Brainscape's Knowledge GenomeTM

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


See full index

PAT > PAT 2 > Flashcards

PAT 2 Flashcards

1
Q

Microscopic picture of Autoimmune associated gastritis

A
  1. Chronic inflammation:
    - The inflammatory infiltrate is predominantly lymphocytes, macrophages, & plasma cells; lymphoid aggregates can be present.
  2. There is marked glandular atrophy & fibrosis of the lamina propria.
  3. In long standing cases, intestinal metaplasia occurs.
    - This is a premalignant condition and carcinoma develops in a small proportion of patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Clinical picture of autoimmune associated Gastritis

A

Hypoacidity & anemia.
- B12 deficiency can also manifest with
( Atrophic glossitis - Peripheral neuropathy & Spinal cord lesions. )

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

complication of B12 deficiency

A

( Atrophic glossitis - Peripheral neuropathy & Spinal cord lesions. )

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

the most common cause of chronic gastritis

A

H. pylori infection

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

Pathogenesis of Helicobacter pylori (HP) associated chronic gastritis

A
  • The organism is found in the mucus layer of gastric epithelium.
  • The acute inflammatory response is mediated by complement activation and attraction of neutrophils
  • The neutrophils release proteases and reactive oxygen species which may be responsible for glandular destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is type B gastritis

A

Helicobacter pylori (HP) associated chronic gastritis

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

what is responsible for glandular destruction in HP gastritis

A

The neutrophils release proteases and reactive oxygen species which may be responsible for glandular destruction

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

Morphology of HP gastritis

A

1) antral gastritis with high acid production; high rik of duodenal ulcer
2) diffuse involvement of antrum and body (pangastritis) with
multifocal glandular atrophy and fibrosis, and decreased acid output: gastric ulcer and carcinoma

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

Microscopic of HP gastritis

A
  • A variable number of neutrophils are present intraepithelial and collect in the lumen of gastric pits.
  • Lamina propria contains abundant plasma cells, macrophages, & lymphocytes, and in case of severe infiltrate the rugal folds are seen grossly thickened.
  • Long-standing gastritis is associated with diffuse mucosal atrophy, with prominent lymphoid aggregates occasionally with germinal centers
  • The organisms are generally seen in the mucus layer on the cell surface as slender, curved rods.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnosis of H. pylori

A

© Antibody serologic test,
© Urea breath test,
© Bacterial culture,
© Direct bacterial visualization in gastric biopsy, or
© DNA-based tests.

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

Fate & complications of HP gastritis

A
  • Severe cases usually proceed to atrophy with intestinal metaplasia which is precancerous, and can lead to adenocarcinoma.
  • H. pylori infection is also a risk factor for peptic ulcer disease, & gastric lymphoma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Microscopic Picture of Acute Gastric Ulceration

A
  • Ulcers include layers of necrosis, inflammation, & granulation tissue.
  • Fibrotic scar is absent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Fate and complications of acute gastric ulceration

A
  • Severe bleeding can occur.
  • Healing with complete re-epithelialization occurs, after the injurious factors are removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lesions associated with
brain injury are due to direct vagal stimulation causing gastric acid hypersecretion

A

cushing ulcers

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

types of acute gastric ulceration

A

stress ulcer, curling ulcer, cushing ulcer

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

Gross Picture of acute gastric ulceration

A
  • Ulcers are usually smaller than 1 cm in diameter, multiple, and shallow
  • Found anywhere in the stomach.
  • The ulcer base is brown (blood), while the adjacent mucosa is normal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Definition of the peptic ulcer

A

§ Chronic mucosal defects, also affecting submucosa,
as a result of acid and pepsin attack.
§ They occur mostly in stomach & duodenum
(but also anywhere exposed to the action of acid & pepsin secretion)

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

Sites of the peptic ulcer

A

1- First part of the duodenum.
2- Stomach: lesser curvature & pyloric antrum..
3- Lower esophagus associated with reflux of acid from stomach.
4- Meckel’s diverticulum:
a congenital remnant of the vitello-intestinal duct containing heterotropic
gastric mucosa (foci of gastric mucosa amidst the intestinal mucosal lining).
5- Distal duodenum & jejunum in Zollinger Ellison syndrome.
6- Gastro-jejenostomy stomal ulcer (surgical opening of stomach into the jejunum) due to dumping of acid & pepsin.

