Midterm Flashcards

1
Q

What level in the spine does the esophagus start at

A

C6 behind the cricoid cartilage

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2
Q

What’s final level does the esophagus enter the diaphragm

A

T10

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3
Q

where is the cardia of the stomach located?

A

t11

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4
Q

what type of cells make up the esophagus?

A

stratified squamous epithelial cells

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5
Q

which layer of muscle in the esophagus is voluntary?

A

the top third layer which is made of striated muscle

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6
Q

which layer of muscle in the esophagus is involuntary?

A

the bottom third layer which is made of smooth muscle

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7
Q

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

A

a mixture of striated and smooth muscle

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8
Q

rugae

A

the inside of the stomach

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9
Q

what secretes pepsinogen and HCl

A

The stomach body

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10
Q

what does the pylorus produce?

A

mucus, gastrin, and pepsinogen

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11
Q

parietal cells secrete

A

HCl, intrinsic factor

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12
Q

Chief (Zymogen) cells secrete

A

pepsinogen

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13
Q

enteroendocrine cells (g-cells) secrete

A

gastrin hormone

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14
Q

primary digestion of protein happens where and due to what?

A

in the stomach, due to pepsin

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15
Q

digestion of carbs takes place where?

A

in the mouth due to amylase

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16
Q

three main sections of small intestine

A

duodenum, jejunum, ileum

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17
Q

what kind of digestion takes place in the small intestine?

A

mechanical digestion and absorption

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18
Q

size of the duodenum

A

25-30 cm (12 fingers length)

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19
Q

where does the pancreatic duct enter the descending duodenum

A

major duodenal papilla - hepatopancreatic ampulla

=ampulla of Vater

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20
Q

accessory pancreatic duct aka

A

papilla of santorini

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21
Q

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

A

back pain close to spine

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22
Q

by percussion the mean liver size is?

A

6cm f

12cm m

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23
Q

size of pancreas

A

15 cm (6in)

