Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GE > Midterm > Flashcards

Midterm Flashcards

1
Q

What level in the spine does the esophagus start at

A

C6 behind the cricoid cartilage

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

What’s final level does the esophagus enter the diaphragm

A

T10

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

where is the cardia of the stomach located?

A

t11

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

what type of cells make up the esophagus?

A

stratified squamous epithelial cells

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

which layer of muscle in the esophagus is voluntary?

A

the top third layer which is made of striated muscle

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

which layer of muscle in the esophagus is involuntary?

A

the bottom third layer which is made of smooth muscle

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

what type of muscle is the middle layer of the esophagus?

A

a mixture of striated and smooth muscle

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

rugae

A

the inside of the stomach

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

what secretes pepsinogen and HCl

A

The stomach body

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

what does the pylorus produce?

A

mucus, gastrin, and pepsinogen

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

parietal cells secrete

A

HCl, intrinsic factor

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

Chief (Zymogen) cells secrete

A

pepsinogen

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

enteroendocrine cells (g-cells) secrete

A

gastrin hormone

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

primary digestion of protein happens where and due to what?

A

in the stomach, due to pepsin

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

digestion of carbs takes place where?

A

in the mouth due to amylase

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

three main sections of small intestine

A

duodenum, jejunum, ileum

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

what kind of digestion takes place in the small intestine?

A

mechanical digestion and absorption

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

size of the duodenum

A

25-30 cm (12 fingers length)

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

where does the pancreatic duct enter the descending duodenum

A

major duodenal papilla - hepatopancreatic ampulla

=ampulla of Vater

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

accessory pancreatic duct aka

A

papilla of santorini

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

issues with the hepatopancreatic ampulla (of vater) cause pain where?

A

back pain close to spine

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

by percussion the mean liver size is?

A

6cm f

12cm m

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

size of pancreas

A

15 cm (6in)

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

α (alpha) cells of the pancreas secrete

A

glucagon (increases blood glucose

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

β (beta) cells of the pancreas secrete

A

insulin (decrease blood glucose)

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

Δ (delta) cells of the pancreas secrete

A 
somatostatin regulates
function of α and β cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

γ (gamma) cells of the pancreas secrete

A

pancreatic polypeptide

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

glycogen is stored where?

A

liver and skeletal muscles

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

pancreatic enzymes help to break-down what?

A

carbohydrates, proteins and lipids in chyme

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

proteins in saliva

A

mucin, lysozyme, IgA

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

electrolytes

A

Na, K, Cl, phosphate, bicarbonate ions

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

Gastrointestinal Tract Stomach Physiology

A 
food 
↓
 G-cells 
↓ 
Gastrin 
↓ 
hydrochloric acid 
↓ 
pepsinogen (non-active enzyme) 
↓ 
pepsin (active enzyme) 
↓ 
digestion of proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

stomach there is also absorption

A

alcohol
medications
water

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

small intestine is responsible for digestion of what

A

major digester of carbs

final digestion of proteins and first digestion of fat

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

what do c cells produce

A

secretin (with bicarbonate?)

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

duodenal mucosal cells produce and release what hormones

A

secretin—> pancreatic juice

cholecystokinin —-> bile from liver and gallbladder, and pancreatic enzymes

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

enzymes from the pancreas

A 
chymotrypsin
trypsin
carboxypeptidase
elastase
they break down short chain peptides to amino acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

lipase from the pancreas breaks down ?

A

fat to fatty acids and glycerol

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

pancreatic amylase finishes the breaking down of

carbohydrates to simple sugars

A

in the small intestine

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

Small Intestine enzymes

A
  • maltase breaks down maltose to two glucose molecules
  • sucrase breaks down sucrose to glucose and fructose
  • lactase breaks down lactose to glucose and galactose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

majority of nutrients are absorbed in the

A

Jejunum

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

vitamin B12 and bile salts are absorbed in the

A

terminal Ileum

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

In the liver there is production of:

A
  • bile - albumins
  • lipoproteins
  • clotting factors (e.g. prothrombin, fibrinogen)
  • angiotensinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Normal Bilirubin Pathway

A 
RBC  →  spleen (lysis)
↓          ↓ 
globulin   heme
↓      ↓ 
iron  porphyrin
ring 
↓ 
biliverdin 
↓ 
bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

bilirubin + albumin =

A

unconjugated (indirect, non-H2O soluble)

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

unconjugated bilirubin aka

A

indirect, non-H2O soluble

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

direct bilirubin →

A 
stercobilinigen
↓
stercobilin
↓
excretion with feces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

direct bilirubin

↓

A 
liver  ←   reabsorption to blood
(urobilinogen) 
↓ 
kidneys 
↓ 
urobilin 
↓
excretion with urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Bile is a mixture of:

A
  • water
  • bile salts
  • cholesterol
  • the pigment bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

liver stores?

