Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

STEP > GI > Flashcards

GI Flashcards

1
Q

Foregut becomes

A

Esophagus to upper duodenum

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

Midgut becomes

A

Lower duodenum to prox 2/3 transverse colon

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

Hindgut becomes

A

Distal 1.3 of transverse colon to anal canal over pectinate line

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

Midgut herniates at…

A

6wks

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

Midgut returns to cavity and rotates around SMA at…

A

10 wks

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

Degree rotation of midgut

A

270

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

Rostral fold closure defect–>

A

Sternal defect (ectopic cordis)

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

Lateral fold closure defect–>

A

Omphalocele and gastroschisis

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

Caudal fold closure defect–>

A

Bladder extrophy

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

Gastroschisis

A

Abdomen contents extrude through abdominal folds (usually rt of umbilius) – no covering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Omphalocele

A

Persistent herniation of abdomen contents into umbility cord – SEALED by peritoneum

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

Congenital umbility hernia

A

Incomplete closure of umbilical ring - can close spontaneously

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

Most common tracheoesophageal abnormality

A

Esophageal atresia w/ distal TEF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Esophageal atresia w/ distal TEF symptoms

A

Polyhydramnios (can’t swallow), drool/choke/vomit at first feeding, air in stomach, cyanosis due to reflux mediated larygospasm, cannot pass nasogastric tube into stomach

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

Pure EA presentation

A

CXR – gasless abdomen

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

Intestinal atresia presentation

A

Billious vom and abdominal distension w/ first 1-2 days of life

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

Duodenal atresia

A

Didn’t recanalize! Double bubble (dilates stomach, prox duodenum), DS association

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

Jejunal and ileal atresia

A

Disruption of mesenteric vessels, ischemic necrosis, segmental resorption (bowel discontinuity/apple peel)

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

Most common gastric outlet obstrxn in infants

A

Hypertrophic pyloric stenosis – palpable olive shaped mass at epigastric region, visible peristaltic waves, nonbiliious projective vom at 2-6 wks
First born male assc, macrolide exposure
Results in hypokalemic hypochloremia metabolic alkalosis (2o to vom and volume contraction
Tx: incision pyloromyotomy

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

Pancreas derivation

A

Foregut

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

Ventral pancreatic buds –>

A

Uncinate process and main pancreatic ducts

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

Dorsal pancreatic bud–>

A

Body, tail, isthmus, accessory pan duct – both cont to pancreatic head

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

Annular pancreas

A

Ventral bud encircles 2nd part of duoedenum -> ring of pancreatic tissue can cause obstruction

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

Pancreas divisum

A

Ventral and dorsal dont fuse at 8 wks – common, usually asymptomatic but can cause chronic abdominal pain/pancreatitis

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

Spleen arises in…

A

Mesentery of stomach

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

Spleen derivation

A

Mesodermal

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

Spleen blood supply

A

Celiac truck –> splenic a.

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

Retroperitoneal stuctures defined

A

GI structures w/ no messentery and non GI structures

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

Injuries to retroperitoneal structures ->

A 
Suprarenal glands (adrneal)
Aorta and IVC
Duodenum (2-4 parts)
Pancreas (except tail)
Ureters
Colon (Descending and ascending)
Kidneys
Esophagus (thoracic)
Rectum (partial)

SAD PUCKER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Falciform ligament

A

Connects liver –> ant abdominal wall, has ligamentum teres hepatis in it

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

Falciform ligament derivation

A

Ventral mesentery

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

Ligatmentum teres hepatis derivation

A

Fetal umbilical v

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

Hepatoduodenal ligament

A

Connects liver–>duodenum

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

In the hepatoduodenal ligament…

A

Portal triad – proper hep a, portal v., common bile duct

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

Pringle maneuver

A

Compress ligament between thumb/index finger in omental foramen to control bleeding

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

Gastrohepatic ligament

A

Connects liver to lesser curvature of stomach

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

Contents of gastrohepatic ligament

A

Gastric arteries

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

Separates greater/lesser sacs on the right

A

Gastrohepatic ligament

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

Lesser omentum ligamnets

A

Hepatoduodenal, gastrohepatic

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

Gastrocolic

A

Connects greater curvature and transverse colon

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

Within gastrocolic

A

Gastroepiploic aas.

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

Greater omentum ligatments

A

Gastrocolic, gastrosplenic

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

Gastroc splenic

A

Connects greater curvature and spleen

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

Contents of gastrosplenic

A

Short gastrics, left gastroepiploic vessels

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

Separates greater/lesser sac on the left

A

Gastrosplenic lig

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

Splenorenal ligament

A

Spleen to post ab wall

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

Splenorenal lig contents

A

Splenic a and v, tail of pancreas

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

Serosa

A

Intraperitoneal

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

Adventitia

A

Retroperitoneal

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

Ulcer

A

Extend into submucosa, muscle layers

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

Erosion

A

Mucosa only

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

Freq of stomach basal waves

A

3/min

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

Freq of duodenal basal waves

A

12/min

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

Freq of ileal basacl waves

A

8-9/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Brunner glands

A

Secrete HCO3, in submucosa of duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Crypts of Lieberkuhn

A

Have stem cells to replace enterocytes/goblet cells; in small intestine and colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Paneth cells

A

Secrete defensins, lysozyme, TNF – duodenal

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

Plicae circulares

A

In distal duodenum, jejunum, ileum

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

Peyer patches

A

Lymphoid aggs in lamina propia, submucosa – ileum

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

Villi are in…

A

SI but not colon

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

Colon has many

A

Goblet cells

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

SMA syndrome

A

Intermittent intestinal obstruction sx (postprandial pain) when transverse (3rd portion duodenum) is compressed between SMA and aorta – usually in conditions w/ diminished mesenteric fat (e.g. low body wt, malnutrition)

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

Forgut artery

A

Celiac

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

Foregut PNS

A

Vagus

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

Foregut vertebral level

A

T12/L1

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

Foregut structures

A

Pharynx (vagus only), lower esophagus (celiac a only) to prox duodenum, liver, gallbladder, pancreas, spleen (mesoderm)