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

Pathogenesis of peptic ulcer

A
  • Hyperacidity or
  • Failure of mucosal defence mechanism,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is meckel’s diverticulum

A

a congenital remnant of the vitello-intestinal duct containing heterotropic gastric mucosa (foci of gastric mucosa amidst the intestinal mucosal lining)

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

why peptic ulcer in distal duodenum & jejunum

A

due to Zollinger Ellison syndrome

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

stomal ulcer related to

A

Gastro-jejenostomy surgery

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

causes of hyperacidity

A
  • Helicobacter pylori causes excess HCL secretion.
  • Gastrinoma (gastrin producing tumor) in Zollinger Ellison syndrome:
  • Chronic stress with high vagal tone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

cause of damage of mucus barrier of stomach

A

Duodeno-gastric reflux

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

epithelial barrier is damaged by

A
  • Chronic NSAID use (direct damage, blocking prostaglandin production)
  • High doses of corticosteroids (suppress prostaglandin synthesis).
  • Chronic alcoholism.
  • H pylori infection (cytotoxins or inflammatory reaction).
  • Smoking especially in presence of H pylori infection

الكاس و المزاج و الكورتيزون و البيلوري

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

The mucosal defence mechanism of the stomach consist of

A
  • A mucus-bicarbonate barrier
  • The surface epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Fate of peptic ulcer

A

Ulcers heal by epithelial regeneration and underlying fibrosis.

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

Microscopically: the peptic ulcer

A

The base of the ulcer shows necrotic tissue
with polymorphs overlying granulation tissue merging with fibrosis.

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

Gross of the peptic ulcer

A

© usually solitary (80% of patients), 1-2 cm,
© round or oval in shape with sharp sloping or terraced edges.
© The floor is smooth due to peptic digestion of any exudate.
© The base is firm due to fibrosis.

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

clinical picture of peptic ulcer

A
  • Chronic recurrent disease in middle aged or older adults.
  • Epigastric pain 1-3 hours after meals, releaved by alkali or food (duodenal ulcer)
  • gastric ulcer after food immediatly .
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

complication of peptic ulcer

A
  1. Bleeding, from eroded vessels at base of ulcer, manifests as:
    * Hematemesis.
    * Melena (in acute bleeding).
    * Iron deficiency anemia (chronic bleeding).
  2. Penetration into solid viscera as pancreas (organs of stomach bed).
  3. Pyloric obstruction in ulcers of pyloric antrum. The fibrosis causes narrowing &
    obstruction of gastric outlet
  4. Perforation into peritoneal cavity causing peritonitis.
  5. Malignant transformation only in gastric ulcer can rarely occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ulcer causes iron def anemia

A

peptic ulcer (complication)

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

benign epithelial tumors of stomach

A

Polyps

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

benign mesechymal tumors of the stomach

A
  • Leiomyoma
  • Schwannoma
  • Benign gastrointestinal stromal tumor (GIST)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

malignant mesenchymal stomach

A
  • Lymphoma
  • Leiomyosarcoma .
  • Neurogenic sarcoma
  • Malignant gastro intestinal stromal tumor (GIST)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

malignant epithelial stomach

A

Gastric carcinoma

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

predisposing factors of carcinoma of stomach

A
  1. In H pylori gastritis, there is a sequence of events of atrophy, intestinal metaplasia, dysplasia and carcinoma.
  2. Smoked food
  3. Autoimmune gastritis type A
  4. Genetic factors
  5. Adenomatous polyp
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

why H pylori causes carcinoma of stomach

A
  • Hypochlorohydria associated with atrophy favors the growth of bacteria that catalyse the formation of carcinogenic nitrosamines.
  • High cell turnover
  • The epithelial damage induce increased cell proliferation, with probable acquired mutations which are transmitted to daughter cells
  • Loss of E cadherins (in diffuse gastric cancer) and mutations of tumor suppressor genes have been demonstrated in gastric cancer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

morphology of Gastric carcinoma

A

Lauren classification separates gastric carcinoma to intestinal adenocarcinoma

40
Q

lauren classifiction related to

A

morphology of gastric carcinoma

41
Q

lauren classification of gastric carcinoma

A

p 68

42
Q

difference of early gastric carcinoma and advanced

A

Early gastric cancer is confined to the mucosa or submucosa and
The advanced cancer have extended in or beyond the muscle layer

43
Q

exophytic
masses or an ulcerated mass appear in carcinoma

A

Intestinal type adenocarcinoma

44
Q

morphology of intestinal type adenocarcinoma

A
  • Tend to be bulky, appear as exophytic masses or an ulcerated mass.
  • Composed of glands with variable degree of differentiation, and secrete mucin.
  • If in excess the term mucoid adenocarcinoma is used.
  • Intestinal type predominates in high risk areas and develop from dysplasia and adenoma.
45
Q

morphology of Diffuse gastric cancer

A
  • Shows an infiltrative growth pattern.
  • Composed of dyscohesive cells which infiltrate the mucosa as single cells.
  • They evoke a desmoplastic reaction that stiffen the gastric wall and cause diffuse flattening of gastric rugae giving the stomach a leather bottle appearance (linitis plastica).
  • The cells may have large intracytoplasmic mucin vacuoles that push the nucleus to one side (signet ring carcinoma).
  • No definite precursor lesion.
46
Q

clinical picture of gastric carcinoma

A

Ø early symptoms resemble those for chronic gastritis (i.e., dysphagia, dyspepsia, & nausea).
Ø Advanced stages present with weight loss, anorexia, altered bowel habits, anemia, & hemorrhage.

