MindMap Gallery Digestive system diseases
Pathology summarizes and organizes knowledge points to help learners understand and remember. Straight to the point, it can be used as study notes and review materials to help you systematically review and consolidate the knowledge you have learned. The knowledge points are systematic and comprehensive. I hope it will be helpful to everyone! Suitable for exam review.
Edited at 2024-10-01 23:35:46In order to help everyone use DeepSeek more efficiently, a collection of DeepSeek guide mind map was specially compiled! This mind map summarizes the main contents: Yitu related links, DS profile analysis, comparison of DeepSeek and ChatGPT technology routes, DeepSeek and Qwen model deployment guide, how to make more money with DeepSeek, how to play DeepSeek, DeepSeek scientific research Application, how to import text from DeepSeek into MindMaster, the official recommendation of DeepSeek Wait, allowing you to quickly grasp the essence of AI interaction. Whether it is content creation, plan planning, code generation, or learning improvement, DeepSeek can help you achieve twice the result with half the effort!
This is a mind map about DeepSeek's 30 feeding-level instructions. The main contents include: professional field enhancement instructions, interaction enhancement instructions, content production instructions, decision support instructions, information processing instructions, and basic instructions.
This is a mind map about a commercial solution for task speech recognition. The main content includes: text file content format:, providing text files according to the same file name as the voice file.
In order to help everyone use DeepSeek more efficiently, a collection of DeepSeek guide mind map was specially compiled! This mind map summarizes the main contents: Yitu related links, DS profile analysis, comparison of DeepSeek and ChatGPT technology routes, DeepSeek and Qwen model deployment guide, how to make more money with DeepSeek, how to play DeepSeek, DeepSeek scientific research Application, how to import text from DeepSeek into MindMaster, the official recommendation of DeepSeek Wait, allowing you to quickly grasp the essence of AI interaction. Whether it is content creation, plan planning, code generation, or learning improvement, DeepSeek can help you achieve twice the result with half the effort!
This is a mind map about DeepSeek's 30 feeding-level instructions. The main contents include: professional field enhancement instructions, interaction enhancement instructions, content production instructions, decision support instructions, information processing instructions, and basic instructions.
This is a mind map about a commercial solution for task speech recognition. The main content includes: text file content format:, providing text files according to the same file name as the voice file.
Digestive system diseases
Esophagitis
Reflux esophagitis
concept
Gastric reflux causes chronic inflammation of the lower esophageal mucosa
clinical manifestations
heartburn
Pathological changes
Local mucosal congestion, infiltration of inflammatory cells, and superficial ulcers may occur. Long-term lesions may lead to fibrosis and esophageal stenosis.
Barrett's esophagus
concept
Columnar metaplasia in the lower esophagus
source
Reflux esophagitis
Pathological changes
in general
Irregular orange-red, velvety appearance changes on gray-white normal mucosa
under the mirror
The esophageal mucosa is composed of epithelial cells and glands from the gastric mucosa or small intestinal mucosa
Features
Barrett's esophageal adenocarcinoma
appendicitis
acute appendicitis
acute uncomplicated appendicitis
Early disease, limited to mucosa and submucosa
acute cellulitis appendicitis
Purulent exudation on the surface
A large amount of inflammatory exudation was seen in all layers
acute gangrenous appendicitis
Often accompanied by perforation and periappendicitis
chronic appendicitis
Appendiceal fibrosis to varying degrees, chronic inflammatory cell infiltration (lymphocytes)
gastritis
The histological structure of the stomach
epithelium
Mucosal layer
mucosal epithelium
lamina propria
muscularis mucosa
submucosa
Muscle layer
fundic glands
chief cell
secrete pepsin
Gland-like structure, hollow, nucleus on one side
parietal cell
Secrete hydrochloric acid and intrinsic factor
The cytoplasm is very red (strongly eosinophilic)
The nucleus is in the middle, round
Pyloric gland
Contains a small number of specific cells and more G cells
G cells are tubular mucus cells (to be confirmed)
chronic gastritis
nature
Chronic nonspecific inflammation of gastric mucosa
Cause
Helicobacter pylori HP infection
long term chronic irritation
duodenal fluid reflux
autoimmune damage
Classification
Non-atrophic (chronic superficial)
Predisposed areas
gastric antrum
under the mirror
Superficial mucosal lymphocyte and plasma cell infiltration
The lamina propria is congested and edematous, and the glands proper are intact (typical structure)
in general
Mucosal congestion and edema, local erosion, and spot hemorrhage
atrophic
Lesion characteristics
Mucosal intrinsic gland atrophy
Intestinal metaplasia (the basis of precancerous lesions)
Cause
HP infection (main cause)
Pathological changes
Gastroscopy
Mucosal atrophy
The mucous membrane becomes thinner and the wrinkled walls become flattened and disappear.