A
  • vitamins A, D, B12, K, E
  • glycogen
  • iron
  • copper
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

liver detoxification:

A
  • converts ammonium to urea
  • breaks down insulin and other hormones
  • breaks down toxic substances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Kupffer cells

A

fixed macrophages within the liver
capture bacteria, fungi, parasites, worn out blood cells, cellular debris
clean large volume software blood very fast

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

Exocrine enzymes produced by the pancreas:

A 
chymotrypsin, 
trypsin, 
carboxypeptidase, 
elastase, 
amylase, 
lipase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Except production of digestive enzymes,

the pancreas also produces hormones:

A
  • Insulin, Amylin (beta cells) - Glucagon (alpha cells) - Somatostatin (delta cells)
    [ is also secreted by the hypothalamus and the intestine ]
  • Pancreatic polypeptide (gamma cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Amylin actions

A
  • inhibits the secretion of glucagon
  • slows emptying of the stomach
  • sends a satiety signal to the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Somatostatin has a variety of functions:

A
  • reduces the rate at which food is absorbed from

the content of the intestines - regulates/stops α- and β-cell functions

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

Achalasia (Cardiospasm) is

A

an
esophageal motility disorder involving the
smooth muscle layer of the esophagus,
and the lower esophageal sphincter (LES).

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

achalasia presentation

A

esophagus dilation

pain behind sternum

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

achalasia is characterized by

A

incomplete relaxation of LES
increased tone
lack of peristalsis of esophagus

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

primary/ congenital achalasia

A

most common
failure of DISTAL esophageal inhibitory neurons
auerbacks plexus, myenteric

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

auerbach’s plexus (aka myenteric plexus)

A

parasympathetic and sympathetic

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

meissner’s plexus

A

parasympathetic

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

secondary achalasia

A

results from :

  • cancer of esophagus or upper stomach
  • trypanosoma cruzi aka chagas disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

chagas disease

A

trypanosome cruzi

causes achalasia

65
Q

dysphagia

A

difficulty in swallowing of solid AND liquid food (with achalasia)

66
Q

signs and symptoms of achalasia

A 
dysphagia
regurgitation
chest pain (worse after eating)
coughing
aspiration of food or liquid
67
Q

bird’s beak or rat’s tail sign

A

X-ray with contrast of barium, diagnosis = achalasia

68
Q

complications due to achalasia

A 
aspiration pneumonia or airway obstruction 
lower esophageal diverticulum
esophageal cancer (5% adenocarcinoma)
69
Q

hiatal hernia

A

is protrusion of the upper part of the stomach into thorax through the space between the muscular crura of the diaphragm and the esophageal wall

70
Q

2 forms of hiatal hernia

A

sliding hernia

rolling or paraesophageal

71
Q

sliding hernia

A

gastroesophageal
junction together with the stomach move above the diaphragm. Creates a bell-shaped dilation.

It is the most common form of hiatal
hernia (95%).

72
Q

acquired sliding hiatal hernia

A

peritoneum moves with the stomach

73
Q

rolling or paraesophageal hernia,

A

when a separate portion of the stomach,
usually along the greater curvature,
enters the thorax through the widening
foramen.

74
Q

etiology of hiatal hernia

A
  • congenital kyphoscoliosis
  • increased pressure within the abdominal cavity
  • congenital diaphragmatic weakness
  • obesity, trauma
  • marfan’s syndrome
75
Q

hiatal hernia aka

A

great mimic disease

76
Q

signs and symptoms of hiatal hernia

A
  • dull pain in the chest
  • shortness of breath
  • heartburn (sliding)
  • heartpalpitation
77
Q

hiatal hernia diagnosis

A

UPPER ENDOSCOPY

xray w/ barium

78
Q

complications of rolling hernia

A

venous infarction due to strangulation by diaphragm

79
Q

GERD

A

is a chronic syndrome resulting in mucosal
damage caused by stomach acid coming
up from the stomach into the esophagus.

80
Q

GERD etiology

A 
-failure of the lower esophageal sphincter
due to:
CNS depressants 
-hypothyroidism pregnancy (MC)
-alcohol or tobacco exposure (#2)
-sliding hernia
-obesity
-H. Pylori
-visceral diseases (lupus, asthma, gallstones, laryngitis)
81
Q

h pylori does what?

