPS” Transjugular Intrahepatic Portosystemic Shunt between Portal Vein and Hepatic Vein percutaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the Pectinate (Dentate) Line

A

Where endoderm (hindgut) meets ectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q 
Above the pectinate line
What kind of hemorrhoids?
What kind of cancer?
Arterial Supply
Venous drainage
A

Internal Hemorrhoids
Adenocarcinoma
Superior Rectal Artery from IMA
Superior Rectal Vein –> IMV –> Portal Vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q 
Below the pectinate line
What kind of hemorrhoids?
What kind of cancer?
Arterial Supply
Venous drainage
A

External Hemorrhoids
Squamous Cell Carcinoma
Inferior Rectal Artery from Internal Pudendal
Inferior Rectal Vein –> Internal Pudendal Vein –> Internal Iliac –> IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Internal Hemorrhoids
Innervation?
Pain?
Lymphatic drainage?

A

Visceral Innervation, therefore NOT painful

Drained by Deep Nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

External Hemorrhoids
Innervation?
Pain?
Lymphatic drainage?

A 
Somatic Innervation (inferior rectal branch of pudendal nerve) and therefore Painful
Drained by Superficial Inguinal Lymph Nodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Apical Surface of hepatocytes face

A

Bile Canaliculi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Basolateral Surface of hepatocytes face

A

Sinusoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Zones of Liver

What is each one vulnerable to?

A

I: periportal –> Affected 1st by viral hepatitis
II: intermediate
III: pericentral vein (centrilobular)
Affected 1st by ischemia, Contains P450 system, most sensitive to toxin injury, site of alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Common Hepatic Duct
Formed from
Goes to

A

R and L Hepatic Ducts

Joins Cystic duct to form Common Bile Duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Common Bile Duct
Formed from
Goes to

A

Cystic Duct + Common Hepatic Duct

Joins Main Pancreatic Duct at Ampulla of Vater in Duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Ampulla of Vater

A

Where the Main Pacreatic Duct joins the Common Bile Duct in the 2nd part of the Duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Sphincter of Oddi

A

Sphincter around ampulla of vater

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Gallstones lodged in ampulla of Vater block

A

Both bile and pancreatic ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Tumors that arise near the head of the pancreas near the duodenum can cause

A

Obstruction of the common bile duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Organization of Vessels in Femoral Region

A

Lateral to Medial to find your “NAVEL”

Nerve, Artery, Vein, Empty space, Lymphatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Femoral Triangle contains

A

Femoral Vein, Artery, and Nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Femoral Sheath
Location
Contents

A

3-4cm below inguinal ligament

Contains femoral vein, artery, and canal (deep inguinal lymph nodes) but not the femoral nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Relation between IVC and the Aorta

A

IVC is to the R of Aorta in MRI/CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Contents of Inguinal Canal

A

Ilioinguinal nerve
Male: Spermatic Cord
Female: Round Ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Diaphragmatic Hernia
Definition
Think what kind of pt?
Most common kind of DH?

A

Abdominal structures enter the thorax
May occur in infants a a result of defective development of pleuroperitoneal membrane
Most commonly a Hiatal Hernia (stomach herniates through esophageal hiatus of diaphragm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Sliding Hiatal Hernia
Frequency?
Results in what?

A

Most common hiatal hernia

GE junction is displaced upwards resulting in a hourglass stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Paraesophageal Hernia

A

GE junction is normal

Fundus protrudes into the thorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q 
Indirect Inguinal Hernia 
Goes through
Location
Occurs in what kind of pt?
Follows path of?
What is it covered by?
A

Goes through internal (deep) inguinal ring, external (superficial) inguinal ring and into the scrotum.
Enters internal inguinal ring lateral to the inferior epigastric artery
Occurs in male infants owing to failure of processus vaginalis to close (from hydrocele)
Follows path of descent of the testes
Covered by all 3 layers of spermatic fascia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q 
Direct Inguinal Hernia
Definition
Location
Occurs in what kind of pt?
Goes through
What is it covered by?
A

Protrudes through inguinal (Hesselbach’s) Triangle
Bulges directly through abdominal wall medial to inferior epigastric artery
Older men
Goes through external (superficial) inguinal ring only
Covered by external spermatic fascia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Location of Direct vs Indirect Inguinal Hernias?

A

“MDs don’t LIe”
Medial to inferior epigastric = Direct
Lateral to inferior epigastric = Indirect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q 
Femoral Hernia
Location
Goes through
Most common in 
Leading cause of
A

Protrudes below inguinal ligament
Goes through Femoral Canal below and lateral to pubic tubercle
Most common in Women
Leading cause of bowel incarceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Hesselbach’s Triangle

A

Inferior epigastric vessels
Lateral border of rectus abdominis
Inguinal ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Gastrin
Source
Location of Source
Action

A

G Cells in Antrum of stomach
↑ Gastric H secretion (through ECL cells that release Hist)
↑ Growth of gastric mucosa
↑ Gastric motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Gastrin
↑ by
↓ by
What syndrome produces ↑ Gastrin secretion?

A

↑ by stomach distention, alkalinization, AA (esp Phenylalanine and Tryptophan), peptides, vagal stimulation
↓ by stomach ph < 1.5
↑↑ in Zollinger-Ellison Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Chronic Proton Pump Inhibitors (PPI) lead to

A

↑ Gastrin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q 
Cholecytokinin 
Source 
Location of Source
Action
Regulation
A

I cells in the duodenum and jejunum
↑ pancreatic secretion (via muscarinic pathways) and gallbladder contraction
↓ gastric emptying
Relaxes sphincter of Oddi
CCK secreted in response to ↑ FA and AA in duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q 
Secretin 
Source 
Location of Source
Action
Regulation
A

S cells in duodenum
↑ pancreatic bicarb secretion, bile secretion
↓ gastric acid secretion
Secretion ↑ w/ acid and FA in duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Pancreatic enzymes function at what pH

A

Basic pHs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q 
Somatostatin 
Source 
Location of Source
Action
Regulation 
Affects Re Growth?
A

D cells in pancreatic islets and GI mucosa
↓ gastric acid and pepsinogen secretion, pancreatic and small intestine fluid secretion, gallbladder contraction, insulin and glucagon release
Secretion is ↑ by acid
Secretion is ↓ by vagal stimulation
Antigrowth hormone (inhibits digestion and absorption of substances needed for growth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q 
Glucose Dependent Insulinotropic Peptide 
AKA
Source 
Location of Source
Exocrine 
Endocrine 
Regulation
A 
Gastric Inhibitory Peptide (GIP)
K cells in duodenum and jejunum 
Exocrine: ↓ Gastric H secretion 
Endocrine:  ↑ insulin release 
Secretion is ↑ by FA, AA, and oral glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q 
Vasoactive Intestinal Polypeptide 
Source 
Location of Source
Action
Regulation
A

Parasympathetic ganglia in sphincters, gallbladder and SI
↑ intestinal water and electrolyte secretion and ↑ relaxation of intestinal smooth muscle and sphincters
Secretion is ↑ by distention and vagal stimulation
Secretion is ↓ by adrenergic input

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

VIPoma
Kind of cells
Presentation

A

non-α, non-β islet pancreatic tumors secrete VIP
“WDHA”
Copious Watery Diarrhea, HypoK, and Achlorhydria (no gastric acid produced)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Nitric Oxide
Actions in GI tract
Especially present in
Implicated in what disorder

A

Smooth muscles relaxation
Especially in lower esophageal sphincter
Loss of NO secretion is implicated in achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q 
Motilin 
Location of Source
Action
Regulation 
Agonists? Uses of agonists?
A

Small Intestine
Produced migrating motor complexes
Secretion ↑ in fasting state
Agonists like erythromycin used to stimulate intestinal peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Intrinsic Factor
Source
Location of Source
Action

A

Parietal Cells in Stomach (Body)

Vit B12 binding protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Where is Vit B12 absorbed?

