MindMap Gallery Infectious 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.
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Infectious diseases
tuberculosis
Basic pathological changes
ooze
serous or fibrinitis
Hyperplasia (tuberculous nodules)
Epithelioid cells (mainly)
caseous necrosis
Langhans giant cells
Lymphocytes
proliferating fibroblasts
live tuberculosis bacilli
Necrosis
caseous necrosis
primary tuberculosis
Predisposed areas
Under the upper leaf or on the lower leaf
Near the pleura
primary syndrome
Primary lesions of the lung
Tuberculous granuloma is characterized by
Tuberculous lymphangitis
hilar lymph node union
X-ray
dumbbell shape
mode of dissemination
lymphatic or blood channels
secondary tuberculosis
Predisposed areas
apex of lung
dissemination route
bronchi
Classification
Infiltrating pulmonary tuberculosis (most common)
Mainly exudation
active pulmonary tuberculosis
Cloudy shadow under X-ray
focal pulmonary tuberculosis
Mainly hyperplasia
chronic fibrocavitary tuberculosis
The cavity is divided into 3 layers
inner caseous necrosis
Intermediate tuberculous granulation tissue
Outer layer of fibrous connective tissue
open pulmonary tuberculosis
Late stage diffuse fibrosis of lung tissue
Cause pulmonary heart disease
caseous pneumonia
Extensive cheesy necrosis
Massive serous fibrin exudation in the alveolar space
combined balls
Isolated fibrous-encapsulated spherical caseous necrosis
tuberculous pleurisy
Moisture
Mainly exudation
Dry
Mainly proliferative changes
extrapulmonary tuberculosis
acute systemic miliary tuberculosis
Tuberculosis is characterized by invasion of pulmonary veins
Intestinal tuberculosis
Intestinal primary syndrome (primary)
primary tuberculous ulcer of intestine
Tuberculous lymphangitis
mesenteric lymphadenitis
Secondary
Ulcerative type
Ulcer perpendicular to long axis
Most likely to occur in the ileocecal part
Proliferative type (most common)
Formation of massive granulomas
cause intestinal stenosis
renal tuberculosis
dissemination route
blood channel
Predisposed areas
Unilateral kidney
bladder tuberculosis
Ulceration and fibrous tissue hyperplasia in the trigone area of the bladder
bone tuberculosis
caseous necrosis forming cold abscess
Spinal tuberculosis is the most common
Cerebral tuberculosis
Obvious brain lesions
lymph node tuberculosis
Mesenteric lymph nodes most commonly involved
Typhoid fever
Overview
concept
Acute infectious disease caused by Salmonella typhi
Lesion characteristics
acute proliferative inflammation
Systemic mononuclear macrophage proliferation
lesion site
terminal ileum
Clinical features
Persistent high fever, apathy, relatively slow
Pathogenesis
endotoxin
diagnosis
Serum agglutination test (Feida test)
Transmission route
feces-oral
body pathways
Small intestine (terminal ileum)—lymphoid tissue of the intestinal wall
At this time, the terminal ileal lymph node or mesenteric lymph node is engulfed by typhoid bacilli, grows and reproduces in them, and becomes sensitive to
Intestinal wall lymphoid tissue—thoracic duct—blood circulation (bacteremia)
Proliferation within macrophages in the blood, hepatosplenomegaly
Gallbladder-intestinal (endotoxemia, sepsis)
Repeated invasion of sensitive intestinal lymphoid tissue leads to necrosis and shedding of intestinal mucosa, forming ulcers
Pathological changes (acute proliferative inflammation)
Overview
typhoid cells
The proliferating macrophages engulf typhoid bacilli, red blood cells and debris.