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

Midgut artery

A

SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Midgut PNS innervation

A

Vagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Midgut vertebral level

A

L1

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

Midgut structures

A

Distal duodenum to prox 2/3 transverse colon

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

Hindgut artery

A

IMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Hindgut PNS

A

Pelvic

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

Hindgut vertebral level

A

L3

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

Hindgut structures

A

Distal 1/3 transverse colon to upper portion of rectum

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

T12 arteries

A

inf Phrenic, Sup suprarenal, mid supraprenal, celiac

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

L1 aa’s

A

SMA, Inf suprarenal, half renal

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

L2 aas

A

Half renal, gonadal

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

L3 aas

A

IMA

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

L4…

A

Bifurcation

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

L5 aas

A

Right/left common iliac, int iliac, median sacral

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

Celiac trunk branches

A

Common hepatic, splenic, lft gastric

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

Anastamoses at…

A

Left/right gastroepiploics, lft/right gastrics

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

Post duodenal ulcers–>

A

Pentrate gastroduocenal a –>hemorrhage

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

Ant duodenal ulcer–>

A

Pneumoperitoneum

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

Anastamoses sites

A

Esophagus, umbilicus, rectum

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

Esophageal portal/systemic

A

Lft gastric/azygos

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

Umbilical portal/system

A

Paraumbilical/small epigastric vvs of ant. abdominal wall

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

Rectal portal/systemic

A

Sup rectal/inf. and middle rectal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Tx of portal HTN and complication

A

TIPS hepatic v and portal v shunt but can cause hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Pectinate line

A

Endoderm of hindgut meets ectoderm

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

Above pectinate line – a, v, l, what can go wrong

A

IMA branch – sup. rectal a
Drained by sup rectal v –> IMV –>splenic v–>portal v
Internal iliac lymphatic drainage
Internal hemorrhoids (not painful – visceral innervation, adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Below pectinate line – a, v, l, what can go wrong

A

Inf rectal a. (branch of int. pudendal)
Inf rectal v –>int. pudendal v.–>int iliac v.–> common iliac v–>IVC
Superficial inguinal lymph nodes
Ext. hemorrhoids (painful if thrombose – innervated somatically by inf. rectal branch of int. pudendal n), anal fissures, squamous cell carcinoma

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

Anal fissue

A

Tear in anal mucosa below pectinate line –> pain while pooping, blood on TP – located posteriorly because poor perfusion
Assc. low-fiber diets and constipatioin

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

Stellate cells in liver

A

Store vit A when quiescent

Produce ECM when activated

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

Zone I

A

Periportal – affected 1st by viral hepatitis and ingested toxins (e.g. cocaine)

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

Zone II

A

Intermediate zone – yellow fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Zone III

A

Pericentral vein/centrilobular – affected 1st by ischemia, contains P450 – most sensitive to metabolic toxins, alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Site of gallstone lodging to cause double duct sign

A

Confluence of common bile and pancreatic ducts at the ampulla of Vater –> cholangitis and pancreatitis

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

Tumors in head of pancreas

A

Most often ductal adenocarcinoma –> obstruction of CBD –> large gallbladder, painless jaundice (Courvosier sign)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Femoral triangle

A

Femoral n, a, v

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Femoral sheath

A

Femoral a, v and canacl (deep inguinal lymph nodes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Indirect inguinal hernia –

A

Through internal (deep) inguinal ring, external and into scrotum
Enters inguinal ring LATERAL to inf epigastric vessels
Infants – no closure of processus vaginalis (can form hydrocele)
MALES
Covered by all 3 payers of spermatic fascia and follows descent of testes

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

Laters of fascia on spermatic cord

A

Internal spermatic fascia (transversalis fascia)
Creamasteric muscle/fascia (int. oblique)
External spermatic fascia (Ext. oblique)

ICE TIE

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

Direct inguinal hernia

A

Protrues through inguinal (Hesselbach) triangle – bulges directly through parietal peritoneum MEDIAL to inf epigastric vvs but lateral to rectus abdominis
Goes through external/superficial inguinal ring onlly
Covered by external spermatic fascia
Older men – acquired weakness in transversalis fascia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Femoral hernia

A

Protrudes below inquinal ligament though femoral canal below/lateral to pubic tubercle
FEMALES! (but overall inguinal most common)
More likely to have incarceration or strangulation

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

Hesselbach tirangle

A

Inf epigastric vessels
Lat border of rectus abdominus
Inguinal ligament

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

Gastrin source and location

A

G cells in antrum of stomach, duodenum

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

Actinon of gastrin

A

Increase gastric H secretion, growth of gastric mucosa, motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Gastrin regulation

A

Increased by stomach distension/alkalinization, amino acids, peptides, vagal stim via GRP

Lowered by low pH (<1.5)

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

Gastrin is increased in which syndromes/drugs

A

PPI, chronic atrophic gastritis (H pylori), Z-E syndrome (gastrinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Somatostatin source and location

A

D cells in pancreas and GI mucosa

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

Action of somatostatin

A

Lower gastric acid/pepsinogen secretion, pancreatic/small intestine fluid secretion, gallbladder contraction, insulin/glucagon release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Regulation of somatostatin

A

Increased by acid, decreased by vagal stim

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

Cholecystokinin source and location

A

I cells in duodenum and jejunum

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

CCK action

A

Increases pancreatic secretion (via neural muscarinic pathways), gallbladder contraction, sphincter of Oddie relaxation
Decreases gastric emptying

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

CCK regulation

A

Increased by fatty acids and amino acids

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

Secretin source and location

A

S cells in duodenum

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

Secretin action

A

INcreases pancreatic bicarb secretion (lowers pH so pancreatic enzymes fxn) and bile secretion
Decreases gastric acid secretion

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

Secretin regulation

A

Increased by acid, fatty acids in lumen of duodenum

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

Glucose dependent insulinotropic peptide source/location

A

K cells in duodenum and jejunum

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

Exocrine fxn of GIP

A

Lower gastric H secretion

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

Endocrine fxn of GIP

A

Increased insulin release

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

GIp regulation

A

Increased by fatty acids, amino acids, oral glucose

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

Motilin source

A

Small intestine

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

Motilin action

A

Produces migrating motor complexes

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

Motilin regulation

A

Increased in fastin state

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

Motilin receptor agonists

A

Erythromycin – can stimulate intestinal peristalsis

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

VIP source

A

Parasympathetic ganglia in sphincters, gallbladder, small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

VIP action

A

Increase intestinal water and electrolyte secretion, as well as relxation of intestinal smooth muscle/sphincters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Regulation of VIP

