MindMap Gallery Pathology—digestive system
The key points of the pathology examination include the structure of the digestive tract, Chronic gastritis, peptic ulcer, Appendicitis, viral hepatitis, alcoholic liver disease, Cirrhosis, etc.
Edited at 2024-01-12 22:39:49マンダラチャート:キャリア発展プランは、ビジネスパーソンのキャリア成長を体系的に計画・管理するための専門的な可視化ツールで、EdrawMind の強力なマンダラチャート作成機能を活用して開発されました。本テンプレートは、「キャリア発展(コア)」を中心に、人脈・昇進・効率・スキル・財務・健康・ブランド・学習という 8 つのコアキーワードを展開し、さらに各分野ごとに具体的な行動目標をマトリクス状に細分化することで、キャリア成長の全側面を可視化・体系化します。人脈構築・昇進戦略・業務効率化・スキルアップ・資産管理・健康維持・個人ブランディング・継続学習という 8 つの次元で、日次・週次・月次の具体的なアクションを明確に定義し、バランスの取れたキャリア成長を実現し、「偏り」を防ぎます。EdrawMind の柔軟なカスタマイズ機能により、目標の追加・修正・進捗管理が容易に行え、キャリア計画・自己管理・成長戦略立案など、あらゆる場面で活用できます。キャリア発展の可視化と体系化を実現し、持続的な成長をサポートする最適なツールです。
マンダラチャート:キャリア発展プランは、個人のキャリア成長を体系的に計画・管理するための専門的な可視化ツールで、EdrawMind の強力なマンダラチャート作成機能を活用して開発されました。本テンプレートは、キャリア発展の 8 つのコアキーワード(人脈・昇進・効率・スキル・財務・健康・ブランド・学習)を中心に、各分野ごとに具体的な行動目標をマトリクス状に展開し、キャリア成長の全側面を可視化・体系化します。人脈構築・昇進戦略・業務効率化・スキルアップ・資産管理・健康維持・個人ブランディング・継続学習という 8 つの次元で、月次・週次・日次の具体的なアクションを明確に定義し、バランスの取れたキャリア成長を実現し、「偏り」を防ぎます。EdrawMind の柔軟なカスタマイズ機能により、目標の追加・修正・進捗管理が容易に行え、ビジネスパーソンのキャリア計画・自己管理・成長戦略立案など、あらゆる場面で活用できます。キャリア発展の可視化と体系化を実現し、持続的な成長をサポートする最適なツールです。
これは、専門家、起業家、キャリアプランナー向けに設計された、再利用可能な「マンダラチャートキャリア開発プラン」テンプレートです。このテンプレートは「キャリア開発」を中心とし、8つの主要な成長分野へと展開していきます。視覚的かつ体系的なデザインにより、抽象的なキャリア目標を具体的な行動計画へと落とし込みます。テンプレートは明確な構造を持ち、読みやすく快適なピンクとブルーの配色を採用しています。中心領域は黒い四角で「キャリア開発」のテーマを強調し、周囲の青い四角は8つの成長方向を示しています。これは、個人の能力開発計画や業界育成戦略の策定に役立ちます。中心テーマと枝のラベルを置き換えるだけで、ニーズに合わせたキャリアプランマップを素早く作成でき、断片化された目標を体系的なキャリア開発の道筋へと統合するのに役立ちます。これは単なるキャリアプランニングの「ナビゲーションマップ」ではなく、断片化された目標を体系的なキャリア開発の道筋へと統合する、継続的に改善していく成長ツールです。
マンダラチャート:キャリア発展プランは、ビジネスパーソンのキャリア成長を体系的に計画・管理するための専門的な可視化ツールで、EdrawMind の強力なマンダラチャート作成機能を活用して開発されました。本テンプレートは、「キャリア発展(コア)」を中心に、人脈・昇進・効率・スキル・財務・健康・ブランド・学習という 8 つのコアキーワードを展開し、さらに各分野ごとに具体的な行動目標をマトリクス状に細分化することで、キャリア成長の全側面を可視化・体系化します。人脈構築・昇進戦略・業務効率化・スキルアップ・資産管理・健康維持・個人ブランディング・継続学習という 8 つの次元で、日次・週次・月次の具体的なアクションを明確に定義し、バランスの取れたキャリア成長を実現し、「偏り」を防ぎます。EdrawMind の柔軟なカスタマイズ機能により、目標の追加・修正・進捗管理が容易に行え、キャリア計画・自己管理・成長戦略立案など、あらゆる場面で活用できます。キャリア発展の可視化と体系化を実現し、持続的な成長をサポートする最適なツールです。
マンダラチャート:キャリア発展プランは、個人のキャリア成長を体系的に計画・管理するための専門的な可視化ツールで、EdrawMind の強力なマンダラチャート作成機能を活用して開発されました。本テンプレートは、キャリア発展の 8 つのコアキーワード(人脈・昇進・効率・スキル・財務・健康・ブランド・学習)を中心に、各分野ごとに具体的な行動目標をマトリクス状に展開し、キャリア成長の全側面を可視化・体系化します。人脈構築・昇進戦略・業務効率化・スキルアップ・資産管理・健康維持・個人ブランディング・継続学習という 8 つの次元で、月次・週次・日次の具体的なアクションを明確に定義し、バランスの取れたキャリア成長を実現し、「偏り」を防ぎます。EdrawMind の柔軟なカスタマイズ機能により、目標の追加・修正・進捗管理が容易に行え、ビジネスパーソンのキャリア計画・自己管理・成長戦略立案など、あらゆる場面で活用できます。キャリア発展の可視化と体系化を実現し、持続的な成長をサポートする最適なツールです。