A

converts pepsinogen to pepsin

pepsin then increases HCl production

82
Q

signs and symptoms of GERD

A
  • heartburn
  • regurgitation
  • dysphagia
  • increased salivation
  • nausea
  • chest pain (radiating to arms and chest)
83
Q

GERD Diagnosis

A

xray barium

UPPER endoscopy

84
Q

GERD Complications

A
  • reflux esophagitis necrosis (ulcer near
    the junction between stomach and
    esophagus)
  • esophageal stricture- Barrett esophagus
  • aspiration pneumonia
  • esophageal cancer
85
Q

Barrett Esophagus

A

– is an abnormal change
(metaplasia) in the cells of the lower portion of
the esophagus.
-In Barrett esophagus the squamous epithelial cells of the esophageal mucosa are replaced by columnar epithelial cells containing goblet mucus-producing cells.

86
Q

Barrett Esophagus Etiology:

A
  • smoking = MC
  • GERD
  • central obesity
87
Q

Barrett Esophagus

A

Signs and symptoms:

  • heartburn
  • dysphagia (in case of complication by
    stricture) - hematemesis
  • painful eating
88
Q

Barrett Esophagus diagnosis

A

upper endoscopy with biopsy ONLY

89
Q

Barrett Esophagus Complications:

A
  • stricture
  • bleeding
  • frank esophageal adenocarcinoma
90
Q

what cells is the issue with in frank esophageal adenocarcinoma

A

goblet cells

91
Q

Barrett Esophagus chiro issue?

A

adjusting could cause bleeding

92
Q

Mallory-Weiss Syndrome

A

bleeding from longitudinal tears in the
mucosa (not muscular layer) at the
esophagogastric junction.
5 – 10% of upper gastrointestinal bleeding episodes.

93
Q

Mallory-Weiss Syndrome Pathogenesis:

A
  • inadequate relaxation of the musculature
    of the lower esophageal sphincter during
    vomiting, with stretching and tearing of
    the esophageal junction during
    propulsive expulsion of gastric contents.
94
Q

Mallory-Weiss Syndrome Etiology:

A
  • alcoholism, after frequent severe retching and vomiting (the most common cause)
  • hiatal hernia
  • overdose/use of NSAIDs (3-5 yrs)
  • severe vomiting in pregnancy/ bulimia
95
Q

Mallory-Weiss Syndrome Signs and symptoms:

A
  • episodes of vomiting with
  • –bright blood = acute esophageal issue
  • –dark blood = stomach issue
96
Q

Mallory-Weiss Syndrome Complications:

A
  • hematemesis
  • esophageal rupture (known as
    Boerhaave syndrome)
97
Q

Esophageal Varicies

A

– are extremely
dilated submucosal veins in low third of
the esophagus
-due to portal hypertension

98
Q

Portal hypertension – causes:

A

1) posthepatic (suprahepatic), 2) hepatic (intrahepatic),

3) prehepatic (infrahepatic),

99
Q

prehepatic (infrahepatic), associated with:

A

-portal vein thrombosis
- portal vein sclerosis
- portal vein congenital stenosis or
atresia

100
Q

hepatic (intrahepatic), associated with:

A
  • liver cirrhosis
  • liver tumors
  • amyloidosis
101
Q

1) posthepatic (suprahepatic), associated with:

A
  • chronic right-sided cardiac failure
  • Budd-Chiari syndrome (endophlebitis
    of the liver veins)
102
Q

Esophageal varicies appear in __% of patients with liver cirrhosis.

A

65%

103
Q

Zenker’s diverticulum –

A

immediately

above the upper esophageal sphincter.

104
Q

Midesophageal, a.k.a.Traction

diverticulum –

A

-near the midpoint of the
esophagus.
-Usually results from mediastinal lymphadenitis (as from tuberculosis).

105
Q

Epiphrenic diverticulum –

A

immediately above the lower

esophageal sphincter

106
Q

Zenker’s diverticulum signs +symptoms

A

– food regurgitation
in the absence of dysphagia, can be
complicated by aspiration pneumonia.

107
Q

Epiphrenic diverticulum S+s

A

gives rise

to nocturnal regurgitation.