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24
Q

α (alpha) cells of the pancreas secrete

A

glucagon (increases blood glucose

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25
β (beta) cells of the pancreas secrete
insulin (decrease blood glucose)
26
Δ (delta) cells of the pancreas secrete
``` somatostatin regulates function of α and β cells ```
27
γ (gamma) cells of the pancreas secrete
pancreatic polypeptide
28
glycogen is stored where?
liver and skeletal muscles
29
pancreatic enzymes help to break-down what?
carbohydrates, proteins and lipids in chyme
30
proteins in saliva
mucin, lysozyme, IgA
31
electrolytes
Na, K, Cl, phosphate, bicarbonate ions
32
Gastrointestinal Tract Stomach Physiology
``` food ↓ G-cells ↓ Gastrin ↓ hydrochloric acid ↓ pepsinogen (non-active enzyme) ↓ pepsin (active enzyme) ↓ digestion of proteins ```
33
stomach there is also absorption
alcohol medications water
34
small intestine is responsible for digestion of what
major digester of carbs | final digestion of proteins and first digestion of fat
35
what do c cells produce
secretin (with bicarbonate?)
36
duodenal mucosal cells produce and release what hormones
secretin---> pancreatic juice | cholecystokinin ----> bile from liver and gallbladder, and pancreatic enzymes
37
enzymes from the pancreas
``` chymotrypsin trypsin carboxypeptidase elastase they break down short chain peptides to amino acids ```
38
lipase from the pancreas breaks down ?
fat to fatty acids and glycerol
39
pancreatic amylase finishes the breaking down of | carbohydrates to simple sugars
in the small intestine
40
Small Intestine enzymes
- maltase breaks down maltose to two glucose molecules - sucrase breaks down sucrose to glucose and fructose - lactase breaks down lactose to glucose and galactose
41
majority of nutrients are absorbed in the
Jejunum
42
vitamin B12 and bile salts are absorbed in the
terminal Ileum
43
In the liver there is production of:
- bile - albumins - lipoproteins - clotting factors (e.g. prothrombin, fibrinogen) - angiotensinogen
44
Normal Bilirubin Pathway
``` RBC → spleen (lysis) ↓ ↓ globulin heme ↓ ↓ iron porphyrin ring ↓ biliverdin ↓ bilirubin ```
45
bilirubin + albumin =
unconjugated (indirect, non-H2O soluble)
46
unconjugated bilirubin aka
indirect, non-H2O soluble
47
direct bilirubin →
``` stercobilinigen ↓ stercobilin ↓ excretion with feces ```
48
direct bilirubin | ↓
``` liver ← reabsorption to blood (urobilinogen) ↓ kidneys ↓ urobilin ↓ excretion with urine ```
49
Bile is a mixture of:
- water - bile salts - cholesterol - the pigment bilirubin
50
liver stores?
- vitamins A, D, B12, K, E - glycogen - iron - copper
51
liver detoxification:
- converts ammonium to urea - breaks down insulin and other hormones - breaks down toxic substances
52
Kupffer cells
fixed macrophages within the liver capture bacteria, fungi, parasites, worn out blood cells, cellular debris clean large volume software blood very fast
53
Exocrine enzymes produced by the pancreas:
``` chymotrypsin, trypsin, carboxypeptidase, elastase, amylase, lipase ```
54
Except production of digestive enzymes, | the pancreas also produces hormones:
- Insulin, Amylin (beta cells) - Glucagon (alpha cells) - Somatostatin (delta cells) [ is also secreted by the hypothalamus and the intestine ] - Pancreatic polypeptide (gamma cells)
55
Amylin actions
- inhibits the secretion of glucagon - slows emptying of the stomach - sends a satiety signal to the brain
56
Somatostatin has a variety of functions:
- reduces the rate at which food is absorbed from | the content of the intestines - regulates/stops α- and β-cell functions
57
Achalasia (Cardiospasm) is
an esophageal motility disorder involving the smooth muscle layer of the esophagus, and the lower esophageal sphincter (LES).
58
achalasia presentation
esophagus dilation | pain behind sternum
59
achalasia is characterized by
incomplete relaxation of LES increased tone lack of peristalsis of esophagus
60
primary/ congenital achalasia
most common failure of DISTAL esophageal inhibitory neurons auerbacks plexus, myenteric
61
auerbach's plexus (aka myenteric plexus)
parasympathetic and sympathetic
62
meissner's plexus
parasympathetic
63
secondary achalasia
results from : - cancer of esophagus or upper stomach - trypanosoma cruzi aka chagas disease
64
chagas disease
trypanosome cruzi | causes achalasia
65
dysphagia
difficulty in swallowing of solid AND liquid food (with achalasia)
66
signs and symptoms of achalasia
``` dysphagia regurgitation chest pain (worse after eating) coughing aspiration of food or liquid ```
67
bird's beak or rat's tail sign
X-ray with contrast of barium, diagnosis = achalasia
68
complications due to achalasia
``` aspiration pneumonia or airway obstruction lower esophageal diverticulum esophageal cancer (5% adenocarcinoma) ```
69
hiatal hernia