これは、専門家、起業家、キャリアプランナー向けに設計された、再利用可能な「マンダラチャートキャリア開発プラン」テンプレートです。このテンプレートは「キャリア開発」を中心とし、8つの主要な成長分野へと展開していきます。視覚的かつ体系的なデザインにより、抽象的なキャリア目標を具体的な行動計画へと落とし込みます。テンプレートは明確な構造を持ち、読みやすく快適なピンクとブルーの配色を採用しています。中心領域は黒い四角で「キャリア開発」のテーマを強調し、周囲の青い四角は8つの成長方向を示しています。これは、個人の能力開発計画や業界育成戦略の策定に役立ちます。中心テーマと枝のラベルを置き換えるだけで、ニーズに合わせたキャリアプランマップを素早く作成でき、断片化された目標を体系的なキャリア開発の道筋へと統合するのに役立ちます。これは単なるキャリアプランニングの「ナビゲーションマップ」ではなく、断片化された目標を体系的なキャリア開発の道筋へと統合する、継続的に改善していく成長ツールです。
digestive system
Digestive tube structure
Mucous membrane
epithelium
lamina propria (glands)
muscularis mucosa
submucosa
Muscle layer
adventitia
chronic gastritis
Cause
Helicobacter pylori (HP) infection
long term chronic irritation
duodenal fluid reflux
autoimmune damage
type
Non-atrophic gastritis/chronic superficial gastritis
parts
gastric antrum
Pathological changes
Features
Diffuse or focal distribution
naked eye
Gastric mucosa is congested and edematous, light red
There may be punctate bleeding and erosion
May be covered with gray-yellow or gray-white mucus exudate
under the mirror
Superficial mucosal lymphocyte and plasma cell infiltration
glands intact
In severe cases, inflammation involves the deep layers of the mucosa
ending
get well
chronic atrophic gastritis
chronic atrophic gastritis
Cause
Smoking, alcoholism, improper medication
Non-atrophic gastritis develops
autoimmune disease
Types
Type A
Commonly seen abroad
autoimmune disease
gastric body and fundus
combined with pernicious anemia
Type B
Common in China
Smoking, alcohol, drugs, HP
gastric antrum
cancer
Features
Mucosal atrophy and thinning, gland reduction or disappearance, intestinal metaplasia
Lymphocyte and plasma cell infiltration of the lamina propria
Pathological changes
naked eye
Gastric mucosa changes from normal orange-red to gray
The mucosal layer becomes thinner and the wrinkles disappear
Submucosal blood vessels are clearly visible, with occasional bleeding and erosion.
under the mirror
Mucous membranes become thinner and glands become smaller and fewer in number
A large number of lymphocytes and plasma cells infiltrate the lamina propria, which can form lymphoid follicles
Gastric mucosa may have fibrous tissue hyperplasia
Intestinal metaplasia (more), pseudopyloric gland metaplasia (rare)
peptic ulcer
Pathological changes
gastric ulcer
parts
Lesser curvature of stomach near pylorus
naked eye
usually one
round or oval
Within 2cm in diameter
The edges are neat and shaped like a knife cut
flat bottom
Deep into the muscle layer and even the serosa layer
Cardia side—deep, shallow digging-like shape; pyloric side—shallow, stepped shape
The mucosal folds at the edge of the ulcer radially converge toward the ulcer.