A

Increased by distension and vagal stim

Lowered by adrenergic input

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

VIPoma

A

non alpha or beta islet cell pancreatic tumor –> secretes VIP –> Watery Diarrhea, Hypokalemia, Achlorhydria syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

NO action

A

Relaxes smooth muscle, including lower esophageal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

NO in achalasia

A

Lower NO secretion–> increased LES tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Ghrelin source

A

Stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Ghrelin action

A

Increase appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Ghrelin regulation

A

Increased in fasting state

Decreased by food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Ghrelin is increased in

A

Prader Willi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Ghrelin is decreased in

A

Post-gastric bypass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Intrinsic factor source and location

A

Parietal cells in stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Action of IF

A

Binds B12 for uptake in terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Pernicious anemia pathophys

A

Autoimmune destruction of parietal cells–>chronic gastritis and pernicious anemia from low B12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Gastric acid source/location

A

Parietal cells in stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Action of gastric acid

A

Lower stomach pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Gastric acid is increased by

A

Histamine, ACh, gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Gastric acid decreased by

A

Somatostatin, GIP, prostaglandin, secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Pepsin source and location

A

Chief cells in stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Pepsin action

A

Protein digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Pepsin regulation

A

INcreased by vagal stim and local acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What activates pepsinogen

A

H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Bicarb source and location

A

Mucosal cells in stomach/duodenum/salivary glands/pancreas

Brunner glands in duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Bicarb action

A

Acid neutralization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Bicarb regulation

A

Increased by panctreatic/biliary secretion w/ secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Main method of gastrin mediated acid secretion

A

+ on ECL –> Histamine –> + on parietal cells –> H+ (indirect – also works direct but this is more of the primary effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

WHen pancreas senses low flow

A

More Cl- secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

When pancreas senses high flow

A

More HCO3 secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Alpha amylase

A

Starch digestion – secreted active by pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Lipases

A

Secreted by pancreas for fat digestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Proteases

A

Protein digestion enzymes trypsin, chymotripsin, elastase, carboxypeptidases secreted by pancreas as zymogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Trypsinogen

A

First converted by brunch border enteropeptidase in duodenum and jejunal mucoase – cleaved to be activated and cleaves more enzymes and itself – secreted by pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Carb absorption

A

Must be monosaccharides
SGLT1 (Na dependent – glucose and galactose)
GLUT5 (fructose – facilitated diffusion)
Blood transported via GLUT2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Fe absorbed

A

Fe2+ in duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Folate absorption

A

Small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

B12 absorption

A

Terminal ileum w/ bile salts, req IF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Peyer patches – capsule?

A

Nope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Peyer patches found

A

Malmina propria and submucosa of ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Fxn of M cells

A

Sample/present ags to immune cells in peyer patches –> IgA plama cells which ultimately reside in LP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Bile composition

A

Bile salts (bile acids conjugate to glycine or taurine to be water soluble), pospholipids, cholesterol, bilirubin, water, ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Rate limiting step of bile acid synthesis

A

Catalyzed by cholesterol 7a hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Fxns of bile

A

Digest/absorb lipids and fat soluble vitamins, cholesterol excretion (primary method), antimibrobial (membrane disruption)

170
Q

Heme–>biliverdin enzyme

A

Heme oxygenase

171
Q

Biliverdin–>

172
Q

Unconjugated bilirubin–>

A

removed from blood by liver–> conjugated w/ glucuronate –> excreted in bile

173
Q

Direct bilirubin=

A

Conjugated –water soluble

174
Q

Indirect bilirubin

A

Unconjugate –water insoluble

175
Q

Conjugation of bilirubin enzyme

A

UDL glucouronosyl transferase

176
Q

Suggestion of malignancy in salivary gland tumor

A

Smaller glands, facial pain or paralysis (involvedment of CN7)

177
Q

Pleomorphic adenoma

A

Benign mixed tumor – most common; chondromyxoid stroma/epithelium and recurs if incompletely excised or ruptured intraoperatively

178
Q

Mucoepidermoid carcinoma

A

Most common malignant tumor – mucinous and squamous components

179
Q

Warthin tumor

A

Papillary cystadenoma lymphomatosum – benign cystic tumor w/ germinal centers typically in smokers, can be bilateral/malignant (10%)

180
Q

Cause of achalasia

A

Lost of myenteric (Auerbach plexus)–> lost of post ganglionic inhibitory neurons w/ NO and VIP –> failure of LES to relax/uncoordinated/absent peristalsis–>progressive dysphagis to solids and liquirds

181
Q

Achalasia imagin

A

Dilated esophagus and are aof distal stenosis – birds beak

182
Q

Achalasia assocation

A

Increased risk of esophageal cancer, can arise 2o to Chagas diease or extra esophageal malignancies (mass effect or paraneoplastic)

183
Q

Boerhaave syndrome

A

Transmural usually distal esophageal rupture w/ pneumomediastinum due to biolent retching – may detect subcutaneous emphysema due to dissecting air w/ crepitus in neck or chest wall – surgical emergency

184
Q

Eosinophilic esophagitis

A

Infilitration of eos in the esophagus in atopic patients; food allergy–>dysphagia/food impaction; see esophageal rings and linear furrows on endoscopy and will be unresponsive to GERD therapy

185
Q

Esophageal strictures assocatiation

A

Caustic ingestion and acid reflux

186
Q

Esophageal varices

A

Dilated submucosa vvs in lower 1/3 of esophagus due to portal HTN – common in cirrhosis and may cause life threatening hematemesis

187
Q

Esophagitis associations

A

Reflux, infxn in immunocompromised (candida, HSV, CMV), caustic ingestion or pill esophagitis (bisphosphonates, tetracycline, NSAIDs, iron, KCl)

188
Q

Candida esophagitis

A

White pseudomembrane (immunocompromised)

189
Q

HSV 1 esophagitis

A

Punched out ulcers (immunocompromised)

190
Q

CMV esophagitis

A

Linear ulcers (immunocompromised)

191
Q

GERD

A

Heartburn, regurg, dysphagia, chronic cough, hoarseness (laryngopharyngeal reflux) due ot transient decrease in LES tone

192
Q

GERD assocation

193
Q

Mallory Weiss syndrome

A

Partial thickness mucosal lacerations at GE jxn due to severe vomiting –> hematemesis – alcoholics and bulemics

194
Q

Plummer Vinson

A

Dysphagia, Iron deficiency anemia, Esophageal webs – can be associated w/ glossitis; higher risk of esophageal SCC
“Plumbers DIE”