A

Bound to IF in terminal ileum along with bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Autoimmune destruction of parietal cells leads to

A

Chronic gastritis and pernicious anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q 
Gastric Acid
Source 
Location of Source
Action 
Regulation
A

Parietal Cells in Stomach
↓ stomach pH
Secretion ↑ by Hist, ACh, Gastrin
Secretion ↓ Somatostatin, GIP, prostaglandins, secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Gastrinoma

A

Gastrin secreting tumor that causes high levels of acid secretion and ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q 
Pepsin
Source 
Location of Source
Action 
Regulation
A

Chief Cells in Stomach (Body)
Protein digestion
Secretion is ↑ by vagal stimulation and local acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Activation of pepsinogen

A

Converted to pepsin in presence of H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q 
Bicarb
Source 
Location of Source
Action 
Regulation
A

Mucosal cells of stomach, duodenum, salivary glands, pancreas and Brunner’s Glands (in the duodenum)
Neutralizes acid
Secretion is ↑ from pancreatic and biliary secretion with secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Mucus that covers the gastric epithelium traps what?

A

Traps bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Saliva
Secreted from
Stimulated by

A

Parotid, Submandibular and Sublingual glands

Supplied by sympathetic (β –> cAMP) and parasympathetic activity (M –> IP3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Components of Saliva with function

A

Amylase digests starch
Bicarb neutralizes bacterial acids
Mucin lubricates food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Tonicity of Saliva

A

Normally hypotonic because of absorption but more isotonic with higher flow rates (less time for absorption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

How would Atropine affect parietal cells vs. G cells

A

Atropine –/ parietal cells

Atropine leaves G cells unaffected because the Vagus nerve releases GRP, not ACh to activate them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Brunner’s Glands
Location
Function
Hypertrophied in…

A

Duodenal submucosa
Secrete Alkaline mucus
Hypertrophied in peptic ulcer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Receptors on Parietal Cells

A

ACh –> M3 –> Gq –> IP3 –> ATPase
Gastrin –> CCKB –> Gq –> IP3 –> ATPase
Hist –> H2 –> cAMP –> ATPase
Prostaglandins/misoprostol Receptors –> Gi –/ cAMP
Somatostatin Receptors –> Gi –/ cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Pancreatic Secretions
Tonicity of Fluid
How does [electrolyte] change with flow?

A

Isotonic fluid
Low flow –> High [Cl]
High flow –> High [HCO3]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Pancreatic Secretions

Names and Roles

A

α amylase –> Starch digestion (secreted in active form)
Lipase. Phospholipase A, Colipase –> fat digestion
Proteases
Trypsinogen –> Activation of proenzymes (including trypsinogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Pancreatic Proteases
Names
Secreted as…

A

Trypsin, Chymotrypsin, Elastase, Carboxypeptidase

Secreted as proenzymes (zymogens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What converts trypsinogen into trypsin

A

Enterokinase/enteropeptidase and then trypsin itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Where is enterokinase/enteropeptidase secreted from?

A

Duodenal mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Salivary Amylase
Role
MoA
Yields

A

Starts digestion

Hydrolyzes α(1-4) linkages to yield disaccharides (maltose and α-limited dextrins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Pancreatic Amylase
Concentrated in
MoA

A

Highest concentration in duodenal lumen

Hydrolyzes starch to oligosaccharides and disaccharides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Oligosaccharide Hydrolase
Location
Role
MoA

A

At brush border of intestines
Rate limiting step in carbohydrate digestion
Produces monosaccharides from oligo- and disaccharides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q 
Carbohydrate absorption 
What kind of carbs?
By what cells?
What enzymes remove them from lumen?
What enzymes transport them to the blood?
A

Only monosaccharides (glucose, galactose, and fructose are absorbed by enterocytes
Glucose and Galactose are taken up by SGLT1 (Na dependent)
Frucose taken up by facilitated diffusion through GLUT5
All sugars enter blood via GLUT2

130
Q

How to distinguish GI mucosal damage from other causes of malabsorption?

A

D-xylose absorption test

131
Q

Iron absorption
Ionic state?
Location

A

As Fe2+ in duodenum

132
Q

Folate absorption

Location

133
Q

Peyer’s Patches
What are they?
Where are they?
Contain what kind of specialized cells?

A

Unencapsulated lymphoid tissue in LP and submucosa of ileum

Contains specialized M cells that take up antigen

134
Q

Peyer’s Patches

What happens in germinal centers? Where do cells from germinal centers go? What do they do?

A

In germinal centers, B cells are stimulated to differentiate into IgA secreting plasma cells
IgA cells migrate to LP
IgA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen

135
Q

Antibody in the gut?

A

Secretory IgA

“Intra Gut Antibody”

136
Q

Composition of Bile

A

Bild salts (bile acids conjugated to glycine and taurine to be made water soluble), Phospholipids, Cholesterol, Bilirubin, Water, Ions

137
Q

Rate limiting step in bile production

A

Cholesterol 7α hydroxylase

138
Q

Functions of Bile

A 
Digestion and absorption of lipids and fat soluble vitamins
Cholesterol excretion (the body's only means)
Antimicrobial activity (via membrane disruption)
139
Q 
Bilirubin 
Product of
Removed from blood by
Conjugated with
Excreted in
A

Product of heme metabolism
Removed from blood by liver
Conjugated with glucuronate
Excreted in bile

140
Q

Direct Bilirubin

A

Conjugated with glucuronic acid

Water soluble

141
Q

Indirect Bilirubin

A

Unconjugated

Water insoluble

142
Q

How is unconjugated bilirubin transported in the blood

A

Bound to albumin

143
Q

What enzyme conjugates bilirubin

A

UDP glucuronsyl transferase

144
Q

What happens to conjugated bilirubin in the gut?

A

Gut bacterial break it down into urobilinogen
80% of excreted in feces as stercobilin to give stool its brown color
20% is reabsorbed

145
Q

What happens to the reabsorbed urobilinogen?

A

10% goes to kidneys and excreted in urine as urobilin (gives urine yellow color)
90% enters enterohepatic circulation

146
Q

Salivary Gland Tumor
Dangerous?
Common Location?