under the mirror
exudate layer
necrotic layer
granulation tissue layer
scar layer
proliferative endoarteritis
Performance
Arteriolar wall thickening, lumen stenosis, and thrombosis
as a result of
Insufficient local blood supply →affects tissue healing
Prevent ulcers and blood vessels from rupturing and bleeding
Duodenal ulcer (common)
duodenal bulb
Ulcers are small and shallow and heal easily
ending
heal
complication
Bleeding (10-35%)
Piercing (5%)
Duodenal ulcers are more likely to perforate
pyloric stenosis
Cancer (<1%)
Duodenal ulcers are almost never cancerous
clinical
cyclic upper abdominal pain
Pain attacks in the middle of the night
Acid reflux, belching
ulcer comparison
appendicitis
clinical
Metastatic right lower quadrant pain
Pathological changes
acute appendicitis
Acute uncomplicated appendicitis—early stage
Acute cellulite appendicitis—simple development
naked eye
The appendix is highly swollen and congested, with pus on the surface
under the mirror
Inflammatory lesions spread from superficial to deep layers in a fan-leaf shape
There is a large amount of neutrophil infiltration in all layers
Inflammatory edema, cellulose exudation
Acute gangrenous appendicitis—severe
chronic appendicitis
inflammatory bowel disease
Crohn disease
Site—Terminal ileum (main)
anti-colon antibodies in blood
Pathological changes
naked eye
segmental disease
The intestinal wall becomes thicker and harder, and the intestinal mucosa is highly edematous
Wrinkled paving stone pattern changes
under the mirror
transmural inflammation
Tuberculoid granuloma without caseous necrosis
ulcerative colitis
Site—rectum (main)
Pathological changes
Continuous distribution of lesions
ulcer
pseudopolyps
viral hepatitis
hepatitis virus
Basic lesions
degenerative inflammation
Degeneration of liver cells
spoil
transsexual
Cellular edema
Cytoplasmic loosening → ballooning
eosinophilia
Liver cells are reduced in size, cytoplasmic eosinophilia is enhanced, and nuclear staining is dark
Steatosis
Necrosis and apoptosis
Lytic necrosis
Punctate necrosis—acute vulgaris hepatitis
Fragmented necrosis—chronic hepatitis
Interface hepatitis—focal necrosis and disintegration of hepatocytes in the boundary plates around the liver lobules
Bridging necrosis—chronic severe hepatitis
Massive necrosis—severe hepatitis
apoptosis
eosinophilic body
Eosinophilia develops
The cytoplasm is condensed and the nucleus disappears → dark red densely stained round bodies
Exudation - infiltration of inflammatory cells
hyperplasia
Liver cell regeneration
Necrosis is light, fiber scaffold is intact, and regeneration is complete
Severe necrosis, collapse of the fibrous scaffold, and incomplete regeneration (nodular regeneration)
interstitial hyperplasia
Kupffer cells
Fibroblasts
Small bile duct hyperplasia
Fibrosis
Various types
Hepatitis A
Basic lesions
Hepatitis B
Light microscopy
ground glass hepatocytes
Electron microscopy
Smooth endoplasmic reticulum—HBsAg particles
Nuclei—HBcAg particles (sand-like nuclei)
Hepatitis C
Obvious fatty degeneration
Lymphocyte infiltration in the portal area and formation of lymphoid follicles
bile duct injury
Clinicopathological type
common viral hepatitis
Acute hepatitis (most common, mostly hepatitis B)
Pathological changes
naked eye
The liver is enlarged, soft, and has a smooth surface
under the mirror
Hepatocellular edema, ballooning, punctate necrosis, eosinophilic bodies
A small amount of inflammatory cell infiltration
The proliferation is not obvious
chronic hepatitis
Indicator—Viral hepatitis lasts for more than half a year
Evolution—depends on the type of virus infected (independent of the degree of initial liver disease)
The rate of hepatitis C chronic hepatitis turning into cirrhosis is extremely high
Pathological changes
Mild
punctate necrosis
Few inflammatory cells
Mild fibrous tissue hyperplasia
The leaflet structure is intact
Moderate
fragmentary necrosis, bridging necrosis
Moderate infiltration of inflammatory cells
Significant interstitial proliferation
The leaflet structure is basically complete
Severe
Large areas of necrosis → nodular regeneration of liver cells (cirrhosis)
Massive infiltration of inflammatory cells
Significant interstitial proliferation
Incomplete leaflet structure
severe viral hepatitis
acute severe hepatitis
Features
Acute onset, short course, severe lesions, and high mortality
Pathological changes
naked eye
The liver is reduced in size, weight, and texture
Cut surface yellow/red—acute yellow liver atrophy/acute red liver atrophy
under the mirror
Diffuse large necrosis of liver cells (central area→peripheral area), with only remaining mesh scaffolding
Liver sinusoids are dilated and congested, and Kupffer cells are hyperplasia and hypertrophy.