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
2 forms of hiatal hernia
sliding hernia | rolling or paraesophageal
71
sliding hernia
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
acquired sliding hiatal hernia
peritoneum moves with the stomach
73
rolling or paraesophageal hernia,
when a separate portion of the stomach, usually along the greater curvature, enters the thorax through the widening foramen.
74
etiology of hiatal hernia
- congenital kyphoscoliosis - increased pressure within the abdominal cavity - congenital diaphragmatic weakness - obesity, trauma - marfan's syndrome
75
hiatal hernia aka
great mimic disease
76
signs and symptoms of hiatal hernia
- dull pain in the chest - shortness of breath - heartburn (sliding) - heartpalpitation
77
hiatal hernia diagnosis
UPPER ENDOSCOPY | xray w/ barium
78
complications of rolling hernia
venous infarction due to strangulation by diaphragm
79
GERD
is a chronic syndrome resulting in mucosal damage caused by stomach acid coming up from the stomach into the esophagus.
80
GERD etiology
``` -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
h pylori does what?
converts pepsinogen to pepsin | pepsin then increases HCl production
82
signs and symptoms of GERD
- heartburn - regurgitation - dysphagia - increased salivation - nausea - chest pain (radiating to arms and chest)
83
GERD Diagnosis
xray barium | UPPER endoscopy
84
GERD Complications
- reflux esophagitis necrosis (ulcer near the junction between stomach and esophagus) - esophageal stricture- Barrett esophagus - aspiration pneumonia - esophageal cancer
85
Barrett Esophagus
– 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
Barrett Esophagus Etiology:
- smoking = MC - GERD - central obesity
87
Barrett Esophagus
Signs and symptoms: - heartburn - dysphagia (in case of complication by stricture) - hematemesis - painful eating
88
Barrett Esophagus diagnosis
upper endoscopy with biopsy ONLY
89
Barrett Esophagus Complications:
- stricture - bleeding - frank esophageal adenocarcinoma
90
what cells is the issue with in frank esophageal adenocarcinoma
goblet cells
91
Barrett Esophagus chiro issue?
adjusting could cause bleeding
92
Mallory-Weiss Syndrome
bleeding from longitudinal tears in the mucosa (not muscular layer) at the esophagogastric junction. 5 – 10% of upper gastrointestinal bleeding episodes.
93
Mallory-Weiss Syndrome Pathogenesis:
- 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
Mallory-Weiss Syndrome Etiology:
- 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
Mallory-Weiss Syndrome Signs and symptoms:
- episodes of vomiting with - --bright blood = acute esophageal issue - --dark blood = stomach issue
96
Mallory-Weiss Syndrome Complications:
- hematemesis - esophageal rupture (known as Boerhaave syndrome)
97
Esophageal Varicies
– are extremely dilated submucosal veins in low third of the esophagus -due to portal hypertension
98
Portal hypertension – causes:
1) posthepatic (suprahepatic), 2) hepatic (intrahepatic), | 3) prehepatic (infrahepatic),
99
prehepatic (infrahepatic), associated with:
-portal vein thrombosis - portal vein sclerosis - portal vein congenital stenosis or atresia
100
hepatic (intrahepatic), associated with:
- liver cirrhosis - liver tumors - amyloidosis
101
1) posthepatic (suprahepatic), associated with:
- chronic right-sided cardiac failure - Budd-Chiari syndrome (endophlebitis of the liver veins)
102
Esophageal varicies appear in __% of patients with liver cirrhosis.
65%
103
Zenker’s diverticulum –
immediately | above the upper esophageal sphincter.
104
Midesophageal, a.k.a.Traction | diverticulum –
-near the midpoint of the esophagus. -Usually results from mediastinal lymphadenitis (as from tuberculosis).
105
Epiphrenic diverticulum –
immediately above the lower | esophageal sphincter
106
Zenker’s diverticulum signs +symptoms
– food regurgitation in the absence of dysphagia, can be complicated by aspiration pneumonia.
107
Epiphrenic diverticulum S+s
gives rise | to nocturnal regurgitation.
108
leiomyomas (most common benign tumors | of esophagus)
– originate from the smooth muscle cells Most commonly locates in distal (lower = MC) two thirds of the esophagus, usually they are multiple
109
polyps
– are usually composed of a combination of fibrous, vascular, or adipose tissue, covered by an intact mucosa - mediastinum , middle or upper
110
Benign Tumors of Esophagus
1) leiomyomas 2) polyps 3) fibromas 4) lipomas 5) hemangiomas 6) neurofibromas 7) squamous papillomas
111
Benign Tumors of Esophagus
• 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
Benign tumors of the esophagus Signs and Symptoms:
-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
The most common malignant esophageal | tumors are
squamous cell carcinoma and adenocarcinoma
114
squamous cell carcinoma