A

Generally benign and occurs in the parotid gland

147
Q 
Salivary Gland Pleomorphic Adenoma 
Dangerous?
Kind of tumor? Composition?
Frequency?
Presentation
Recurrence?
A 
Benign
Mixed tumor of cartilage and epithelium 
Most common salivary gland tumor
Painless and mobile mass
Frequently recurs
148
Q 
Warthin's Tumor
Kind of tumor?
Descriptive name?
Dangerous?
Description
A

Salivary Gland Tumor
Papillary Cystadenoma Lymphomatosum
Benign
Cystic tumor with germinal centers

149
Q 
Achalasia 
What is it?
Presentation
Diagnosis
Increased Risk of...
A

Failure of the lower esophageal sphincter to relax due to loss of myenteric plexus
Progressive dysphagia to solids and liquids
Barium swallow shows dilated esophagus with area of distal stenosis (Birds Beak)
Increased risk of squamous cell carcinoma

150
Q

Secondary Achalasia may arise from…

A

Chagas disease

151
Q

Scleroderma and Esophagus?

A

Associated with esophageal dysmotility involving low pressure proximal to LES

152
Q

DDx for progressive dysphagia to solids and liquids?

A

Achalasia and Scleroderma

153
Q

GERD
Common Presentation
May also present with
Pathology

A

Heartburn and regurgitation upon lying down
May also present with nocturnal cough, dyspnea, adult onset asthma
Decrease in LES tone

154
Q

Esophageal varices
What are they?
Secondary to?

A

Painless bleeding of dilated submucosal veins in the lower 1/3 of the esophagus
Secondary to portal HTN

155
Q

DDx for Esophagitis

A

Reflux, Infection, chemical ingestion

156
Q

What organisms cause infectious Esophagitis?

A

Candida (white pseudomembrane), HSV1 (punched out ulcers), CMV (linear ulcers)

157
Q 
Mallory-Weiss Syndrome 
What is it?
What causes it?
What does it lead to?
Usually found in what kind of pt?
A

Painful Mucosal laceration at the GE junction
Due to severe vomiting
Leads to hematemesis
Alcoholics and bulimics

158
Q

Boerhaave Syndrome

A

“Been Heaving Syndrome”

Transmural esophageal rupture due to violent retching

159
Q

Esophageal Strictures are associated with…

A

Lye ingestion and acid reflux

160
Q

Plummer Vinson Syndrome

A

Triad of: Dysphagia (due to esophageal webs), Glossitis, Iron Deficiency Anemia

161
Q

Barrett’s Esophagus
What is it?
Due to
Associated with

A

Glandular metaplasia: replacement of stratified squamous epithelium with intestinal (non-ciliated columnar with goblet cells) epithelium in the distal esophagus
Due to GERD
Associated with esophagitis, esophageal ulcers, and increased risk for esophageal adenocarcinoma

162
Q

SCJ or Z line?

A

Squamocolumnar Junction at LES

163
Q

Esophageal Cancer
What kinds of cancer?
Presentation
Prognosis

A

Squamous Cell Carcinoma or Adenocarcinoma Presents with progressive dysphagia (first solids, then liquids) and weight loss
Prognosis is poor

164
Q

Risk factors for Esophageal Cancer

A

“AABCDEFFGH”

Achalaisa, Alcohol (squamous), Barrett’s (adeno), Cigarettes, Diverticula (Zenker’s) (squamous), Esophageal webs (squamous), Familial, Fat (adeno), GERD (adeno), Hot liquids (squamous)

165
Q

Most common Esophageal cancer
Worldwide?
US?

A

Worldwide: squamous
US: adenocarcinoma

166
Q

Esophageal Cancers

Location of Squamous vs Adenocarcinoma?

A

Squamous: upper 2/3
Adenocarcinoma: lower 1/3

167
Q

Malabsorption Syndromes can cause…

A

Diarrhea, Steatorrhea, Wt loss, Weakness, Vitamin and Mineral deficiencies

168
Q

Malabsorption Syndromes Names

A

“These Will Cause Devastating Absorption Problems”

Tropical Sprue, Whipple’s Disease, Celiac Sprue, Disaccharidase deficiency, Abetalipoproteinemia, Pancreatic insufficiency

169
Q 
Tropical Sprue
Cause
Responds to
Similar to
Can affect
A

Unknown cause
Responds to antibiotics
Similar to Celiac Sprue
Can affect entire small bowel

170
Q 
Whipple's Disease
What is it?
Histology
Presentation 
Most often in what kind of pt?
A

“Foamy Whipped cream in a CAN”
Infection with Tropheryma whipplei (gram +)
PAS+ fomay macrophages in the intestinal LP and mesenteric nodes
Cardiac Symptoms, Arthralgias, and Neurologic Symptoms
Most often in older men

171
Q 
Celiac Sprue
Pathology
Stool?
Ethnicity?
Genetics 
What part of GI tract?
A

AutoAbs to gluten (gliadin) in wheat and other grains
Leads to steatorrhea
Northern European descent
HLA-DQ2 and 8
Primarily affects distal duodenum or proximal jejunum

172
Q 
Disaccharidase Deficiency 
Most common kind?
Histology 
Diarrhea?
Self limiting kind?
A

Most common is lactase deficiency
Normal appearing villi
Osmotic diarrhea
Lactase normally at tips of villi, so self limiting kind can occur following infection

173
Q

Lactase deficiency diagnosis?

A

Administration of lactose produces symptoms and glucose rises < 20mg/dL

174
Q

Abetalipoproteinemia
PathoPhys?
Presentation?

A

↓ synthesis of apolipoprotein B –> inability to generate chylomicrons –> ↓ secretion of choesterol, VLDL into blood and fat accumulates in enterocytes
Presents in early childhood with malabsorption and neurologic manifestations

175
Q

Pancreatic Insufficiency
What can cause it?
What does it lead to
Stool?

A

Caused by CF, Obstructing Cancer, Chronic Pancreatitis
Causes malabsorption of fat and fat soluble vitamins (A, D, E, K)
↑ neutral fat in stool

176
Q 
Celiac Sprue
Histology 
Ab findings?
Screening 
Associated with
Increased risk for
A

Blunting of villi. Crypt hyperplasia. Lymphocytes in LP
Anti-endomysial, anti-tissue transglutaminase, and anti-gliadin Abs
Serum levels of tissue transglutaminase Abs used for screening
Associated with dermatitis herpetiformis
Moderately increased risk for malignancy (T cell lymphoma)

177
Q

Acute Gastritis
MoA
What can cause it?
Especially common among

A

Disruption of mucosal barrier –> inflammation
“U want a SNAC?”
Caused by stress, NSAIDs (↓ PGE –> ↓ gasric mucosa protection), Alcohol, Uremia, Burns (Curling’s ulcer), Brain Injury (Cushing’s ulcer)
Especially common among alcoholics and NSAID users (RA pts)

178
Q

Curling’s Ulcer

A

↓ plasma volume –> sloughing of gastric mucosa

179
Q

Cushing’s ulcer

A

↑ vagal stimulation –> ↑ ACh –> ↑ H production

180
Q

Acute vs Chronic Gastritis

A

Erosive vs Non-Erosive

181
Q 
Type A Chronic Gastritis 
What part of stomach?
Pathology
Produces what?
Associated with what?
A

Fundus and Body
AutoAbs to parietal cells
Produces pernicious Anemia and Achlorhydria
Associated with other immune disorders