Massive inflammatory cell infiltration
clinical
A large amount of bilirubin enters the blood → hepatocellular jaundice
Coagulation factor synthesis disorder → bleeding tendency
liver failure, kidney failure
subacute severe hepatitis
Features
Slow onset, long course, mostly delayed from acute severe hepatitis
Pathological changes
under the mirror
Massive necrosis of liver cells Nodular regeneration of liver cells
Massive infiltration of inflammatory cells (lymphocytes, Kupffer cells)
interstitial hyperplasia, small bile duct hyperplasia
naked eye
Liver shrinks in size, loses weight, and becomes harder in texture
ending
Most cirrhosis
alcoholic liver disease
Pathological changes
Fatty Liver Disease – Most Common with Alcoholism
under the mirror
Liver cells are swollen with large fat droplets inside, pushing the cell nucleus to one side
The central lobule area is most obviously affected, accompanied by varying degrees of hepatocellular edema.
naked eye
liver big soft yellow
alcoholic hepatitis
hepatocellular steatosis
Mallory corpuscle
Focal hepatocellular necrosis with neutrophil infiltration
Alcoholic cirrhosis – Alcoholic liver disease is the most severe
Cirrhosis
Basic pathological characteristics
Chronic, diffuse hepatocyte degeneration and necrosis, intrahepatic fibrous tissue hyperplasia, and nodular regeneration of hepatocytes
pseudolobule
Cause
Viral hepatitis (my country)
Chronic alcoholism (Western)
cholestasis
Drugs, metabolic disorders, nutritional disorders
Classification
Micronodular (less than 3 mm)/alcoholic cirrhosis
Mild hepatitis/chronic alcoholism develops
Macronodular (more than 3 mm)/post-hepatitis cirrhosis
Severe hepatitis/toxic hepatitis develops
Mixed nodularity (half and half)
Pathological changes
under the mirror
The structure of the liver lobules is destroyed and replaced by pseudo lobules
Central lobular veins: absent/deviated/multiple
Liver cells: degeneration, necrosis, proliferation (large size, large and deeply stained nuclei, double nuclei), disordered arrangement
The periphery of the pseudolobules is surrounded by fibrous septa, and there is infiltration of inflammatory cells in the fibrous septa. Small bile duct hyperplasia
naked eye
Early stage - no significant changes
Late stage
Liver shrinks in size, loses weight, and becomes harder in texture
There are fiber-encircled nodules on the surface and cut surface (normal color/yellow-green/yellow-brown)
clinicopathological link
portal hypertension
reason
Intrahepatic fibrous tissue hyperplasia, hepatic sinusoidal occlusion, and portal vein circulation obstruction (sinusoidal obstruction)
Pseudolobules compress the sublobular veins and block blood outflow in the liver sinusoids (postsinusoidal obstruction)
The small branches of the intrahepatic hepatic artery and the small branches of the portal vein abnormally anastomose before they merge into the liver sinusoids, and high-pressure arterial blood flows into the liver sinusoids (pre-sinusoidal obstruction).