Submucosal vascular branches are clearly visible (not visible at normal thickness)
Fine granular on mucosal surface
The result of alternating between atrophic and normal mucosa
The mucous membrane turns from orange to gray, alternating with red and white (mainly white)
under the mirror
Mucosal atrophy
Reduced intrinsic glands (characteristic pathological changes, diagnostic basis)
Decreased number, decreased density, cystic expansion (compensation)
glandular metaplasia
Intestinal metaplasia (major)
Features
Papillary epithelium of the small intestinal mucosa (stalactite-like) with goblet cells (unique to the intestine)
Classification
complete metaplasia type 1
Goblet cells, absorptive cells, and Paneth cells all exist
Incomplete metaplasia type 2
Goblet cells only
gastric type 2a
Colonic type 2b
Associated with intestinal type gastric cancer
intestinal gland epithelium
goblet cells
Almost transparent, lightly tinted
absorbing cells
striated border
Paneth cells
Very orange
pseudopyloric gland metaplasia
Pyloric glands appear in the lower body of the stomach (no goblet cells)
The gastric mucosa is jungle-like, with a thick basal layer and no goblet cells.
Inflammatory cell infiltration
lymph, plasma, lymph follicle
chronic inflammatory hyperplasia
intramucosal fibroplasia
Classification
Type A
Autoimmunity (antibody positive)
gastric fundus body
Yes (parietal cells disappear, intrinsic factor is absent)
none
None (reduced gastric acid secretion)
Type B
direct damage
gastric antrum
none
have
Yes (gastric acid secretion is normal)
chronic hypertrophic gastritis
mucosal wall hypertrophy
verrucous gastritis
Central depression in gastric mucosa
peptic ulcer disease
feature
Beyond the muscularis mucosae
caused by self-digestion
Classification
Duodenal ulcer (bulbar)
Gastric ulcer (lesser curvature of the antrum)
under the mirror
exudate layer
necrotic layer
granulation tissue layer
scar tissue layer
proliferative endarteritis
Location
Scar base
Performance
Small and medium A is thickened and narrowed
thrombosis
Influence
Prevent blood vessel bleeding
Local circulation disorder and non-healing ulcers
hepatitis
viral hepatitis
Overview
nature
degenerative inflammation
Pathogenesis (Hepatitis B)
Cellular immune damage is the main
HBV antigen on the surface of liver cells
Pathological changes
transsexual
Cellular edema (most common)
Cytoplasmic loosening
Liver cells are swollen, and the cytoplasm is loose to reticular and translucent.
Ballooning
The liver cells further swelled, changing from polygonal to spherical, and the cytoplasm was almost transparent.