108
Q

leiomyomas (most common benign tumors

of esophagus)

A

– originate from the smooth
muscle cells
Most commonly locates in distal (lower = MC) two thirds of the
esophagus, usually they are multiple

109
Q

polyps

A

– are usually composed of a
combination of fibrous, vascular, or adipose
tissue, covered by an intact mucosa
- mediastinum , middle or upper

110
Q

Benign Tumors of Esophagus

A

1) leiomyomas
2) polyps
3) fibromas
4) lipomas
5) hemangiomas
6) neurofibromas
7) squamous papillomas

111
Q

Benign Tumors of Esophagus

A

• The potentials for malignancy for all these
benign tumors are extremely low
• They typically occur in the age between 20 and
50 y/o
• No gender predominance

112
Q

Benign tumors of the esophagus Signs and Symptoms:

A

-They are usually asymptomatic, silent and
undetected
However, if their size is more than 5 cm in
diameter, they can come to the clinical attention
- dysphagia – on some types of food (e.g. meat
and bread)
-pain while swallowing – less common, usually
it is retrosternal

  • food regurgitation
    -bleeding or hematemesis result from
    ulceration or necrosis of benign tumors.
    These manifestations are extremely rare.
113
Q

The most common malignant esophageal

tumors are

A

squamous cell carcinoma
and
adenocarcinoma

114
Q

squamous cell carcinoma

A 
1) Represents 90-95%
of esophageal cancer
worldwide                                      USA
2) Arises from the squamous
3) Usually occurs in the
proximal two thirds of
esophagus
4) Direct correlation with:
- Celiac disease
- hot tea with increasedconcentration of tannins - Tylosis (palmar/plantar
hyperkeratosis)
115
Q

adenocarcinoma

A 
1) Represents 50-80% of
esophageal cancer in 
2) Arises from
epithelium
metaplastic columnar epithelium
3) Usually occurs in
the distal third of
esophagus or gastro-
esophageal junction
4) direct correlation with:
-GERD
-Baret esophagus
-Scleroderma
-Zollinger-ellison syndrome
116
Q

Metastases of malignant esophageal tumors:

A
  • regional lymphnodes
  • aorta
  • liver and lungs
  • mediastinum
117
Q

Pyloric Stenosis

A 
– is a narrowing( stenosis)
of the pylorus due to hypertrophy of the
sphincter muscle, or scarring of the tissue
surrounding the opening from the stomach
to duodenum.
118
Q

congenital pyloric stenosis -

A

hypertrophic pyloric stenosis = male : female = 4 : 1
= prevalence 2-4 per 1,000
newborns

119
Q

acquired pyloric stenosis

A 
- scarring of
stomach peptic ulcer
or duodenal bulb
- tumors
(stomach, pancreatic etc.)
120
Q

Signs and Symptoms of pyloric stenosis

A
  • severe worsening vomiting
  • weight loss
  • dehydration
  • constant hunger
  • visible or palpable peristaltic waves
  • in hypertrophic pyloric stenosis in
    babies:
    = first symptoms appear in the
    first 2-6 weeks of the life
    = there is progressive vomiting with partially digested food after each or few feedings
121
Q

pangastritis

A

diffuse acute gastritis

122
Q

Chronic gastritis

A

–chronic mucosal
inflammatory changes in the stomach wall
that eventually result in mucosal atrophy
and mucosal (intestinal) metaplasia

123
Q

Chronic gastritis etiology

A
  • Helicobacter pylori (in 90% of C.G.)
  • bile reflux

–These etiological factors affect the antral part of the stomach.
- NSAIDs
- autoimmune diseases (autoimmune
chronic gastritis, SLE)
- allergic response

–These etiological factors cause multiple focal damages of the stomach mucosa.

124
Q 
Intestinal (mucosal) metaplasia is very
important predisposing factor for
development of one the most common
stomach cancers, known as:
Intestinal-type
A

Adenocarcinoma

125
Q

5 forms of chronic gastritis

A
  • hypertrophic
  • hyperplastic
  • erosive
  • antral
  • atrophic
126
Q

Hypertrophic, erosive and antral forms s+s

A 
- acute pain in epigastrium and left upper
abdominal area 
- this pain is local, without radiation 
- usually this pain develops in 30 – 60
minutes after the meal
- heartburn 
- belching 
- constipation
127
Q

Signs and Symptoms (cont.):

Atrophic form:

A
  • heaviness in epigastrium and left upper
    abdominal area
  • fullness in the stomach after small amount
    of meal
  • diarrhea
  • signs of pernicious anemia
128
Q

organs effected by peptic ulcers

A

stomach, duodenum, esophagus

129
Q

peptic ulcers

A
  • 80% of peptic ulcer develops in the duodenum
    and
  • 20% in the stomach
    Etiology:
    Helicobacter pylori is found in:
  • 100% of duodenal peptic ulcer
  • 70% of stomach peptic ulcer
    -Corticosteroid Hormones and Nonsteroidal
    Antinflammatory Drugs
    They suppress the production of Prostaglandins which inhibit secretion of Gastrin.
130
Q

peptic ulcer etiology

A
  • h pylori
  • corticosteroids+ NSAIDS
  • cigs
  • zollinger- ellison
  • stress
  • genetics
131
Q

early pain (30 minutes – 1 hour after the meal) –

A

typical for stomach peptic ulcer

132
Q

late pain (1.5 – 2 hours after the meal)