Performance
chronic congestive splenomegaly
Gastrointestinal congestion and edema
ascites
Causes
Portal hypertension → plasma leaks into the abdominal cavity
Hypoalbuminemia → decreased plasma colloid osmotic pressure
Liver dysfunction → elevated blood ADH and aldosterone → sodium and water retention
collateral circulation formation
Lower esophageal varices
Rupture → fatal bleeding (common cause of death from cirrhosis)
Rectal varicose veins
Rupture → bloody stool
Periumbilical varicose veins
brittlehead phenomenon
Liver dysfunction
protein synthesis disorder
bleeding tendency
Bile pigment metabolism disorder
Inactivated estrogen weakens → testicular atrophy, breast development, menstrual disorders, spider nevi, liver palms
Hepatic encephalopathy (hepatic coma)
pancreatitis
acute pancreatitis
Cause
Middle-aged men overeating
Biliary tract disease
Pathological type
Acute edematous (interstitial) pancreatitis (common)
Site—Tail of Pancreas
Good prognosis
naked eye
The pancreas becomes enlarged and hardened
under the mirror
Interstitial congestion, edema, neutrophil infiltration
acute hemorrhagic pancreatitis
The onset is urgent and the condition is serious
naked eye
Pancreatic enlargement, dark red, turbid yellow-white spots
under the mirror
Large areas of coagulative necrosis and massive bleeding
few inflammatory cells
clinicopathological link
shock
peritonitis
Elevated levels of amylase in blood
Serum ion changes
chronic pancreatitis
naked eye
Pancreatic nodular atrophy, hard texture
Diffuse fibrosis on cut surface
pseudocyst
under the mirror
Pancreatic cell degeneration and necrosis, interstitial lymphocyte and plasma cell infiltration, and extensive fibrosis
tumor
Esophageal cancer
source
Esophageal mucosal epithelium and glands
Pathological changes
early stage cancer
No clinically obvious symptoms
The lesion is localized and does not invade the muscle layer (regardless of whether there is lymphatic metastasis)
naked eye
Mild erosion of the mucosa at the cancer site/granular surface
under the mirror
Squamous cell carcinoma
Intermediate and advanced cancer/advanced cancer
clinical dysphagia
naked eye
Medullary type (diffuse wall thickening)
Fungi type (exophytic)
Ulcerative type
Coarctation type (diffuse wall thickening)
under the mirror
Squamous cell carcinoma
stomach cancer
source
gastric mucosal epithelium, glandular epithelium
Predisposed areas
gastric antrum
Pathological changes
early gastric cancer
Infiltration is limited to the mucosa and submucosa (raised, superficial, depressed)
Microcarcinoma - diameter <0.5cm
Small gastric cancer—0.6-1.0cm in diameter
A little bit of cancer - after the pathology was taken and the cancer was confirmed, the surgery did not find it
tubular adenocarcinoma
Intermediate and advanced cancer (advanced cancer) (polypoid/fungus type, ulcer type, invasive type)
Infiltration beyond the submucosa
"Leather Stomach"
Infiltration type: Diffuse infiltration causes the stomach wall to thicken and harden, and the gastric cavity becomes smaller and looks like leather.
"Colloid carcinoma"
Cancer cells secrete a large amount of mucus, and the cancer tissue appears translucent jelly to the naked eye.
Adenocarcinoma
transfer
Lymphatic metastasis (main)
Late metastasis via thoracic duct to left supraclavicular lymph node (Vichow signal node)
Hematogenous metastasis (late stage)
liver, lungs, brain
Implantation transfer
Krukenberg tumor—metastatic mucinous carcinoma that develops in both ovaries
Colorectal cancer (mostly rectum)
naked eye
Raised type, ulcerated type, infiltrative type, colloid type (worst prognosis)
under the mirror
Tubular adenocarcinoma, mucinous carcinoma (poor prognosis)
WHO classification—Colorectal tumor tissue is called cancer only if it invades the muscularis mucosa and reaches the submucosa (beyond the muscularis mucosa)
Not exceeded—Intraepithelial neoplasia
primary liver cancer
origin
Hepatocytes or intrahepatic bile duct epithelial cells
Classification
hepatocellular carcinoma
Cause
Hepatitis B, cirrhosis, alcohol, aflatoxin
Pathological changes
naked eye
Small liver cancer type—early liver cancer
The diameter of a single cancer nodule is less than 3cm/the total diameter of 2 cancers is less than 3cm
Multinodular type—most common
Diffuse type
Huge type
Tumor volume >10cm
Satellite carcinoma nodules
under the mirror
Hepatocyte differentiation varies greatly
cholangiocarcinoma
mixed cell liver cancer
pancreatic cancer