secondary lesions
The swelling ruptures, releasing cytoplasm (lytic necrosis)
eosinophilia
Accumulated number of liver cells
Eventually become eosinophilic bodies (apoptosis)
The nucleus is bluer and the cytoplasm is redder
fatty change
Spherical lipid droplets of varying sizes appear in the cytoplasm of liver cells
liquefaction necrosis
Spotty necrosis SN (spotty)
concept
Necrosis of a few liver cells in the liver lobules, accompanied by eye cell infiltration, common in acute hepatitis vulgaris
parts
Within the liver lobules (on the liver cords)
scope
several liver cells
form
Punctate or focal inflammatory cell infiltration
Fragmented necrosis PN (piecemeal)
concept
Focal necrosis and disintegration of hepatocytes in the boundary plates around the liver lobules, seen in chronic hepatitis
lead to
Perilobular fibrosis
Features
Common characteristics of chronic hepatitis
Bridging necrosis BN (bridging)
concept
The necrotic zone that connects liver cells in the central vein and portal area
seen in
Moderate to severe chronic hepatitis
lead to
bridging fibrosis, fibrous septation
Massive necrosis (massive)
concept
Extensive hepatocyte necrosis (without structural debris-like material) involving almost the entire liver lobule, common in severe hepatitis
as a result of
acute liver failure
Basic lesions
Inflammatory cell infiltration
parts
Intralobule, portal area
Element
lymphocytes (viruses), monocytes
regeneration
full regeneration
Mesh fiber stent complete
nodular regeneration
Destruction of mesh fiber scaffold
Regenerating liver cells arrange into disordered hepatocyte clumps
interstitial reactive hyperplasia
Kupffer cell proliferation
Mesenchymal and fibroblast proliferation
Fibrosis
source
Fibroblast proliferation in portal areas and perilobules
Hepatic stellate cells become myofibroblast-like cells
Mesh fibrous scaffold collapse
as a result of
liver fibrosis
Reversible
early cirrhosis
Diffuse fibrosis and insufficient hepatic lobular structural reconstruction
Cirrhosis
The liver lobule structure is mostly remodeled into pseudo lobules
Fibrous septa surround pseudolobules
apoptosis
Eosinophilic bodies: apoptosis of single cells
Various hepatitis
Hepatitis A
Hepatocyte lytic necrosis around the central veins of the hepatic lobules
Hepatitis B
ground glass hepatocytes
Fine granular substances in the cytoplasm of stem cells in patients with HbsAg and chronic hepatitis
Essential slippery surface endoplasmic reticulum hyperplasia, containing large amounts of HbsAg
psammoid nuclei
Synthesis of HBcAg in the nucleus
Hepatitis C
hepatocellular steatosis
Lymphocyte infiltration in portal area, lymphoid follicles visible
bile duct injury
Hepatitis E
Can be infected vertically
Clinicopathological type
Ordinary type (light)
Acute (most common)
Ballooning
eosinophilic body
punctate necrosis
Chronic
Mild (G2)
SN, mild PN
Moderate to severe (G3-4)
spoil
PN and BN
ooze
Massive chronic inflammatory cell infiltration
Hyperplasia (severe)
Formation of massive fibrous septa (pseudolobules)
Structural disorder of liver lobules, advanced cirrhosis
Severe (extremely poor prognosis)
acute
MN
Basically no regeneration
subacute
Nodular hepatocyte regeneration (secondary cirrhosis)
Renewable
Liver cells around the lobules
Cirrhosis (hyperplasia) of the liver
Overview
Cirrhosis is the end stage of the development of various chronic liver diseases
Pathological features: diffuse fibrosis, pseudolobule formation
Clinical: Hepatic insufficiency and portal hypertension
concept
Due to diffuse degeneration and necrosis of liver cells and the action of hepatic stellate cells
Causes liver fibrosis and nodular regeneration of hepatocytes
Types
Portal cirrhosis (micronodular)
Viral hepatitis (B and C), chronic alcoholism
Small nodules of equal size and smaller than 1cm (essentially pseudolobules) are diffusely distributed on the surface and cut surface.