182
Q 
Type B Chronic Gastritis 
What part of stomach?
Frequency
Pathology
Increased risk of what?
A

Antrum
Most common type of chronic gastritis
Caused by H pylori infection
Increased risk of MALT lymphoma

183
Q

Type A vs B Chronic Gastritis

A

“ABA, BAB”
A is in Body and from Autoimmunity
B is in Antrum and from Bacteria

184
Q

Menetrier’s Disease
What is it?
Cancerous?
Description

A

Gastric hypertrophy with protein loss, Parietal cell atrophy, ↑ mucous cells
Precancerous
Rugae of stomach are so hypertrophied that they look like brain gyri

185
Q

Stomach Cancer
What kind of cancer?
Does it spread?
Often presents with

A

Almost always adenocarcinoma
Early aggressive local spread and node/liver metastases
Often presents with acanthosis nigricans

186
Q

Stomach Cancer: Diffuse
Associated with?
Histology
Gross

A

Not associated with H pylori
Signet ring cells
Stomach wall grossly thickened and leathery (linitis plastica)

187
Q

Virchow’s Node

A

Involvement of Left Supraclavicular Node by metastasis from stomach

188
Q

Krukenberg’s Tumor
Presents with
Histology

A

Bilateral metastases from stomach to ovaries
Presents with abundant mucus
Signet ring cells

189
Q

Sister Mary Joseph’s Nodule

A

Subcutaneous periumbilical metastasis

190
Q 
Intestinal Stomach Cancer
What causes it 
Associated with
Common location
Looks like
A

Caused by H pylori infection, dietary nitrosamines (smoked foods), achlorhydria, chronic gastritis,
Associated with Type A blood
Commonly on lesser curvature
Looks like ulcer with raised margins

191
Q

Peptic Ulcer Disease

A

Gastric Ulcers

Duodenal Ulcers

192
Q 
Gastric Ulcer
Pain
Weight 
H pylori
Causes
Risk 
Often occurs in what kind of pt?
A 
Pain increases with meals 
Weight loss
H pylori in 70%
↓ mucosal protection against gastric acid; NSAID use
Risk of Carcinoma 
Often occurs in older patients
193
Q 
Duodenal Ulcer
Pain
Weight 
H pylori
Causes
Risk 
Histological changes
A 
Pain decreases with meals
Weight gain
H pylori in 100%
↓ mucosal protection or ↑ gastric acid secretion 
Generally benign
Hypertrophy of Brunner's glands
194
Q

Ulcer Complications

A

Hemorrhage or Perforation

195
Q

Location of Hemorrhage from Ulcer

A

Gastric or Duodenal Ulcers

Posterior > Anterior

196
Q

Location of Perforation from Ulcer

A

Duodenal

Anterior > Posterior

197
Q

Ruptured gastric ulcer on the lesser curvature –> bleeding from

A

Left Gastric Artery

198
Q

Ulcer on posterior wall of the duodenum –> bleeding from

A

Gastroduodenal Artery

199
Q

Inflammatory Bowel Disease

A

Crohn’s Disease or Ulcerative Colitis

200
Q 
Crohn's Disease 
Etiology
Distribution
Location
Gross
XR
A

Disordered response to intestinal bacteria (Th1 mediated)
Any portion of the GI tract; usually terminal ileum and colon; rectal sparing
Skip Lesions
Transmural inflammation; Cobblestone mucosa, creeping Fat, linear ulcers, fissures, fistulas
Bowel wall thickening –> “string sign” on barrium swallow x ray

201
Q

Crohn’s disease
Histology
Complications

A

Noncaseating granulomas and lympohid aggregates (Th1 mediated)
Strictures, fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer

202
Q

Crohn’s disease
Intestinal manifestations
Extraintestinal manifestations
Treatment

A

Diarrhea (w/ or w/o blood)
“Just got crushed by a stone –> red eyes, mouth hurts, and an aching back”
Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, kidney stones (Uric Acid from dehydration and CaOxylate from acidic urine), aphthous ulcers
Corticosteroids, azathioprine, methotrexate, infiximab, adalimumab

203
Q

Crohn’s Mnemonic

A

“Fat Granny, and old Crone Skipping down the Cobblestone road away from the Rec”

204
Q 
Ulcerative Colitis 
Etiology
Location
Distribution 
Gross
A

Autoimmune (Th2 mediated)
Colon; always rectal involvement
Continuous lesion
Friable mucosal pseudopolyps with freely hanging mesentery; Loss of haustra –> “lead pipe appearance”

205
Q

Ulcerative Colitis
Histo
Cell mediating the reaction?
Complications

A

Mucosal and submucosal inflammation only, crypt abscesses and ulcers, bleeding, no granulomas (Th2 mediated)
Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse with right sided colitis or pancolitis)

206
Q

Ulcerative Colitis
Intestinal manifestations
Extraintestinal manifestations
Treatment

A

Bloody diarrhea
Pyoderma gangrenosum, Primary sclerosing cholangitis, ankylosing spondylitis, uveitis
ASA preparation (sulfasalazine), 6-mercaptopurine, infliximab, colectomy

207
Q

Dx criteria for IBS

A

Recurrent abdominal pain with ≥2 of:
Pain improves with defecation
Change in stool frequency
Change in appearance of stool

208
Q 
IBS
Structural changes
Classic pt? 
Timeline of symptoms 
Presentation 
Pathophysiology 
Treatment
A 
No structural changes 
Most common in middle aged women
Chronic timeline
May present with diarrhea, constipation or alternating
Multifaceted pathophysiology 
Treat the symptoms
209
Q 
Appendicitis
What is it?
What causes it?
Presentation
If perforates... 
DDx
Treatment
A

Acute inflammation of the appendix
Obstruction by fecalith (adults) or lymphoid hyperplasia (children)
Initial diffuse periumbilical pain migrates to McBurney’s point. Nausea. Fever.
If perforates –> peritonitis
DDx: Diverticulitis (elderly), ectopic pregnancy,
Treatment: appendectomy

210
Q

McBurney’s Point

A

1/3 the distance from ASIS to umbilicus

211
Q

Diverticulum
What is it?
Most are…
Occurs most often in

A

Blind pouch protruding from alimentary tract that communicates with lumen of the gut
Most (esophagus, stomach, duodenum, colon) are acquired and are false (lack or have attenuated muscularis externa)
Occurs most often in sigmoid colon

212
Q 
Diverticulosis
What is it?
Frequency?
Caused by	
Associated with
Most often located in
A 
Many false diverticula
Common (~50% in pts >60)
Caused by Increased intraluminal pressure and focal weakness in colonic wall	
Associated with low fiber diet 
Most often located in sigmoid colon
213
Q

True diverticulum

A

All 3 gut wall layers outpouch

Meckels

214
Q

False diverticulum
AKA
Definition
Occur especially where…

A

Pseudodiverticulum
Only mucosa and submucosa outpouch
Occur especially where vasa recta perforate muscularis externa

215
Q

Diverticulosis
Presentation
Common cause of
Complications

A

Often asymptomatic or associated with vague discomfort
Common cause of hematochezia
Can lead to diverticulitis and fistula