195
Q

Sclerodermal esophageal dysmotility

A

Esophageal smooth muscle atrophy –> lower LES pressure and dysmotility –> acid reflux/dysphagia –> stricture, Barrett esophagus, aspiration
Part of CREST

196
Q

Barrett Esophagus

A

Intestinal metaplasia in previously nonkeratinized strat squamous epithelium in esophagus due to chronic GERD –> increased risk of esophageal ADENOcarcinoma

197
Q

Intestinal metaplasia

A

Nonciliated columnar w/ goblet cells

198
Q

Presentation of esophageal cancer

A

Progressive dysphagia starting w/ solids, wt loss, poor prognosis

199
Q

SCC of esophagus location

A

Upper 2/3 esophagus

200
Q

SCC of esophagus risk factors

A

Alcohol, hot liquires, caustic strictures, smoking, achalasia

201
Q

Adenocarcinoma of esophagus location

202
Q

Adenocarcimona risk factors

A

GERD, Barrett esophagus, obesity, smoking, achalasia

203
Q

Prevalence of esophageal cancers

A

SCC more worldwide but adeno more in America

204
Q

Cause of erosions (acute gastritis)

A

NSAIDs –> less PGE2–>less gastric mucosa protection
Burns (curling ulcer) hypovolemia–>mucosal ischemia
Brain injury (Cushing ulcer) – more vagal stim–> more ACh–>more H prodxn

205
Q

Chronis gstritis

A

Mucosal inflamation –> atrophy (hypochlorhydria–>hypergastrinemia) and intestinal G cell metaplasia (higher risk of gastric cancers)

206
Q

H pylori

A

Most common chronic gastritis; increased risk of PUD, MALT lymphoma – antrom first and spreads to body

207
Q

Autoimmune chronic gastritis

A

Autoabs to parietal cells and IF –> higher risk of pernicious anemia; affects body/fundus of stomach

208
Q

Menetrier disease

A

Hyperplasia of gastric mucosa –> hypertrophied rugae (look like brain gyri), excess mucus and protein loss/parietal cell atrophy –> less acid production
Precancerous

209
Q

Gastric cancer most common

A

Gastric adenocarinoma

210
Q

Signs of gastric cancer

A

Usually present late – wt loss, early satiety, acanthosis nigricans or Leser Trelat

211
Q

Instestinal gastric cancer associations

A

H pylori, dietary nitrosamines, tobacco smoking, achorhydria, chronic gastritis

212
Q

Intestinal gastric cancer most commonly located

A

Lesser curvature (ulcer w/ raised margins)

213
Q

Diffuse gastric cancer histology

A

Signet ring cells

214
Q

Diffuse gastric cancer grossly

A

Stomach wall grossly thickend and leathery (linitus plastica)

215
Q

Virchow node

A

Left suprclavicular spread from gastric metastatses

216
Q

Krukenberg tumor

A

Bilateral ovarian metastatses in diffuse CA

217
Q

Sister mary joseph nodule

A

Subcutaneous periumbilical metastatsis

218
Q

Gastric ulcer pain

A

Made greater w/ meals –> wt loss

219
Q

Gastric ulcer causes

A

H pylori, NSAIDs

220
Q

Gastric ulcer cause

A

Less mucosal protection against gastric acid

221
Q

Duodenal ulcer pain

A

Less w/ meals –> weight gain

222
Q

Mechanism of duodenal ulcer

A

Less mucosal protection or increased gastric acid secretion

223
Q

Causes of duodenal ulcer

A

H pylori or ZE syndrome

224
Q

Seen in duodenal ulcer

A

Hypertrophy of Brunner glands

225
Q

Complications of ulcers

A

Hemorrhage (gastric or duodenal (post>ant), obstruction (pyloric channel, duodenal) perforation (duodenal – ant>post)

226
Q

Lesser curvature ulcer hemorrhage–>

A

Bleeding from lft gastric a

227
Q

Duodenal post. hemorrhage–>

A

Bleeding form gastroduodenal a

228
Q

Duodenal ulcer –>perforation –> sx

A

Free air under diaphragm w/ referred pain to shoulder via phrenic n irritation

229
Q

In celiac disease, autoimmune mediated intolerance of…

A

Gliadin (gluten protein found in wheat)

230
Q

HLA w/ celiac

A

HLA DQ2, DQ8

231
Q

Seen in celiac disease

A

European descent, dermatitis herpetiformis, lower bone density, IgA TTG, antiendomysial and anti deamidated gliadin peptide abs
Histology: villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis
Increased risk of T cell lymphoma
Mucosal malabsorption primary affects distal duodenum/proximal jejunum

232
Q

D xylose test

A

Passively absorbed in prox SI – blood and urine levels decrease w mucosa defects or bacterial overgrowth, normal in pancreatic inufficiency

233
Q

Lactose intolerance causes

A

Lactase deficiency – viral or acquired

234
Q

Histology/labs in lactose intolerance

A

Normal appearing villi (except when 2o injury at tips due to viral enteritis –> osmotic diarrhea w/ low stool pH (colonic bacteria ferment); lactose hydrogen breath test (pos for lactos malabsorption if postlactose breath hydrogen rises > 20 ppm compared to baseline)

235
Q

Pancreatic insufficiency causes

A

Chronic pancreatitis, CF< obstructive cancer

236
Q

Pancreatic insufficiency results in

A

Malabsorption of fat/fat soluble vitamins (ADEK) and B12 – low duodenal pH (bicarb) and fecal elastase

237
Q

Tropical sprue

A

Like celiac sprue but respons to Abx -

238
Q

Whipple disease bug

A

Tropheryma whipplei – PAS +

239
Q

Whipple disease histology

A

PAS foamy macrophages in lamina propia and mesenteric nodes

240
Q

Signs of Whipple disease

A

Cardiac symptoms, Arthralgias, Neuro symptoms, later –> diarrhea/steatorrhea

241
Q

Whpple disease demographic

242
Q

Crjohn disease location

A

Any part of GI tract – usually terminal ileum and colon w/ skip lesion and rectal sparing

243
Q

Grossly Crohn disease

A

Transmural inflamm –> fistula, cobblestone mucosa, creeping fat, bowel wall thickening (string sign on barium swallow), linear ulcers, fissure