47
Q

Complications of gastric carcinoma

A

1- Hematemesis & melena.
2- Pyloric obstruction resulting in severe vomiting & dehydration.
3- Anemia due to recurrent bleeding with microcytic hypochromic anemia.
4- Spread
- Direct spread: to duodenum, pancreas and retroperitoneum. - Lymphatic spread:
to perigastric - celiac- paraortic lymph nodes .and then to left supraclavicular lymph nodes** (Virchows node)**.
- Blood spread : through portal vein to liver.
- Transcoelomic:
producing peritoneal deposits &
deposits in both ovaries causing
enlargement of the ovaries (Krukenberg tumor of the ovaries)

48
Q

the most common mesenchymal tumor of the abdomen

A

GASTROINTESTINAL STROMAL TUMOR GIST

49
Q

origin of GIST

A

interstitial cell of Cajal

50
Q

location of interstitial cell of Cajal

A

located in the muscularis propria and serve as pacemaker for the gut

50
Q

cancer develops from the lymphoid follicles in H pylori gastritis

A

acquired mucosa-associated lymphoid tissue or MALT

51
Q

high grade lymphoma of stomach

A

diffuse large B cell lymphoma

52
Q

fate of acquired mucosa-associated lymphoid tissue or MALT

A

show complete regression after
complete eradication of H pylori infection

53
Q

etiology of GIST

A

tyrosine kinase (C-KIT) mutation

54
Q

treatment of GIST

A

imatinib (an inhibitor of the tyrosine kinase activity)

54
Q

what is kurkenberg tumor

A

metastatic deposits from gastric carcinoma to both ovaries casing enlargment of them

55
Q

Definition of INTESTINAL ATRESIA

A

Failure of the gut to canalize,
most commonly found in the duodenum or small intestine

56
Q

Definition of Meckel’s Diverticulum

A

remnant of the vitello-intestinal duct
which makes tubular blind pouch present on the antimesenteric border of small intestine

57
Q

length of the M diverticulum

A

2 inch (5cm)

58
Q

length from the iliocoecal junction

A

2-3 feet (60-90 cm)

59
Q

complication of meckel’s diverticulum

A
  1. It may contain heterotropic gastric epithelium, which may secrete acid & pepsin resulting in peptic ulcer.
  2. Acute intestinal obstruction: Meckel’s diverticulum can result in
    abnormal twisting of a loop of intestine on itself (volvulus)
    causing acute intestinal obstruction.
  3. May get inflamed and present as acute abdomen mimicking acute ‘appendicitis.
60
Q

location of the meckel’s diverticulum

A

the antimesenteric border of small intestine

61
Q

Etiology of Hirschsprung’s Disease (Megacolon)

A

Ø Congenital absence of the ganglionic cells in the myenteric plexus of the intestine at the recto-sigmoid junction.
Ø Peristalsis stops at the affected site resulting in functional obstruction leading to chronic intestinal obstruction

62
Q

which congentital disorder causes acute intestinal obstruction

A

Meckel’s Diverticulum

63
Q

which congentital disorder causes chronic intestinal obstruction

A

Hirschsprung’s Disease (Megacolon)

64
Q

Clinical picture of Hirschsprung’s Disease (Megacolon)

A

Pain, vomiting, constipation, and distension

PVCD

65
Q

treatment of the megacolon

A

incision of the distal collupsed part

66
Q

Hirschsprung’s Disease (Megacolon) causes which type of intestinal obstruction

A

chronic

67
Q

Gross of Hirschsprung’s Disease (Megacolon)

A

he aganglionic segment is narrow markedly dilated colon proximal to it (Megacolon).
The intestinal wall is thickened due to hypertrophy of the muscle wall

68
Q

Definition of Acute intestinal obstruction

A

Sudden complete bowel obstruction

69
Q

Types of Acute intestinal obstruction

A

function (paralytic ileus) and Organic

70
Q

Causes of the paralytic ileus

A
  • A segment of the intestine loses its peristaltic movement.
  • Caused by operative trauma to the intestine or septic peritonitis disturb the normal autonomic control of peristalsis.
71
Q

causes of organic obstruction

A

a) Strangulated hernia
b) Adhesions of healed peritoneal inflammation
c) Lumen obstruction: by foreign body, worms or fecolith (solid stools) or tumor.
d) Volvulus:
e) Intussusception:
f) Thrombosis or embolism of mesenteric artery