Typhoid granuloma (typhoid fever summary)
Typhoid cells clump together to form small nodules
It is a characteristic lesion of typhoid fever and can be diagnosed
intestinal lesions
Myeloid swelling period (1 week)
Peyer's lymph node lesions are the most prominent
Lymphatic tissue in the lower ileum swells and bulges
The surface of the raised tissue resembles a brain gyrus
Necrosis period (2 weeks)
Local intestinal mucosal necrosis
Typhoid enters the intestines again
Ulcer stage (3 weeks)
The edge of the ulcer is raised and the bottom is uneven
Ulceration of lymph nodes parallel to the intestines
intestinal tuberculosis ulcer vertical
Solitary lymph node ulcer is small and round
Healing period (4 weeks)
Granulation hyperplasia, intestinal mucosal regeneration
Other lesions
heart
Granular degeneration, necrosis
skin
Small red papules (rosacea)
Diaphragm, rectus abdominis, adductor vastus
Coagulative necrosis (waxy degeneration)
gallbladder
No disease, but can reproduce
bacillary dysentery
Overview
Lesion classification
pseudomembranous colitis
lesion site
Large intestine (sigmoid colon, rectum)
Cause
Infection with Shigella dysenteriae
Transmission route
feces-oral
body pathways
Colon multiplication, invasion of intestinal mucosa
Propagation of the lamina propria of the mucosa, release of endotoxins, and ulceration of the intestinal mucosa
Intestinal mucosa complicated by exudative inflammation
Pseudomembrane falls off and forms mucus, pus and bloody stools
Endotoxins enter the blood, causing toxemia
Among them, Shigella can produce exotoxins, which are the main cause of watery diarrhea.
Pathological changes
acute bacillary dysentery
acute catarrhal inflammation
Early stage hypersecretion of mucus, mucosal congestion and edema, and spotting bleeding may be seen.
Characteristic pseudomembranous inflammation
Superficial necrosis of the mucosa, with large amounts of cellulose in the exudate
Necrotic tissue, inflammatory cells, red blood cells, and bacteria form pseudomembranes
First appears on the top of the mucous membrane wall, chaff-like
Grayish white, dark red if bleeding, green if bile staining
Ulcer formation
Pseudomembrane falls off and forms ulcer
Map-like, superficial
heal
Exudation and necrosis are cleared, and surrounding tissue is regenerated
chronic bacillary dysentery
Recurrent episodes of acute bacillary dysentery in four stages
cause deep ulcers
virulent bacillary dysentery
Catarrhal inflammation of the gastrointestinal tract (without pseudomembrane formation)
Can quickly lead to shock
Amebiasis
Overview
parasitic site
colon
Pathogenic stage
large trophozoite
infection stage
cyst
Pathogenesis
The cyst wall is acid-resistant and can safely enter the ileocecal part.
Alkaline intestinal fluid dissolves cysts and releases small trophozoites
Small trophozoites multiply and invade the intestinal mucosa to become large trophozoites
Large trophozoites phagocytose tissue/red blood cell fragments, destroy the intestinal wall and cause ulcers
Intestinal amoebiasis
Overview
lesion site
cecum, ascending colon
Lesion classification
degenerative inflammation
liquefaction necrosis
acute phase
in general
Early days
Punctate necrosis (mucosal layer)
progress period
Button necrosis (submucosa)
Formation of a flask-shaped ulcer with a small base in the mouth (diagnosis)
Late stage
Adjacent ulcers are connected and fall off, forming a huge ulcer
Involvement of the muscularis leading to intestinal perforation and subsequent peritonitis
under the mirror
Trophozoites can be found at the edge of the ulcer and in the small veins of the intestinal wall.
Chronic phase
Amoebiasis
meningitis and Japanese encephalitis
meningococcal meningitis
Upper respiratory tract infection stage (septicemia stage): Petechiae appears on the skin and mucous membranes; develops into meningitis stage
subarachnoid suppurative inflammation
The subarachnoid space is filled with purulent exudate
The subarachnoid space is widened and filled with gray-yellow purulent exudation
Cerebrospinal fluid: turbid or purulent, many pus cells, reduced sugar, and positive bacterial culture Meningitis irritation symptoms, increased intracranial pressure
Meningoencephalitis B
Mosquitoes are vectors
Cerebrospinal parenchymal degenerative inflammation
Millet-sized translucent softening stove
Degeneration and necrosis of nerve cells: satellite phenomenon, neurophagocytosis, disappearance of Nissl bodies Formation of sieve-like softening lesions (characteristics) perivascular lymphocyte cuff
Cerebral edema, increased intracranial pressure, motor neuron damage