244
Q

Microscopic Crohns

A

Moncaseating granulomas and lymphoid aggregates – Th1 mediated

245
Q

Complications of Crohn

A

Malabsorption/malnutrition, colorectal cancer, fistulas (enterovesicular –> recurrent UTI, pneumaturia), phlemon/abcess, strictures (–>obstruction), perianal disease

246
Q

Crohn disease diarrhea

A

Bloody or nah

247
Q

Extraintestinal manifestations common to both IBDs

A

Rash (pyoderma gangrenosum, erythema nodosum), eye inflammation (episcleritis, uveitis), oral ulcers (apthous stomatitis), arhtritis (peripheral, spondylitis)

248
Q

Crohn specific extraintestinal manifestations

A

Kidney stones (Ca oxalate), gallstones, may have positive anti Saccharomyces cervisiae abs (ASCA)

249
Q

Tx of Crohns

A

Corticosteroids, AZA, abx (cipro, metro), infliximab, adalimumab

250
Q

Ulcerative colitis location

A

Continuous from rectum up (not past end of colon)

251
Q

Grossly ulcerative colitis

A

Mucosal and submucosal inflam only – firable mucosa w/ superficial/deep ulcerations, loss of haustra (lead pipe appearance on imaging)

252
Q

Histology of UC

A

Crypt abcesses and ulcers, bleeding, no granulomas, Th2 mediated

253
Q

Complications of UC

A

Malabsorption/malnutrition, colorectal CA 9increased risk w pancolitis), fulminant colitis, toxic megacolon, perf

254
Q

Diarrhea in UC

A

Always bloody

255
Q

UC specific extraintestinal manifestations

A

1o sclerosing cholangitis (pANCA)

256
Q

Tx of UC

A

5ASA preps (mesalamine), 6MP, infliximab, colectomy

257
Q

IBS

A 
Recurrent abdominal pain w/ 2+:
- Related to defecation
-Change in stool freq
-Chain in form (consistency) of stool
w/ no structural abnormalities
Can be diarrhea predom, constipation predom, or mix
258
Q

IBS demographic

A

Middle aged women

259
Q

Appedicitis most common cause

A

Kids: lymphoid hyperplasia
Adults: fecalith

260
Q

Complication of appendicits

A

Perf–>peritonitis

261
Q

Buzzwords for appendicits

A

McBurney’s point pain, posas, obturator, Rovsing signs

262
Q

True diverticulum

A

All 3 gut wall layers outpouch (meckl)

263
Q

False diverticulum

A

Only mucosa and submucosa outpouch (esp where vasa recta perforate muscularis externa)

264
Q

Diverticulosis

A

Many false diverticula of colon, commonly in sigmoid

265
Q

Diverticulosis cause

A

Increased intraluminal pressure and focal weakness in colonic wall, low fiber diets

266
Q

Complications of diverticulosis

A

Diverticular bleeding (painless hematochezia) or diverticulitis

267
Q

Diverticulitis

A

Inflammation fo diverticula – LLQ pain, fever, leukocytosis (tx w/ abx)

268
Q

Diverticulitis complications

A

Abscess, fistula (colovesical–>pneumaturia), obstruction (inflammatory stenosis), perf –>peritonitis

269
Q

Zenker diverticulum

A

Pharyngoesophageal false diverticulum – esophageal dysmotility –> herniation of mucosa at Killian triangle vtween thyropharyngeal and cricopharygeal parts of inf pharyngeal contricture –> dysphagia, obstruction, gurgling, aspiration, foul breath, neck mass (usually elderly males)

270
Q

Meckle diverticulum

A

True diverticulum – persistence of vitellin duct, may contain ectopic acid secreting gastric mucosa +/- pancreatic tissue; most common congenital anomaly of GI tract –> hematochezia/melena, RLQ pain, intussusception, volvulus, obstruction near terminal ileum

271
Q

Omphalomestnteric cycst

A

Cystic dilation of vitelline duct

272
Q

Diagnose meckel diverticulum

A

Pertechnetate study for uptake by ectopic gastric mucosa

273
Q

Rule of 2s in Meckle’s

A

2x more likely in males, 2 inches long, 2 feet from ileocecal vavle, 2% of population, presents in first 2 years of life, 2 types of epithelia

274
Q

Hirschprung disease

A

Congenital megacolon due to lack of ganglion cells/enteric nervous plexuses (Auerbach, Meissner) in distal colon due to failure of neural crest migration

275
Q

Hirschprung genetics

A

RET mutations, higher in DS

276
Q

Presentation of Hirschprung

A

Bilious emesis, abdominal distention/failure to pass meconium w/in 48 hrs –> chronic constipation; explosive expulsion of feces (squirt sign) –> empty rectum on digital exam

277
Q

Hirschsprung diagnosis

A

Rectal suctino biopsy

278
Q

Malrotation

A

Anomaly of midgut rotation during fetal development –> improper position of bowel, formation of fibrous bands (Ladd bands)

279
Q

Malrotation complications

A

Volvulus, duodenal obstruction

280
Q

Volvulus

A

Twisting of part of bowel around its mesentary –> obstruction or infactrion

281
Q

Common volvulus in kids

282
Q

Elderly volvulus

A

Sigmoid (coffee bean)

283
Q

Intussusception

A

Telescoping of prox bowel into distal – usually at ileocecal jxn –> compromised blood supply –> abdominal pain w/ currant jelly stools

284
Q

Cause of intussusception in adults

A

Intraluminal mass or tumor

285
Q

Most common lead point in intussuception

A

Meckel diverticulum (usually kids)

286
Q

Associations w/ intussusception

A

Recent viral infxn (adenovirus –> Peyer patch hypertrophy –> lead point; rotavirus vax

287
Q

Acute mesenteric ischemia

A

Critical blockage of intestinal blood flow (often embolic occlusion of SMA) –> SI necrosis –> abdominal pain out of proportion to physical findings, may see current jelly stools

288
Q

Chronic mesenteric ischemia

A

Intestinal angina – atherosclerosis of celiac a, SMA, IMA –> intestinal hypoperfusion –> posprandial epigastric pain –> food aversion/wt loss

289
Q

Colonic ischemia

A

Reduction in intestinal blood flow –> ischemia –> crampy abdominal pain followed by hematochexia

290
Q

Location of colonic ischemia

A

Watershed areas (splenic flexure, distal colon)