``` 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
adenocarcinoma
``` 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
Metastases of malignant esophageal tumors:
- regional lymphnodes - aorta - liver and lungs - mediastinum
117
Pyloric Stenosis
``` – 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
congenital pyloric stenosis -
hypertrophic pyloric stenosis = male : female = 4 : 1 = prevalence 2-4 per 1,000 newborns
119
acquired pyloric stenosis
``` - scarring of stomach peptic ulcer or duodenal bulb - tumors (stomach, pancreatic etc.) ```
120
Signs and Symptoms of pyloric stenosis
- 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
pangastritis
diffuse acute gastritis
122
Chronic gastritis
–chronic mucosal inflammatory changes in the stomach wall that eventually result in mucosal atrophy and mucosal (intestinal) metaplasia
123
Chronic gastritis etiology
- 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
``` Intestinal (mucosal) metaplasia is very important predisposing factor for development of one the most common stomach cancers, known as: Intestinal-type ```
Adenocarcinoma
125
5 forms of chronic gastritis
- hypertrophic - hyperplastic - erosive - antral - atrophic
126
Hypertrophic, erosive and antral forms s+s
``` - 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
Signs and Symptoms (cont.): | Atrophic form:
- heaviness in epigastrium and left upper abdominal area - fullness in the stomach after small amount of meal - diarrhea - signs of pernicious anemia
128
organs effected by peptic ulcers
stomach, duodenum, esophagus
129
peptic ulcers
- 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
peptic ulcer etiology
- h pylori - corticosteroids+ NSAIDS - cigs - zollinger- ellison - stress - genetics
131
early pain (30 minutes – 1 hour after the meal) –
typical for stomach peptic ulcer
132
late pain (1.5 – 2 hours after the meal)
–typical for duodenal peptic ulcer
133
“starving” pain (6 – 7 hours after the meal)
- is characteristic for duodenal peptic ulcer
134
night pain (at 4 – 5 a.m.) for
duodenal peptic ulcer
135
pain radiation from area of cardia - postbulbar area – mid back on the level of T5–T7 around right scapula
– left upper quadrant and | retrosternal area
136
pain radiation from postbulbar area
– mid back on the level of | T5–T7 around right scapula
137
Dyspepsia
``` – heartburn (in 30-80%), may be the only peptic ulcer symptom – nausea – vomiting (relieves the pain) – belching with sour taste ```
138
Penetration
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
Perforation
When the stomach or duodenal wall is perforated, the stomach content spreads into the peritoneal cavity, resulting in peritonitis. pain worse at night
140
“Hourglass stomach”
This complication develops as a result of peptic ulcer healing, with development of scar tissue – so called
141
linitis plastica
leather bottle stomach
142
benign mesenchymal tumors
1) polyps 2) leiomyoma 3) lipoma 4) neurogenic (neuroma aka schwannoma, aka neurilemmoma) 5) vascular (gloms tumors)
143
Malignant tumors of the stomach:
``` 1) carcinomas (90-95% of all stomach malignant tumors) 2) lymphomas 3) carcinoids 4) sarcoma 5) non hodgkins lymphoma ```
144
early gastric carcinoma –
when a lesion | confined to the mucosa and submucosa
145
advanced gastric carcinoma –
when a neoplasm has extended below the submucosa into the muscular wall
146
exophytic gastric carcinomas
– with protrusion of tumor | into the lumen
147
``` flat or depressed gastric carcinomas aka linitis plastica aka leather bottle scirrhous cancer (scirr) ```
– in which there is no | obvious tumor mass within the mucosa
148
excavated gastric carcinomas
– whereby the shallow or | deeply erosive crater is present in the wall of the stomach
149
intestinal type adenocarcinoma
- 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
diffuse gastric carcinoma
- 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
darkness of the skin, frequently locating in axilla and groin, known as
“ acanthosis nigricans”
152
acanthosis nigricans
1-2 month onset no discomfort darkening of armpit and groin
153
``` tripe palms (a.k.a. “acanthosis palmaris”) ```
``` 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
(Leser-Trelat sign)
sudden eruption of multiple seborrheic keratosis
155
lymphatic node in the left supraclavicular fossa
known as Virchow’s node
156
stomach carcinoma metastases area that mimics hodgkins lymphoma
virchow's node (left supraclavicular fossa)
157
metastases of stomach carcinoma go to?
- Lymph nodes, local and occasionally to virchow's node - liver via blood (portal vein) - pancreas - lungs (constant back pain) - ovaries
158
krukenberg tumors
secondary ovarian cancer caused by metastasis of stomach carcinoma
159
Diagnosis of stomach carcinoma
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