72
Q

Definition of stangulated hernia

A

A hernia is a loop of intestine which passes through a congenital or acquired defect in the abdominal wall results in obstructing the mesentry vessels

73
Q

Definition of Volvulus

A

Volvulus is complete twisting of a bowel loop about its mesenteric
vascular base, leading to vascular and luminal obstruction with infarction

74
Q

causes of lumen acute obstruction

A

foreign body, worms or fecolith (solid stools) or tumor

75
Q

common part that volvulus occur

A

sigmoid colon

76
Q

Intussusception is common in

A

infants and children

77
Q

in older age intussusception is caused by

A

benign tumor, parasitic irritation, bilharzial polyps or abnormal motility

78
Q

results of thrombosis of the mesenteric artery

A

Producing hemorrhagic infarction
of a segment which loses its peristalsis & doesn’t function

79
Q

Gross of acute intestinal obstruction

A
  • The proximal segment is markedly dilated, edematous wall.
  • The mucosa is congested with loss of its folds (stretched), with
    accumulation of fluid & gas in the lumen.
  • The distal segment is collapsed
80
Q

Complications of acute Intestinal obstruction

A

1- Septic peritonitis; bacteria pass through the devitalized wall from the lumen into the sterile peritoneum.

2- Gangrene: the marked dilatation causes compression on the vessels of the wall leading to ischemic necrosis, which quickly undergoes putrefaction, wet gangrene perforation, septic peritonitis.

3- Septicemia 2ry to peritonitis

81
Q

Clinical Picture of acute intestinal obstruction

A
  • Abdominal distention, persistent vomiting leading to dehydration & shock (hypovolemic). Loss of K affects the cardiac rhythm.
  • No passage of stools or flatus (gas).
  • Plain X ray shows distention of intestine with gas and presence of a fluid level.
82
Q

Definiton of chronic intestinal obstruction

A

Gradual incomplete obstruction

83
Q

Etiology of Chronic intestinal obstruction

A

1- Lumen obstruction.
2- Fibrous stricture following dysentries, ulcerative colitis, Crohn’s disease or TB.
3- Endophytic tumor benign or malignant growing into the lumen
4- Obstruction from outside: Pressure of a tumor & adhesions between intestinal loops.
5- Annular stricture carcinoma.
6- Hirschsprung’s disease

84
Q

Defintion of Malabsorption

A

Malabsorption is a disease characterized by defective absorption of fats, proteins, carbohydrates, water, electrolytes, minerals, fat and water soluble vitamins

85
Q

Gross of chronic intestinal obstruction

A

§ Proximal segment: Above obstruction there is dilatation, hypertrophy of wall (muscle contracts more forcibly to enable pushing of contents beyond the obstruction).
The lumen contains accumulating liquified food & gases (action of bacteria).
§ Distal segment: Below obstruction: the segment is collapsed (no contents)

86
Q

Etiology of malabsorption

A

1- Celiac Disease (gluten-induced enteropathy)
2- Tropical sprue
3- Giardiasis
4- Secondary malabsorption:

87
Q

pathogenesis of Celia disease

A
  • Hypersensitivity reaction to a protein in wheat.
  • Characterized by total villous atrophy of small intestine
88
Q

Characterized by partial villous atrophy of the small intestine

A

Tropical sprue causing malabsorption

89
Q

Characterized by total villous atrophy of small intestine

A

Celiac Disease (gluten-induced enteropathy)

89
Q

Clinical Picture of mal absorption

A

Chronic diarrhea, weight loss, abdominal distension and muscle wasting.
A hallmark of malabsorption is steatorrhea characterized by excessive fecal fat and bulky, frothy, greasy, yellow or clay colored stools.

90
Q

what is secondary malabsorption

A

omplicating other diseases with diffuse distruction
of small intestinal mucosa, eg:
- Intestinal lymphomas.
- TB ulcers (2ry),
- Crohn’s disease (regional ileitis).
- Surgical intestinal anastomosis (reduce the intestinal length.
- leading to decrease surface absorption).
- Extensive surgical resections (short gut)

91
Q

Bronchial asthma G & M

A

Gross:
Lungs are overinflated
Bronchial wall is thick, swollen & red.
Bronchial lumen contains large amounts of thick mucus plugs
Microscopic:
Bronchial lumen
§ Occlusion of bronchi and bronchioles by mucus
plugs which contain whorls of shed epithelium
known as Curschmann spirals.
§ Numerous eosinophils and Charcot-Leyden
crystals derived from eosinophils are also
present.
Bronchial wall
§ mucous gland hypertrophy.
§ smooth muscle hypertrophy,
§ thickening of basement membrane

92
Q

Curschmann spirals related to

A

bronchial asthma

93
Q

Charcot-Leyden crystals related to

A

bronchial asthma

PAT (5 decks)

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