291
Q

Colonic ischemia demographics

292
Q

Clonoic ischemia imaging

A

Thumbprint sign due to mucosal edema/hemorrhage

293
Q

Angiodysplasia

A

Tortuous dilation of vessels –>hematochezia; confirmed by angiography

294
Q

Angiodysplasia location

295
Q

Angiodysplasia demographics

296
Q

Adhesion

A

Fibrous band of scar tissue, commonly after surgery –> most common cause of SI obstruction, can have well demarkated necrotic zones

297
Q

Ileus

A

Intestinal mypomotility w/o obstruction –> constipation and less flatus

298
Q

Presentation of ileus

A

Constipation, less flatus, distended/tympanic abdomen w/ less bowel sounds

299
Q

Associations w/ ileus

A

Abdominal surgeries, opiates, hypokaemia, sepsis,

300
Q

Tx of ileus

A

Bowel rest, electrolyte correction, cholinergic drugs (stim intestinal motility)

301
Q

Meconium ileus

A

In CF – meconium plub obstructs intesting preventing stool passage at birth

302
Q

Necrotizing enterocolitis

A

Premature forumla fed infants w/ immature immune system – necrosis of intestinal mucosa (esp colonic) w/ possible perfs –> pneumatosis intestinalis, free air in abdomen, portal venous gas

303
Q

Hamartmoatous polyps

A

Generally non neoplastic and solitary – growths of normal colonic tissue w/ distorteed architecture

304
Q

Associated with hamartomatous polyps

A

Peutz-Jeghers, juvenile polyposis

305
Q

Mucosal polyps

A

Small, less than 5 mm, look similar to normal, clinically insignificant (non neoplastic)

306
Q

Inflammatory pseudopolyps

A

Result of mucosal erosion in inflam bowel disease (non neoplastic)

307
Q

Submucosal polyps

A

Lipomas, leimyomas, fibromas, etc (non neoplastic)

308
Q

Hyperplastic polyps

A

Smaller and mostly in rectosigmoid region – only rarely evolve into serrated and more advanced lesions

309
Q

Adenomatous polyps

A

Neoplastic via chromosomal instability pathway with mutation in APC and KRAS – tubular worse than villous, tubulovillous in the middle; usually asymptomatic but may present w/ occult bleeding

310
Q

Serrated polyps

A

Premalignant via CpG hypermethylation phenotype w/ microsatillite instability and BRAF mutations; saw tooth crypts – up to 20% of sporadic CRC

311
Q

FAP genetics

A

AD mutation of APC tumor suppressor (2 hit) on chr 5q21

312
Q

FAP sx

A

Thousands of polyps after puberty – pancolonic and always involves rectum

313
Q

FAP tx

A

Prophylactic colectomy – 100% progression

314
Q

Gardner syndrome

A

FAP+osseous and soft tissue tumors, congenital hypertrophy of RPE, impacted/supernumerary teeth

315
Q

Turcot syndrome

A

FAP/Lynch syndrome and malignant CNS tumor (medulloblastoma, glioma)

316
Q

Peutz Jeghers syndrome genetics

317
Q

Peutz Jeghers sx

A

Numerous hamartomas through GI tract, hyperpigmented mouth, lips, hands, genitalia

318
Q

Peutz Jeghers assoc

A

Higher risk of breast and Gi cancers (colorectal, stomach, SI, pancreatic

319
Q

Juvenile polyposis syndrome genetics

320
Q

JPS demographics

A

Children under 5

321
Q

JPS sx

A

Numerous hamartomatous polyps in colon, stomach, SI

322
Q

JPS assoc

A

Higher risk of CRC

323
Q

Lynch syndrome aka

324
Q

Lynch syndrome genetics

A

AD mutation of DNA mismatch repair gene –> microsatillite instability

325
Q

Lynch prognosis

A

80% progression to CRC

326
Q

Lynch syndrome assoc

A

Endometrial, ovarian, skin CA and CRC

327
Q

CRC demographics

A

most >50, 25% family hx

328
Q

CRC risk factors

A

Adenomatous/serrated polyps, familiar CA syndromes, IBD, tobacco use, diet of processed meat w/ low fiber

329
Q

CRC sx

A

Rectosigmoid>
ascending – exophytic, IDA, wt loss>
descending – infiltrating, partial obstruction, colicky pain, hematochezia

330
Q

Assoc w/ CRC

A

S bovis bacteremia

IDA in males >50 and postmenopausal females

331
Q

Screening for CRC

A

Starts at 50 w/ colonoscopy (40 or 10 yrs prior to family member if family hx in 1st degree relative)

332
Q

Tumor marker for CRC

A

CEA – mointors recurrence/tx, not screening

333
Q

Molecular pathogenesis of CRC chromosomal instability

A

APC mutation –> less adhesion and more proliferation (at risk) –> KRAS mut –> unregulated incracell signalling –> adenoma –> loss of tumor suppressor gene (e.g. p53) –>increased tumorienesis –> carcinoma

334
Q

Molecular pathogenesis of CRC microsatilite instability

A

Mutations or methylation of mismatch repair genes (e.g. MLH1)

335
Q

May cause or prevent CRC

A

Overexpression of COX2 linked to CRC – NSAIDs chemoprotective

336
Q

Cells most involved in cirrhosis

337
Q

Causes of portal HTN

A

Cirrhosis (most), vascular obstruction (e.g. portal vein thrombosis, Budd chiari), schistosomiasis

338
Q

Metabolic changes in portal HTN

A

Hyponatremia, hyperbilirubinemia

339
Q

Spontaneous bacterial peritonitis aka

A

Primary bacterial peritonitis

340
Q

Predisposes to spontaneous bacterial peritonitis

A

Cirrhosis/ascites

341
Q

Sx of spontaneous bacterial peritonitis

A

Often asymptomatic, but can cause fevers, chiils, abdominal pain, ileus, worsening encephalopathy

342
Q

Causes spontanoeous bact peritonitis

A

Aerobic gram neg organism – esp E coli

343
Q

Diagnose spont. bact peritonitis

A

Paracentesis w/ ascitic fluid abs. neutrophil count >250cells/mm3

344
Q

Most liver disease liver enzymes and exception to rule

A

ALT>AST
Exception alcohol (AST>ALT)
If AST>ALT in non alcoholic liver disease – probably progression to advanced fibrosis of cirrhosis

345
Q

Alk phos

A

Increased in cholestasis, infiltrative disorders, and bone disease

346
Q

GGT

A

Increased in liver and billiary disease (like alk phos) but not in bone disease; assc w/ alcohol use

347
Q

Why are plts low in liver disease?