216
Q 
Diverticulitis 
What is it?
Classic presentation 
May lead to
If perforates
Treatment
A

Inflammation of diverticula
LLQ pain, fever, leukocytosis, Stool occult blood +/- hematochezia
May lead to colovesical fistula which would cause pneumaturia
Perforation –> peritonitis, abscess formation, or bowel stenosis
Treat with antibiotics

217
Q

Zenker’s Diverticulum
What kind?
Where is it?
Presentation

A

False diverticulum
At Killian’s Triangle
Halitosis (due to trapped food particles), dysphagia, obstruction

218
Q

Killian’s Triangle

A

Between Thyropharyngeal and Cricopharyngeal parts of the inferior pharyngeal constrictor

219
Q 
Meckel's diverticulum 
What kind?
Caused by?
May contain
Frequency
Presentation 
What can it do to the GI tract?
Diagnostic test
A

“5 2s: 2in long, 2ft from ileocecal valve, 2% of pop, First 2 years of life, 2 types of tissue”
True diverticulum
Caused by persistence of the vitelline duct
May contain ectopic acid-secreting gastric mucosa +/or pancreatic tissue
Most common congenital anomaly of the GI tract
Melena, RLQ pain
Can cause intussusception, volvulus or obstruction near terminal ileum
Pertechnetate study for ectopic uptake

220
Q

Omphalomesenteric cyst

A

Cystic dilation of the vitelline duct

221
Q 
Intussusception 
What is it?
Common location
Presentation
Can lead to
Frequency and Cause 
Urgency
A

Telescoping of 1 bowel segment into distal segment
Commonly at ileocecal junction
Currant jelly stools
Can compromise blood supply
Unusual in adults (intraluminal mass or tumor). Majority in children (idiopathic, adenovirus)
abdominal emergency in children

222
Q 
Volvus
What is it?
Can lead to 
Common locations 
What kind of pt?
A

Twisting of portion of bowel around its mesentery
Can lead to obstruction and infarction
May occur at cecum and sigmoid colon (redundant mesentery)
Usually in elderly pt

223
Q 
Hirschsprung's Disease
What is it?
PathoPhys
Presentation 
Gross 
Location  
Risk Increases with  
Diagnosed with 
Treatment
A

Congenital megacolon
Failure of neural crest cells –> lack of ganglion cells/enteric nervous plexus (Auerback’s + Meissner’s)
Chronic constipation in early life. Failure to pass meconium
Grossly dilated portion of the colon proximal to the aganglionic segment, resulting in a transition zone
Involves rectum
Risk Increases with Down Syndrome
Diagnosed with suction biopsy
Treatment: resection

224
Q

Source of Inferior and Superior Epigastric Arteries?

A

Inferior: External Iliac Artery
Superior: Internal Thoracic Artery

225
Q

Meconium Ileus

A

Seen in CF

Meconium plug obstructs intestine preventing passage of stool at birth

226
Q 
Necrotizing enterocolitis 
What is it?
Risk of...
Where is it usually?
Classic pt?
A

Necrosis of intestinal mucosa
Risk of perforation
Usually in colon but can involve entire tract
Neonates, more common in preemies

227
Q 
Ischemic colitis 
What is it?
Presentation
Common location
Classic pt?
A

Reduction in intestinal blood flow –> ischemia
Pain out of proportion with physical findings. Pain after eating –> wt loss
Splenic flexure and distal colon
Elderly

228
Q 
Adhesion
What is it?
When does it happen?
Frequency?
Gross
A

Fibrous band of scar tissue
Commonly forms after surgery
Most common cause of small bowel obstruction
Well demarcated necrotic zones

229
Q 
Angiodysplasia 
What is it?
Presentation 
Common location
What kind of pt?
Diagnostic test
A 
Tortuous dilation of vessels 
Hematochezia
Terminal ileum, Cecum, Ascending Colon
Older pt.
Confirmed by angiography
230
Q 
Colonic Polyps
What are they?
Cancer?
Gross
Types Re Histology?
A

Masses protruding into gut lumen
90% are non-neoplastic
Sawtooth appearance
Tubular Adenoma: Small, rounded, more likely to be benign
Villous Adenoma: Long, finger like projections

231
Q

Adenomatous Polyps
What are they?
Risk Increases w/…
Presentation

A

Precancerous polyps that are precursors to Colorectal cancer
Malignant risk associated with increased size, villous histology (villous = villainous), increased epithelial dysplasia
Often asymptomatic. Lower GI bleed, partial obstruction, secretory diarrhea

232
Q

Hyperplastic Polyps
Frequency
Location

A

Most common non-neoplastic polyp in colon

Most (>50%) are in rectosigmoid colon

233
Q 
Juvenile Polyps 
What are they?
Who gets them?
Where are they?
Malignant?
A 
Sporadic lesion
Children <5
80% in rectum
Single: no malignant potential
Multiple: Increased risk for adenocarcinoma
234
Q 
Peutz-Jeghers
Genetics 
Features 
Presentation 
Risk
A

Autosomal Dominant syndrome
Multiple non malignant harmatomas throughout GI tract
Hyperpigmented mouth, lips, hands and genitalia
Increased risk for colorectal cancer and other visceral malignancies

235
Q

Colorectal Cancer
Frequency
Age of pts?
Genetics

A

3rd most common cancer; 3rd most deadly
Most pts are >50
~25% have family history

236
Q

Genetic disorders leading to Colorectal Cancer

A

Familial Adenomatuous Polyposis (FAP)
Gardner’s Syndrome
Turcot’s Syndrome
Hereditary Nonpolyposis Colorectal Cancer (Lynch Syndrome)

237
Q 
Familial Adenomatuous Polyposis
Dominance?
Mutation w/ chromosome 
Risk of CRC
Gross?
Location
A 
Autosomal dominant 
Mutation of APC gene on chromosome 5q (2 hit hypothesis)
100% progress to CRC
Thousands of polyps; Pancolonic
Always involves rectum
238
Q

Gardner’s Syndrome

A

FAP + Osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium

239
Q

Turcot’s Syndrome

A

“Turcot = Turban”

FAP + malignant CNS tumors

240
Q 
Lynch Syndrome 
Dominance 
Mutation
Risk of CRC
Location
A

Autosomal Dominant
Mutation in DNA mismatch repair genes
~80% progress to CRC
Proximal colon always involved

241
Q

Risk factors for CRC?

A

IBD, tobacco, large villous adenomas, juvenile polyposis syndrome, Peutz Jeghers

242
Q

Common locations for CRC?

A

Rectosigmoid > Ascending > Descending

243
Q

Ascending CRC
Description
Presentation

A

Exophytic mass

Iron deficiency anemia, wt loss

244
Q 
Descending CRC
Description
What does it produce?
Presentation 
Rarely, but can, present as...
A

Infiltrating mass
Produces partial obstruction
Colicky pain, hematochezia
Rarely, but can, present as Streptococcus bovis bacteremia

245
Q

Diagnosis of CRC
What raises suspicion in a pt?
Screening: Initial and Recurrence
XR

A

Iron Deficiency Anemia in males >50 and postmenopausal females
Screen for pts >50 with colonoscopy or stool occult blood test
CEA tumor marker is a screen for recurrence
Apple core lesion on barium enema XR

246
Q

What are they 2 molecular pathogenesises of CRC?