Pseudolobule: Fiber segmentation leads to the absence or deviation of the central vein of the lobule (BN); or the central vein enters the portal area; the arrangement of liver cells is disordered Chronic inflammatory cell infiltration: lymphocytes, monocytes and macrophages
Portal hypertension and hepatic insufficiency, upper gastrointestinal bleeding (death)
Postnecrotic cirrhosis (macronodular)
subacute severe hepatitis
Liver nodules of varying sizes
Pseudolobules of varying sizes (caused by nodular regeneration)
Liver insufficiency
biliary cirrhosis
Autoimmune diseases, biliary obstruction
Liver green-brown
Stem cell reticular or feathery necrosis
Liver insufficiency
digestive system tumors
Esophageal cancer
Predisposed areas
middle section
Histological type
Squamous cell carcinoma (90%)
Adenocarcinoma (10%)
early stage cancer
The lesions are limited, mostly carcinoma in situ or intramucosal cancer or submucosal layer, and do not invade the muscle layer.
Mass or polyp type
Intermediate and advanced cancer
Medullary type (most common) (infiltrative type)
Infiltrative growth in the esophageal wall, thickening the wall and narrowing the lumen
mushroom type
Project into the esophageal lumen
Ulcerative
Superficial ulcer, deep into the muscle layer
Most likely to cause retrosternal pain
Narrow type
Infiltrative growth local annular stenosis
The earliest onset of dysphagia
transfer
lymphatic tract
Gastric cancer (mostly adenocarcinoma)
Cause
Helicobacter pylori
Chronic gastric diseases (atrophic gastritis, ulcers, polyps, intestinal metaplasia)
Duodenal ulcer does not cause tumors
Predisposed areas
Gastric antrum (lesser curvature side)
Early stage cancer (does not invade the muscle layer; depressed type is most common)
A little cancer
Cancer was found in biopsy but not in surgery
Microcarcinoma
diameter less than 0.5
Small gastric cancer
Diameter is 0.6~1.0
Intermediate and advanced cancer (advanced gastric cancer)
exogenous
Polyp or mushroom type
Ulcerative type (most common)
The edge is raised, crater-like
Infiltration type, narrowing type
diffuse infiltration
Leather stomach (signet ring cell carcinoma - a type of mucinous carcinoma)
Narrow type
transfer
Lymphatic tract (most common)
Late metastasis to left supraclavicular lymph node
Implantation transfer
Krukenberg tumor (bilateral ovary)
Differentiation of benign and malignant ulcers
shape
circle or ellipse
Crater shaped
size
diameter less than 2
diameter greater than 2
depth
deep
shallow
edge
tidy
Untidy
bottom
flat
uneven
around
The wrinkled wall is concentrated towards the ulcer
The wrinkle wall is interrupted and nodular hypertrophy
colorectal cancer
Cause
High protein, high fat, low fiber diet
Precancerous lesions
Colorectal adenomatous polyps (APC gene mutations)
ulcerative colitis
Other polyposis
intraepithelial neoplasia
Does not exceed the muscularis mucosae (less than the submucosa), and the 5-year survival rate is 100%
Predisposed areas
Rectum>Colon
Pathological changes
in general
Ulcerative
most common
Colloidal type (poor prognosis)
Appearance
Translucent jelly-like
under the mirror
Mucinous adenocarcinoma (with mucus lakes) or imprinton vilcell carcinoma
Raised type
Infiltrating type
under the mirror
Adenocarcinoma (most common)
papillary adenocarcinoma
tubular adenocarcinoma
signet ring cell carcinoma
mucinous adenocarcinoma
transfer
Lymphatic metastasis is the most common
Hematogenous metastasis (mostly liver removal)
primary liver cancer
Cause
hepatitis virus
Cirrhosis
Aflatoxin B1
Histological type (adenocarcinoma)
Hepatocellular carcinoma (most common)
cholangiocarcinoma
mixed cell liver cancer
Early cancer (small liver cancer)
A single cancer nodule or two cancer nodules combined, with a maximum diameter less than 3cm
advanced liver cancer
Multinodular type (most common)
Often associated with postnecrotic cirrhosis
Huge type
More common in right lobe
Without cirrhosis
Diffuse type
Combined with liver cirrhosis
transfer
Hematogenous metastasis (portal vein intrahepatic metastasis is the most common)