A

Low TPO, liver sequestration

348
Q

Why are plts low in portal HTN?

A

Splenomealy, spenic sequestration

349
Q

Reye syndrome

A

Oft fatal hepatic encephalopathy in kids; sx: mitochondrial abnormalities, fatty liver (microvesicular fatty change), hypoglycemia, vomiting, hepatomegaly, coma

350
Q

Cause of Reyes syndrome

A

Viral infxn (esp VZV and influenza B) tx w/ aspirin

351
Q

Reye syndrome mechanism

A

Aspirin metabolites decrease B-oxidation by reversible inhib of mitochondrial enzymes

352
Q

Hepatic steatosis

A

MACROvesicular fatty change – may be reversible w/ alcohol cessation

353
Q

Alcoholic hepatitis

A

Req sustained long-term consumption – swollen/necrotic hepatocytes w/ neutrophilic infiltration, Mallory bodies (intracytoplasmic eosinophilic inclusions of damaged keratin filaments)

354
Q

Alcoholic cirrhosis

A

Final and irreversible form of liver damage – regnerative nodules surrounded by fibrous bands in response to chronic liver injury –> portal HTN and end stage liver disease; sclerosis around central vein in early disease

355
Q

Nonalcoholic fatty liver disease

A

Metabolic syndrome (insulin resistance, obesity) –> fatty infiltratin of hepatocytes –> cellular ballooning and eventual necrosis –> can –>cirrhosis and HCC

356
Q

Hepatic encephalopathy

A

Cirrhosis –>portosystemic shunts –> less HN3 metabolism –> neuropsych dysfxn (from disorientation/asterixis to difficult arousal or coma)

357
Q

Triggers of hepatic encephalopathy

A

Increase NH3 prodxn and absorption (due to dietary protein, GI bleed, constipation, infxn)
or
Less NH3 removal (due to renal failure, diuretics, TIPS)

358
Q

Tx of hepatic encephalopathy

A

Lactulose (increased NH4 prodxn) and refaximen or neomycin (less NH3 producing gut bacteria)

359
Q

HCC assoc

A

HBV (w/ or w/o cirrhosis), HCV, alcoholic and nonalcoholic fatty liver disease, autoimmune disease, hemochromatosis, alpha1 AT def, aflatoxin

360
Q

Findings in HCC

A

Jaundice, TENDER hepatomegaly, ascites, polycythemia, anorexia

361
Q

Spread of HCC

A

Hematogenously

362
Q

What can HCC progress to cause?

A

Budd chiari

363
Q

Diagnosis of HCC

A

AFP, ultrasound or contrast CT/MRI, biopsy

364
Q

Cavernous hemangioma

A

Common benign liver tumor occuring 30-50 yrs

DO NOT BIOPSY – risk of hemorrhage

365
Q

Hepatic adenoma

A

Rare benign liver tumo r– related to OCP or anabolic steroids – can regress spontaneously or rupture (abdominal pain/shock)

366
Q

Angiosarcoma

A

Malignant tumor of endothelium – assoc w/ exposure to arsenic, vinyl chloride

367
Q

Metastases

A

Most common liver tumor altogether – usually multiple; most commonly GI, breast, and lung cancer

368
Q

Budd chiari

A

Thrombosis/compression of hepatic vvs w/ centrilobular congestion/necrosis –>congestive liver disease (hepatomegaly, ascities, varices, abdominal pain, liver failure) – can cause nutmeg liver
No JVD

369
Q

Budd chiari assoc

A

Hypercoagulable states, polycythemia vera, postpartum, HCC

370
Q

a1 AT deficiency

A

Misfolded gene product protein aggregates in hepatocellular ER –> cirrhosis w/ PAS + globules in liver

371
Q

a1 AT genetics

A

codominant

372
Q

Presentation of a1AT def

A

young pt w/ liver damage and dyspnea and no hx of smoking

373
Q

Common causes of jaundice (increased bili)

A 
HOT Liver
Hemolysis
Obstruction
Tumor
Liver disease
374
Q

Unconjugated hyperbilirubinemia

A

Hemolytic, physiologic in newborns, Crigler-Najjar, Gilbert

375
Q

Conjugated hyperbilirubinemia

A

Biliary tract obstruction – gallstones, cholangiocarcinoma, pancreatic/liver cancer, liver fluke
Biliary tract disease: 1o sclerosis cholangitis or 1o biliary cholangitis
Excretion defect: duin-Johnson, Rotor syndrome

376
Q

Cuase of neonatal jaundice and danger

A

Immature UDP glucuronosyltransferase – can cause kernicterus esp in basal ganglia
Usually w/in 24 hours of life and resolves in 1-2 wks
Tx: phototerapy

377
Q

Gilber syndrome v Crigler Najjar

A 
Mildly low UDPGTase vs. absent UDPGTase
Relatively asymptomatic (sx on fasting/stress) vs early in life presentation and death w/in a few years
378
Q

Type I vs Type II C-N

A

Type II is less severe and responds to phenobarb (increases liver enzyme synth)

379
Q

Dubin johnson

A

Defective liver secretion – grossly black liver (Rotor – same, no black liver)

380
Q

Wilson disease genetics

A

AR mutation in hepatocyte copper transporting ATPase – ATP7B gene on Chr 13

381
Q

Wilson disease mechanism

A

Less Cu exretion into bile and incorporation into apoceruloplasmin –> less serum ceruloplasmi –> Cu accumulation, esp in liver, brain, cornea, kidneys; higher urine Cu

382
Q

Wilson disease presentation

A

Before age 40 – liver disease (hepatitis, acute liver failure, cirrhosis), neurologic disease (e.g. dysarthria, dystonia, treamor, parkinsonism), psych disease, K-F rings (deposits in Descemet membrane of cornea), hemolytic anemia, renal disease (Fanconi syndrome)

383
Q

Tx of Wilson disease

A

Chelation w/ penicillamine or trientine, oral Zn

384
Q

Hemochromatosis genetics

A

AR mutation in HFE gene (C282Y>H63D) chr 6, assc w/ HLA A3

385
Q

Hemochromatosis mechanism

A

Abnormal Fe sensing and increased int absorption (high ferritin, high iron, low TIBC –> high transferrin sat), OR 2o to chronic blood transfusion –> Iron accumulation in liver, pancreas, skin, heart, pituitary, joints