A

Microsatellite instability pathway (15%)

APC/beta catenin (chromosomal instability) pathway (85%)

247
Q

Microsatellite instability pathway for CRC pathogenesis

A

DNA mismatch repair gene mutations –> sporadic CRC and Lynch Syndrome
Mutations accumulate but no defined morphologic correlates

248
Q

Chromosomal instability pathway for CRC pathogenesis

A

“AK-53”

Normal Colon –> loss of APC gene –> decreased intracellular adhesion and increased proliferation –> Colon at risk –> K-RAS mutation –> unregulated intracellular signal transduction –> Adenoma –> Loss of p53 –> Increased tumorigensis –> Carcinoma

249
Q 
Carcinoid Tumor
What kind of tumor?
Frequency?
Location
EM
Produce
Presentation 
Symptoms only observed if...
Treatment
A 
NeuroEndocrine tumor
50% of small bowel tumors
Appendix, ileum, and rectum
EM: Dense core bodies
Produces 5HT
"CARC" --> Cutaneous flushing, Asthmatic wheezing, R heart murmurs, Cramps (diarrhea) 
Symptoms only observed if metastases exist beyond liver because liver will degrade 5HT 
Resection, Octreotide, Somatostatin
250
Q 
Liver Cirrhosis 
Description
Gross
Histo
Increased risk for
Etiologies
A

Diffuse fibrosis w/ nodular regeneration –> destruction of normal architecture of liver
Macronodules
Regenerative nodules and bridging fibrosis
Increased risk for hepatocellular carcinoma
Alcohol (60-70%), viral hepattis, biliary disease, hemochromatosis

251
Q

Presentation of Portal HTN

A 
Esophageal varicies --> Hematemesis + melena 
Peptic ulcers --> melena
Splenomegaly
Caput Medusae
Ascites
Gastropathy 
Hemorrhoids
252
Q

Presentation of Liver Cell Failure

A

Coma, Scleral icterus, Fetor Hepaticus, Spider Nevi, Gynecomastia, Jaundice, Testicular atrophy, Asterixis, Bleeding tendency, Anemia, Ankle Edema

253
Q

Aminotransferases
Names
Marker for
Ratio Re Different Diseases

A

AST and ALT are Liver Enzymes
Marker for Liver Pathology
ALT > AST –> Viral Hepatitis
AST > ALT –> Alcoholic Hepatitis

254
Q

Alkaline Phosphatase is a marker for

A

ALP

Hepatocellular carcinoma, bone disease, bile duct disease

255
Q

Gamma Glutamyl Transpeptidase (GGT)

A

Elevated in liver and biliary disease but not in bone disease

256
Q

Amylase is a marker for

A

Acute Pancreatitis or Mumps

257
Q

Lipase is a marker for

A

Acute Pancreatitis

258
Q

Ceruloplasmin is a marker for

A

Decreases in Wilson’s Disease

259
Q 
Reyes Syndrome 
What is it?
Frequency 
Classic pt
Cellular Findings
Presentation 
Mechanism
A

Fatal Childhood Hepatoencephalopathy
Rare
Child given aspirin for viral infection (especially VZV and Influenza B)
Mitochondrial abnormalities, Fatty Liver (microvesicular fatty change)
Hypoglycemia, vomiting, hepatomegaly, coma
Aspirin metabolites –> decreased beta oxidation by reversible inhibition of mitochondrial enzymes

260
Q

Only time you can give child aspirin?

A

Kawasaki’s Disease

261
Q

Stages of Alcoholic Liver Disease

A

Steatosis –> Hepatitis –> Cirrhosis

262
Q

Hepatic Steatosis
What is it?
Histo
Reversible?

A

Short term change in liver with moderate alcohol intake
Macrovesicular fatty change of hepatocytes
Reversible with cessation

263
Q

Alcoholic Hepatitis
In order to develop, one needs…
Histology
AST/ALT

A

In order to develop, one needs sustained, long term consumption
Swollen, necrotic hepatocytes with neutrophilic infiltration. Mallory Bodies (intracytoplasmic eosinophilic inclusions)
AST > ALT (usually AST/ALT > 1.5) “make a toAST with alcohol!”

264
Q 
Alcoholic Cirrhosis 
Reversible?
Gross
Histology
How does it manifest itself?
A

Irreversible
Micronodular, irregular, shrunken liver with “hobnail” appearance
Sclerosis around central vein (zone III)
Manifests as chronic liver disease (jaundice, hypoalbuminemia…)

265
Q 
Hepatocellular Carcinoma (Hepatoma)
Frequency 
Increased risk w/...
Presentation 
Serum markers?
How does it spread
May lead to...
A

Most common primary malignancy of the liver in adults
Increased risk w/ Hepatitis B and C, Wilson’s, Hemochromatosis, Alpha 1 antitrypsin deficiency, Alcoholic cirrhosis and carcinogens (e.g. aflatoxin from Aspergillus)
Jaundice, Tender Hepatomegaly, Ascities, Polycythemia, Hypoglycemia
Increased Alpha Fetoprotein
Spreads hematogenously
May lead to Budd Chiari Syndrome

266
Q 
Cavernous hemangioma 
Frequency
Danger 
Typical pt
Biopsy?
A

Common, benign liver tumor
Age 30-50
Biopsy contraindicated because of risk of hemorrhage

267
Q

Hepatic Adenoma
Danger
Related to what?
Prognosis

A

Benign liver tumor
Related to oral contraceptives or steroid use
Can spontaneously regress

268
Q

Angiosarcoma
Danger?
Origin?
Associated with exposure to

A

Malignat tumor of endothelial origin

Associated with exposure to arsenic, polyvinyl chloride

269
Q

Nutmeg Liver
What causes it?
Can result in?

A

Mottled appearance because of backup of blood into liver
R sided heart failure or Budd Chiari
Can result in centriolobular congestion and necrosis which will lead to cardiac cirrhosis

270
Q

Budd Chiari Syndrome
What is it?
Presentation
Associations?

A

Occlusion of IVC or hepatic vein –> centriolobular congestion and necrosis –> congestive liver disease
Hepatomegaly, ascites, abdominal pain, varices, visible abdominal and back veins. No JVD
Associated with hypercoagulable state, polycythemia vera, pregnancy, hepatocellular carcinoma

271
Q 
Alpha 1 AntiTrypsin Deficiency
What is it?
Histo
Affects on other organs 
Genetics
A

Misfolded gene products aggregate in hepatocellular ER –> cirrhosis
PAS + globules in liver
Panacinar emphysema because of decreased elastic tissue in lung
Codominant trait

272
Q

Jaundice
What is it?
What literally causes it
What conditions or processes can lead to it?