A

–typical for duodenal peptic ulcer

133
Q

“starving” pain (6 – 7 hours after the meal)

A
  • is characteristic for duodenal peptic ulcer
134
Q

night pain (at 4 – 5 a.m.) for

A

duodenal peptic ulcer

135
Q

pain radiation from area of cardia
- postbulbar area – mid back on the level of
T5–T7 around right scapula

A

– left upper quadrant and

retrosternal area

136
Q

pain radiation from postbulbar area

A

– mid back on the level of

T5–T7 around right scapula

137
Q

Dyspepsia

A 
– heartburn (in 30-80%),
may be the only peptic ulcer symptom
– nausea
– vomiting (relieves the
pain) – belching with sour
taste
138
Q

Penetration

A

stomach content does not enter the peritoneal cavity.

The tissue of adjacent organ undergoes digestion, which is potentially also very dangerous and may result in death.

139
Q

Perforation

A

When the stomach or duodenal wall is perforated, the stomach content spreads into the peritoneal cavity, resulting in peritonitis.
pain worse at night

140
Q

“Hourglass stomach”

A

This complication develops as a result of peptic ulcer healing, with development of scar tissue – so called

141
Q

linitis plastica

A

leather bottle stomach

142
Q

benign mesenchymal tumors

A

1) polyps
2) leiomyoma
3) lipoma
4) neurogenic (neuroma aka schwannoma, aka neurilemmoma)
5) vascular (gloms tumors)

143
Q

Malignant tumors of the stomach:

A 
1) carcinomas (90-95% of all stomach
malignant tumors)
2) lymphomas
3) carcinoids 
4) sarcoma
5) non hodgkins lymphoma
144
Q

early gastric carcinoma –

A

when a lesion

confined to the mucosa and submucosa

145
Q

advanced gastric carcinoma –

A

when a neoplasm has extended below the submucosa into the muscular wall

146
Q

exophytic gastric carcinomas

A

– with protrusion of tumor

into the lumen

147
Q 
flat or depressed gastric carcinomas aka linitis plastica aka leather bottle
scirrhous cancer (scirr)
A

– in which there is no

obvious tumor mass within the mucosa

148
Q

excavated gastric carcinomas

A

– whereby the shallow or

deeply erosive crater is present in the wall of the stomach

149
Q

intestinal type adenocarcinoma

A
  • compsed of neoplastic intestinal glands
  • is an exophytic projectile tumor
  • has relatively long latent period
  • known risk factors
  • ass w/ chronic gastritis due to intestinal metaplasia
150
Q

diffuse gastric carcinoma

A
  • is composed of gastric type mucous cells
  • flat tumor
  • has short latent period (grows fast)
  • risk factors undefined
  • no ass w/ h pylori or Chronic gastritis
151
Q

darkness of the skin,
frequently locating
in axilla and groin,
known as

A

“ acanthosis nigricans”

152
Q

acanthosis nigricans

A

1-2 month onset
no discomfort
darkening of armpit and groin

153
Q 
tripe palms (a.k.a.
“acanthosis palmaris”)
A 
tripe palms are the first sign of an undiagnosed cancer
In over 40% of patients,
a skin condition in which
the skin of the palm
becomes thick and
velvety hyperpigmentation
with pronounced folds in
the lines of the hand
154
Q

(Leser-Trelat sign)

A

sudden eruption of multiple seborrheic keratosis

155
Q

lymphatic node in the left supraclavicular fossa

A

known as Virchow’s node

156
Q

stomach carcinoma metastases area that mimics hodgkins lymphoma

A

virchow’s node (left supraclavicular fossa)

157
Q

metastases of stomach carcinoma go to?

A
  • Lymph nodes, local and occasionally to virchow’s node
  • liver via blood (portal vein)
  • pancreas
  • lungs (constant back pain)
  • ovaries
158
Q

krukenberg tumors

A

secondary ovarian cancer caused by metastasis of stomach carcinoma

159
Q

Diagnosis of stomach carcinoma

A
  1. Tumor markers such as:
    - CEA - elevated CEA in 45-50% of cases
    - CA 19-9 - elevated in about 20% of cases
    - CBC
  2. Endoscopic ultrasonography with Biopsy 3. PET,CT or MRI of the chest, abdomen, and pelvis

GE (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions