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MindMap Gallery local blood circulation disorder
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local blood circulation disorder
The mind map of local blood circulation disorders shares knowledge about blood circulation disorders, congestion and congestion, thrombosis, infarction, and embolism. Come and take a look!
Edited at 2023-06-04 10:28:07
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- Outline
local blood circulation disorder
blood circulation disorder
Classification
systemic blood circulation disorder
local blood circulation disorder
Abnormal local circulation blood volume (congestion and congestion, ischemia)
Abnormal blood properties and vascular contents (thrombosis and embolism) → infarction
Changes in vessel wall permeability and integrity (edema and hemorrhage)
congestion and congestion
hyperemia
Congestion of organs or tissues due to increased arterial blood input is called active congestion.
mechanism
type
Physiological congestion (many)
Pathological congestion
inflammatory hyperemia
Hyperemia after decompression
Tissues and organs that have been under pressure for a long time will reflexively expand arterioles when the pressure is suddenly relieved, causing congestion.
Do not extract too much ascites at one time → avoid congestion after decompression
lesions
under the mirror
Thin A, Cap expands, fills RBC
naked eye
Swelling, bright red, hot (body surface)
as a result of
Mostly physiological, it is a temporary vascular reaction, which is beneficial to the body; if the blood vessels are diseased, they may cause rupture and bleeding.
Blood stasis
Finger venous return is blocked and blood accumulates in small veins and capillaries (passive)
reason
venous compression
venous lumen obstruction
heart failure
lesions
under the mirror
Little V and Cap are expanding but full of RBC
naked eye
Swelling, dark red or purple (cyanosis), cool
Cyanosis: skin and mucous membranes turn blue-purple, reduced HB≥5g/dl
as a result of
Stasis edema and hemorrhage
Parenchymal cell atrophy, degeneration, and necrosis
hemorrhagic sclerosis
Blood stasis in vital organs
Pulmonary congestion (left heart failure)
lesions
under the mirror
Alveolar wall thickening, telangiectasia, congestion, and large amounts of edema fluid, RBC, and heart failure in the alveolar cavities C
heart failure cells
When left heart failure causes chronic pulmonary congestion, macrophages C containing large amounts of hemosiderin can be seen in the alveolar spaces.
naked eye
The lung volume increases, dark red, and foamy red fluid flows out from the cut surface
clinical manifestations
Pink frothy sputum, cyanosis, shortness of breath (orthopnea)
ending
Pulmonary fibroplasia with iron-blooded yellow → brown sclerosis of the lungs
Liver congestion (right heart failure)
lesions
under the mirror
Central V sinusoidal blood stasis Compression atrophy and necrosis of liver C in the central lobule area Perilobular liver C steatosis
naked eye
Increased volume, weight, and membrane tension The cut surface is red (blood stasis) and yellow (fatty change), and looks like betel nut, so it is called betel nut liver.
clinical manifestations
Hepatomegaly, pain in liver area, decreased liver function
ending
Long-term chronic liver congestion → cirrhosis
formation of thrombus
concept
In the cardiovascular system of a living body, certain blood components (platelets) precipitate and aggregate, or blood coagulates to form a solid mass.
forming conditions
Cardiovascular endothelial cell damage (most common)
Endocarditis, myocardial infarction, atherosclerosis (cardiovascular endothelial damage leading to thrombosis)
Hypoxia, shock, sepsis → extensive endothelial injury → DIC
changes in blood flow status
Slow down/vortex
increased blood coagulability
Platelets and coagulation factors↑
Fibrinolytic system activity↓
hypercoagulable state
reason
hereditary
Acquisition
Major surgery, severe trauma, extensive burns, malignant swelling, etc.
The formation of blood clots in the arteries and heart
Intimal damage and eddy currents are common
venous thrombosis
Often slow and stagnant blood flow
The process of thrombosis and the morphology of thrombus
Platelet adhesion and aggregation
blood clotting
Platelet adhesion is the first step in thrombosis (primary) Future development depends on the location and blood flow rate (Continuous venous thrombosis is the most complete)
Types and shapes of blood clots
White thrombus (dissociated thrombus, platelet thrombus)
seen in
Persistent thrombus head, heart valve
naked eye
Gray, rough, hard, tight
under the mirror
A large number of platelets and a small amount of fibrin constitute surface adherent neutrophils
Red thrombus (coagulable thrombus)
seen in
tail of persistent thrombus
naked eye
Dark red, crispy
under the mirror
Cellulose mesh filled with red blood cells
Mixed thrombus (lamellar thrombus)
seen in
Body of persistent thrombus; aneurysm (mural thrombus), left atrium (spherical thrombus)
naked eye
Red and white, arranged in layers
under the mirror
Platelet beams and fibrin mesh filled with red blood cells between beams
hyaline thrombi (microthrombi)
seen in
DIC (disseminated intravascular coagulation)
constitute
Fibrin - fibrinous thrombus
parts
within microcirculation
naked eye
Can't see
ending
Dissolve, absorb, soften and fall off
Mechanization and recanalization
Recanalization
During the process of thrombus organization, due to drying, shrinkage and softening, cracks appear inside it or between it and the blood vessel wall. New endothelial cells cover its surface to form a new lumen and communicate with each other to partially restore blood flow to the blocked blood vessel.
Calcification (incomplete organization): phleboliths/arterioliths
Effects on the body
favorable
Stop bleeding and prevent the spread of infection
unfavorable
block blood vessels
embolism
Heart valve deformation
extensive bleeding
infarction
concept
Necrosis of organs or local tissues due to vascular obstruction and cessation of blood flow leading to ischemia and hypoxia
Reason
Thrombosis (most common)
Arterial embolism
arterial spasm
Vessel compression and occlusion
condition
Tissue sensitivity to ischemia and hypoxia
Collateral circulation status
dual blood supply
Lungs (pulmonary artery and bronchial artery), liver (hepatic artery and portal vein)
Rich anastomotic branches
Forearm and hand (radial and ulnar arteries)
Few anastomotic branches
Brain, spleen, kidney
Pathological changes and types
General morphological features of infarction
The shape of the infarct
Depends on how the organs are vascularized
Portal organs (spleen, kidneys, lungs)
Cone shape (sector-shaped section)
The tip points toward the portal (the site of blood vessel obstruction)
The bottom is close to the surface of the organ
Myocardial infarction
Map graphics
Intestinal infarction
segmental
Texture of the infarct
Depends on the type of necrosis
Coagulative necrosis: heart, liver, spleen, lung, kidney
Liquefied necrosis: brain
Color of infarct
Depends on the blood content in the lesion
Anemic infarction (white infarct)
Hemorrhagic infarct (red infarct)
Types of infarction
Anemic infarction
Reason
Blocked arteries
Part
Heart, kidney, spleen, brain
Dense tissue structure with thin and few side branches
lesions
Grayish white, clear boundary, surrounding congestion and hemorrhage
Hemorrhagic infarction
Reason
Blocked arteries
Conditions
Severe congestion
Part
Lungs, intestines
The tissue structure is loose and the dual arterial supply or anastomotic branches are abundant
Common
pulmonary hemorrhagic infarction
Part
In the peripheral part of the lower lobe of the lung, the costophrenic angle is more common
naked eye
Cone-shaped, dark red, pulmonary membrane fibrinitis
under the mirror
The structure of the alveolar wall is unclear, and the alveolar cavity and interstitium are filled with red blood cells
enterohemorrhagic infarction
naked eye
Segment-shaped, purple-red, thickened intestinal wall
under the mirror
Tissue necrosis and bleeding in various layers of the intestinal wall
septic infarction
Bacteria-containing emboli block blood vessels, common in infective endocarditis
The impact and outcome of infarction on the body
embolism
concept
Abnormal substances that are insoluble in the blood appear in the circulating blood and travel with the blood to block the lumen of the blood vessels.
embolus
Abnormal substance that blocks the blood
solid
liquid
gas
The path of travel of emboli
consistent with blood flow direction
From the venous system (systemic circulation) and right heart
lung
From the left heart and aortic system
The whole body (spleen, brain, kidneys, lower limbs, etc.)
portal venous system
liver (splenic vein)
cross emboli
congenital atrioventricular septal defect
Retrograde embolism (rare)
Seen when chest and abdominal pressure suddenly increase when venous emboli in systemic circulation circulate
Types of embolism and effects on the body
Thromboembolism (99%)
pulmonary embolism
source
Deep veins of lower limbs above the knee (95%) Pelvic vein, right heart mural thrombosis
as a result of
Depends on the size and number of emboli and cardiopulmonary function
The emboli are small and few
Generally does not cause serious consequences
Dual blood supply of pulmonary artery and bronchial artery
Chronic pulmonary congestion
Hemorrhagic infarction of lung tissue
Increased intramicrocirculatory pressure and obstruction of bronchial artery blood supply
The embolus is big
sudden death
The emboli are small and numerous
sudden death
systemic circulatory embolism
Source
Left heart (80%) or artery
parts
More common in brain, kidney, spleen and lower limbs
as a result of
Local tissue infarction when no collateral circulation is established
fat embolism
Fat droplets appear in the circulation and block blood vessels
source
Shaft fractures of long bones, severe bruises and burns to fatty tissue
Lipid droplets → bone marrow sinusoidal capillaries and venules
traumatic Non-traumatic (diabetes, alcoholism, chronic pancreatitis, excessive stress)
gas embolism
concept
A large amount of air quickly enters the blood circulation or the gas dissolved in the blood quickly dissociates to form bubbles and block blood vessels.
Classification
air embolism
seen in
Infusion, blood transfusion, artificial pneumothorax and other accidents Trauma or surgery to the head, neck, chest wall, and lungs Strong uterine contractions during childbirth
as a result of
In small doses, no serious consequences will occur
Sudden death when exceeding 100 ml
Air→enters the blood→foamy blood forms in the heart cavity→sudden death
Nitrogen embolism
concept
When the human body rapidly transitions from a high-pressure environment to a low-pressure environment, the gas dissolved in the blood, interstitial fluid, and fatty tissue rapidly dissociates and forms bubbles, causing gas embolism, which is called decompression sickness.
seen in
diver, pilot
as a result of
Subcutaneous → Subcutaneous emphysema, skin itching
Muscles, tendons, ligaments → Muscle, joint pain
Systemic blood vessels → ischemia, infarction, If it affects the heart and brain, it can be life-threatening
amniotic fluid embolism
Amniotic fluid (containing meconium, vernix, lanugo, mucus, keratinized squamous epithelium, etc.)
concept
During childbirth, the uterus contracts and the amniotic fluid is pressed into the venous sinuses of the uterine wall and enters the maternal blood circulation.
More common in abnormal births such as placenta previa and inappropriate use of oxytocin
process
Amniotic fluid → maternal blood circulation → pulmonary embolism → systemic circulation embolism
sudden death mechanism
Pulmonary artery obstruction and reflex vasospasm
Anaphylactic shock caused by amniotic fluid
DIC caused by coagulogenase-like substances in amniotic fluid