A

Yellow skin +/or sclera resulting from elevated bilirubin

Caused by Direct hepatocellular injury, Obstruction of bile flow, Hemolysis

273
Q

Hepatocellular Jaundice
Hyperbilirubinemia
Urine Bilirubin
Urine Urobilinogen

A

Direct/Indirect
Increased
Normal or Decreased

274
Q

Obstructive Jaundice
Hyperbilirubinemia
Urine Bilirubin
Urine Urobilinogen

A

Direct
Increased
Decreased

275
Q

Hemolytic Jaundice
Hyperbilirubinemia
Urine Bilirubin
Urine Urobilinogen

A

Indirect
Absent (acholuria)
Increased

276
Q

Physiologic Neonatal Jaundice
What causes it
Treatment

A

Immature UDP Glucuronyl transferase –> unconjugated hyperbilirubinemia –> jaundice/kernicterus
Phototherapy (converts UCB to water soluble form)

277
Q

Names of Hereditary Hyperbilirubinemias

A

Gilbert’s Syndrome
Crigler-Najjar Syndrome Type 1
Dubin Johnson Syndrome

278
Q 
Gilbert Syndrome 
What happens?
Presentation
Labs
Aggravation
Clinical Consequences?
A

Mildly decreased UDP-glucuronyl transferase –> decreased bilirubin uptake
Asymptomatic
Elevated unconjugated bilirubin w/o overt hemolysis
Bilirubin increases with fasting and stress
No clinical consequences

279
Q 
Crigler-Najjar Syndrome Type 1
What is it?
When does it present
Prognosis 
Findings 
Labs
Treatment
A 
Absent UDP-glucuronyl transferase
Presents in early life
Patients die within a few years 
Jaundice, kernicterus (bilirubin deposition in brain)
Increased unconjugated bilirubin 
Plasmapheresis and phototherapy
280
Q

Crigler Najjar Syndrome Type II
Severity
Treatment

A

Less severe form

Responds to phenobarbital which increases liver enzyme synthesis

281
Q 
Dubin Johnson Syndrome
What is it?
What is it due to?
Gross
Danger
A

Conjugated hyperbilirubinemia due to defective liver excretion
Grossly black liver
Benign

282
Q

Rotor’s Syndrome

A

Mild form of Dubin Johnson Syndrome that does not cause black liver

283
Q 
Wilson's Disease 
Mnemonic
AKA
MoA
What accumulates where?
Characterized by...
Treatment 
Genetics
A

“Copper is Hella BAD”
Hepatolenticular degeneration
Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin
Accumulates in Liver, Brain, Cornea, Kidneys, and Joints
Ceruloplasmin decreased, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular), Hemolytic anemia, Basal ganglia degeneration (parkinsonism), Asterixis, Dementia, Dyskinesia, Dysarthria
Penicillamine, Zn
Autsoomal recessive (chromosome 13)

284
Q

How is copper normally excreted?

A

ATPase (ATP7B gene) transports copper from hepatocytes into bile

285
Q 
Hemochromatosis 
Inheritance
What is it?
Presentation 
Can result in
Etiology 
Labs
Treatment
A

Autosomal recessive
Disease caused by iron deposition
Micronodular Cirrhosis, Diabetes Mellitus, Skin pigmentation (bronze diabetes)
Can result in CHF, testicular atrophy, hepatocellular carcinoma
Primary: autosomal recessive mutation of HFE gene (associated with HLA-A3)
Secondary: chronic transfusion therapy (e.g. beta thalassemia major)
Increased ferritin and iron. Decreased TIBC –> Increased transferrin saturation
Repeated phlebotomy, deferasirox, deferoxamine

286
Q 
Secondary Biliary Cirrhosis 
PathoPhys
Presentation
Labs
Complication
A

Extrahepatic biliary obstruction (gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head) –> Increased pressure in intrahepatic ducts –> Injury, Fibrosis, and Bile Stasis
Pruritus, jaundice, dark urine, light stool, hepatosplenomegaly
Increased conjugated bilirubin, cholesterol, and ALP
Complicated by ascending cholangitis

287
Q 
Primary Biliary Cirrhosis
PathoPhys
Histo
Presentation
Labs
Associations
A

Autoimmune reaction –> lymphocytic infiltrate + granulomas
Pruritus, jaundice, dark urine, light stool, hepatosplenomegaly
Increased conjugated bilirubin, cholesterol, and ALP
Also increased serum mitochondrial Abs including IgM
Associated with other autoimmune diseases (CREST, RH, Celiac)

288
Q 
Primary Sclerosing Cholangitis 
PathoPhys
Imaging
Presentation
Labs
Associations 
What can in lead to?
A

Unknown cause of concentric “onion skinning” bile duct fibrosis –> alternating strictures and dilation with beading of intra and extrahepatic bile ductrs on ERCP
Pruritus, jaundice, dark urine, light stool, hepatosplenomegaly
Increased conjugated bilirubin, cholesterol, and ALP
Hypergammaglobinemia (IgM)
Associated with UC
Can lead to secondary biliary cirrhosis

289
Q

Cholelithiasis
What causes them?
Risk factors?
Types

A

Increased cholesterol +/or bilirubin, Decreased bile salts, gallbladder stasis
4Fs: Fat, Female, Fertile (pregnant), and Forty
Cholesterol stones and Pigment stones

290
Q

Cholesterol stones
Frequency
Imaging?
Associated with

A

80% of stones
Radiolucent (10-20% opaque due to calcification)
Associated with Obesity, Crohn’s, CF, Age, Clofibrate, Estrogen, Multiparity, Rapid Wt Loss, Native American origin

291
Q 
Pigment Gallstones
Frequency
Imaging
Seen in patients with...
Color Re Etiology
A 
20%
Radiopaque 
Seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infection
Black - hemolysis
Brown - infection
292
Q 
Cholelithiasis 
What can it lead to?
Presentation?
When might the presentation be different?
Diagnosis 
Treatment
A

Cholecystitis, Ascending Cholangitis, Acute Pancreatitis, Bile Stasis, Biliary Colic (neurohormonal activation like CCK trigger contraction of gallbladder which forces stone into cystic duct)
Charcot’s Triad of Jaundice, Fever, RUQ Pain with a + Murphy’s sign (Inspiratory arrest on deep RUQ palpation)
Painless in diabetics
Diagnose with US, Radionuclide Biliary Scan
Cholecystectomy

293
Q

Possible Complication of Cholelithiasis

Image of this complication

A

Fistula between gallbladder and SI –> air in biliary tree

If gallstone obstructs ileocecal valve, air can be seen on the biliary tree on imaging

294
Q

Cholecystitis
What is it?
What causes it?
Labs

A

Inflammation of gallbladder
Usually from gallstones but can be caused by ischemia or infection (CMV)
Increased ALP if bile duct becomes involved (ascending cholangitis)

295
Q 
Acute Pancreatitis 
What is it?
What causes it?
Presentation
Labs
A

Autodigestion of pancreas by pancreatic enzymes
“GET SMASHED”
Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypercalcemia, Hypertriglyceridemia, ERCP, Drugs (Sulfa)
Epigastric pain radiating to the back, anorexia, nausea
Elevated amylase, lipase

296
Q

Acute Pancreatitis
What can it lead to?
Complications

A 
DIC, ARDS, Diffuse fat necrosis, Low Ca (collects in pancreatic soap deposits), pseudocysts, hemorrhage, infection, multiorgan failure 
Pancreatic pseudocyst (lined by granulation tissue, not epithelium) which can rupture and hemorrhage
297
Q 
Chronic Pancreatitis 
What is it?
What causes it?
What can it lead to?
Labs
A