386
Q

Hemochromatosis findings

A

Hemosiderin identified on liver MRI or biopsy w/ Prussian blue stain

387
Q

Demographics of hemochromatosis

A

Pts older than 40 when total body iron >20 g – iron loss through menstruation slows progression in women

388
Q

Presentation of hemochromatosis

A

Cirrhosis, DM, skin pigmentation (bronze), restrictive cardiomyopathy or dilated (reversible), hypogonadism, arthropathy (Ca pyrophosphate deposition – esp in MCP jnts), can lead to HCC

389
Q

Tx of hemochromatosis

A

Repeated phlebotomy, chelation w/ desfersirox, deferoxamine, oral deferiprone

390
Q

Presentation of biliary tract disease

A

Pruritis, jaundice, dark urine, light colored stool, hepatosplenomegaly –> cholestatic pattern of LFT (high conj bilirubin, high chol, high alk phos)

391
Q

PSC pathology

A

Something causes concentric onion skin bile duct fibrosis –> alternating strictures and dilation w/ beading of intra/extrahepatic bile ducts on ERCP or MRCP

392
Q

Epidemiology of PSC

A

Middle aged men w/ IBD

393
Q

Associations of PSC

A

Assc w/ UC, pANCA+, can lead to 2o biliary cholangitis, higher risk of cholangiocarcinoma and gallbladder CA

394
Q

PBC pathology

A

Autoimmune rxn –> lymphocytic infilitrate and granulomas –> destruction of intralobular bile ducts

395
Q

Epidemilogy of PBC

A

Middle aged women

396
Q

Assoc w/ PBC

A

Anti mitochondrial ab +, high igM; assc w/ other autoimmune conditions (Sjogrens, Hashimotos, CREST< RA, celiac)

397
Q

2o biliary cholangitis pathology

A

Extrahepatic biliary obstruction –> higher pressure in intrahepatic ducts –> injury/fibrosis and bile statsis

398
Q

2o BCitis assc.

A

Pts w/ gallstones, biliary strictures, pancreatic carcinoma (can be complicated by ascending cholangitis)

399
Q

Cholesterol stones –

A

Radioluscent (most common_ assc w/ obesity, Crohn disease, advanced age, estrogen therapy, multiparity, rapid wt loss, Native American origin

400
Q

Pigment stone –

A

Radiopaque, bilirubinate, hemolysis (black) or radiolucent from infxn (brown)
Assc w/ Crohn disease, chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infxns, TPN

401
Q

Most common complication of cholelithiasis

A

Cholecystitis (can also cause acute pancreatitis, ascending cholangitis, fistula btween gallbladder and GI tract –>air in biliary tree (pneumobilia) –> passage of gallstones into intestine –>obstruction of ileocecal valve (gallstone ileus))

402
Q

Risk factors for cholelithiasis

A 
Female
Fat
Fertile (preggers)
Forty
(4Fs)
403
Q

Biliary colic

A

Cholelithiasis complicatio. Assc w/ NV, dull RUQ; neurohormonal activation by CCK after fatty meal –> contraction of gallbladder –> stone into cystic duct; normal labs (see stone on US)

404
Q

Choledocholithiasis

A

Gallstone in common bile duct –> elevated ALP, GGT, direct bili, AST/ALT

405
Q

Cholecytisis

A

Acute or chronic inflam of gallbladder from cholelithiasis (stone at neck of gallbladder) w/ gall bladder wall thickening

406
Q

Calculous cholecystitis

A

Most common – gallstone impaction in cystic duct –> inflammation (can produce 2o infxn)

407
Q

Acalculous cholecystitis

A

Due to gallbladder stasis, hypoperfusion, infxn (CMV) in critically ill pts

408
Q

Cholecystitis test

A

Murphy sign (inspiratory arrest on RUQ palpation due to pain), increased ALp if bile duct involved (ascending cholangitis)< diagnosed w/ US or HIDA (can’t visulaize gallbladder on HIDA – obstruction)

409
Q

Porcelain gallblader

A

Calcified gallbladder due to chronic cholecystitis – usually inceidental finding

410
Q

Tx of porcelain gallbladder

A

Prophylactic cholecystectromy – high rates of gallbadder adenocarcinoma

411
Q

Ascending cholangitis

A

Infxn of biliary tree usually due to obstruction –> stasis/bacterial overgrowth

412
Q

Charcot triad of cholangitis

A

Jaundice, fever, RUQ pain; reynolds pentad adds alteed mental status and shock (hypotension)

413
Q

Acute pancreatitis

A

Autodigestion of pancreas by pancreatic enzymes

414
Q

Causes of acute pancreatitis

A

Idiopathic, Gallstones, EtOH, Trauma, Steroids, Mumps< Autoimmune, Scorpion sting, Hypercalcemia/hypertriglyceridemia (>1000 mg/dL), ERCP, Drugs (e.g. sulfa, NRTIs, protease inhibs)

I GET SMASHED

415
Q

Diagnosis of acute pancreatitis

A

2 of 3: acute epigastric pain radiating to back, high serum amylase or lipase (more specific) to 3x ULN, characteristic imaging

416
Q

Complications of acute pancreatitis

A

Pseudocyst (lined by granulation tissue – not epithelium), necrosis, hemorrhage, infxn, organ failures (ARDS, shock, renal failure), hypocalcemia (precipiation of Ca soaps)

417
Q

Chronic pancreatitis major causes

A

EtOH abuse, idiopathic

418
Q

Sx of chronic pancreattitis

A

Pancreatic insufficiency – statorrhea, fat soluble vit def, DM
+/- on lipase/amylase changes

419
Q

Panctic adenocarcinoma

A

Arises from pancreatic ducts (disorganized gladular sturctionw/ cellular infiltration) — most common in pancreatic head –> obstructive jaundice

420
Q

Tumor marker for pancreatic adenocarcinoma

421
Q

Risk factors for pancreatic adenocarcinoma

A

Tobacco use, chronic pancreatitis (esp > 20 yrs), DM, age >50 yrs, Jewish and AfAm males

422
Q

Presentation of pancreatic adenocarcinoma

A

Abdominal pain radiating to neck, wt loss (malabsorption, anorexia), migratory thrombophleibitis (redness and tenderness on palpation of extremeties – Troussea syndrome), obstructive jaundice w/ palpable nontender gallbladder (Courvosier sign)

STEP (15 decks)

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