Chronic inflammation, atrophy, and calcification of the pancreas
EtOH or idiopathic
Can lead to pancreatic insufficiency, DM, and adenocarcinoma
Amylase and Lipase are increased but less than in acute pancreatitis

298
Q 
Pancreatic Adenocarcinoma 
Prognosis
Arises from
Serum markers
Risk factors 
Presentation 
Treatment
A

Poor prognosis
Arises from ducts in pancreatic head
C-19-9 and CEA (less specific)
Tobacco, Chronic Pancreatitis, Age (>50), Jewish or Black
Abdominal pain radiating to back, Weight loss (malabsorption or anorexia), Trousseau’s Syndrome, Obstructive jaundice, Courvoisier’s sign
Whipple procedure, Chemo, Radiation

299
Q

Trousseau’s Sign

A

Migrating thrombophlebitis –> redness and tenderness to palpation of extremities

300
Q

Courvoisier’s Sign

A

Palpable, nontender gallbladder

301
Q 
H2 Blockers
Names
MoA
Use
Tox
A

Cimetidine, ranitidine, famotidine, nizatidine
“Take H2 when you need a table for 2 before you DINE”
–/ H2 resulting in decreased secretion of H by parietal cells
Peptic ulcer disease, gastritis, mild esophageal reflux
C –/ P450 (multiple drug interactions) and anti androgenic (prolactin release, gynecomastia, impotence, decreased libido in males). Crosses BBB (leading to confusion, dizziness, headache) and placenta
R and C decrease renal excretion of Cr

302
Q 
PPI
Names
MoA
Use
Tox
A

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole
Irreversible inhibition of H/K ATPase in Parietal cells
Peptic ulcer disease, gastritis, esophageal reflux, Zollinger Ellison Syndrome
Increased risk for C diff and pneumonia. Hip fractures, decreased serum Mg with long term use

303
Q

Bismuth, Sucralfate
MoA
Use

A

Binds to ulcer base, provides physical protection and allowing HCO3 secretion to reestablish pH gradient in mucous layer
Ulcer healing, travelers diarrhea

304
Q

Misoprostol
MoA
Use
Tox

A

PGE analog –> increased production and secretion of gastric mucous barrier + decreased acid production
Prevention of NSAID-induced peptic ulcers; maintenance of ductus arteriosus; labor induction (ripens cervix)
Diarrhea, Abortifacient

305
Q

Octreotide
MoA
Use
Tox

A

Somatostatin analog
Acute variceal bleeds, acromegaly, VIPoma, carcinoid tumor
Nausea, cramps, steatorrhea

306
Q

Antacids
Names
Use
Tox

A

Aluminum Hydroxide, Magnesium Hydroxide, Calcium Carbonate
Can affect absorption, bioavailability, or urinary excretion or other drugs by altering gastric and urinary pH or delaying gastric emptying
All: HypoK
Al: Constipation (aluMINIMUM amount of feces), HypoPhosphatemia, proximal muscle weakness, osteodystrophy, seizures
Mg: Diarrhea (Must Go to Bathroom), Hypoflexia, Hypotension, Cardiac Arrest
Ca: HyperCa, Rebound acid increase, can chelate other drugs (tetracycline)

307
Q 
Osmotic Laxatives 
Names
MoA
Use
Tox
A

Mg Hydroxide, Mg Citrate, Polyethylene Glycol, Lactulose
Osmotic load to draw out water
L can be used to treat hepatic encephalopathy since gut flora degreate it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4
Use: Constipation
Tox: Diarrhea, dehydration, Abuse by bulimics

308
Q

Inflximab
MoA
Use
Tox

A

Anti TNF Ab
CD, UC, RA
Infection (TB), fever, hypotension

309
Q 
Sulfasalazine 
MoA
Activation
Use
Tox
A

Combination of sulfapyridine (antibacterial), 5-aminosalicylic acid (anti-inflammatory)
Activated by colonic bacteria
UC, CD
Malaise, nausea, Sulfonamide tox, reversible oligospermia

310
Q

Ondansetron
MoA
Use
Tox

A

5HT antagonist = powerful central acting antiemetic “Keep on dancing”
Control vomiting post-op and during chemo
Headache, constipation

311
Q 
Metoclopramide 
MoA
Use
Tox
Contraindications
A

D2 antagonist, Increases resting tone, contractility, LES tone, motility. Does not influence colon transit time
Diabetic and post-surgery gastroparesis, antiemetic
Increased Parkinsonian effect, restlessness, drowsiness, depression, nausea, diarrhea, Interaction with digoxin and diabetic agents.
Contraindicated in pts with small bowel obstruction and PD

312
Q 
Iron Transport, Storage and Regulation 
Ferritin
Transferrin 
Transferrin Receptor
Regulation
A

Ferritin stores Iron in cells (esp liver and kidney). Has IRE in 5’ UTR
Transferrin transports iron in the blood. Has IRE in 3’ UTR
Transferrin Receptor allows iron to enter cells
Regulated at level of translation
Low Fe –> IRP binds UTRs and F is blocked and T is stabilized
High Fe –> IRP cannot bind and F is translated and T is destabilized

313
Q

Muscles That Make Up the Upper Esophageal Sphincter

A

Inferior Constrictor and Cricopharyngeus

314
Q

Protein absorption in small intestine
What can move across apical surface? Via what transporters?
What can move across basolateral surface?

A

AA, dipeptides and tripeptides can move across apical surface.
AA with Na and dis and tris with H+
Only AA can move across basolateral surface

315
Q

Electrolyte transport in Jejunum
Na?
H?
HCO3?

A

Na absorbed with sugars and AA and in exchange for H

Bicarb transported out of cell on basolateral surface into blood

316
Q 
Electrolyte transport in Ileum 
Na?
H?
HCO3?
Cl?
A

Na absorbed with sugars and AA and in exchange for H

Bicarb transported out of cell on apical surface into lumen in exchange for Cl

317
Q

Electrolyte transport in Colon epithelium
Na
K
Regulation

A

Na channels absorb Na
K channels secrete K
Aldosterone upregulates both channels and the Na/K ATPase

318
Q 
Electrolyte transport in Colon crypts 
What happens net?
Basolateral transporters
Apical transporters 
Regulation 
Pathology
A

Net secretion
Na/K ATPase and NaK2Cl cotransporter basolaterally
Cl channel apically
VIP, ACh and other hormones –> cAMP –> Cl Channels
Cholera toxin –> α of G protein –> cAMP –> Cl channels inappropriately open –> Na and water follow

319
Q

How does EtOH cause acute pancreatitis?

A

EtOH –> Ca –> trypsin

320
Q

Hereditary Hemochromatosis Type 1 PathoPhys

A

HFE (chromosome 6) regulates hepcidin
Hepcidin is released by the liver when Iron is high to stop absorption of Fe (blocks Ferroportin channel which allows Fe to enter circulation)
In HHT1, Hepcidin is not produced

USMLE (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions