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pathophysiology
The pathophysiology is summarized based on what we teach. It summarizes the symptoms of fever, stress, Ischemia-reperfusion injury, shock, etc.
Edited at 2024-01-12 00:04:41
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pathophysiology
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This article discusses the Easter eggs and homages in Zootopia 2 that you may have discovered. The main content includes: character and archetype Easter eggs, cinematic universe crossover Easter eggs, animal ecology and behavior references, symbol and metaphor Easter eggs, social satire and brand allusions, and emotional storylines and sequel foreshadowing.
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- Outline
pathophysiology
introduction
A discipline that studies the rules and mechanisms of functional and metabolic changes in the occurrence and development of diseases. Its main content is to reveal the essence of the disease and provide theoretical and experimental basis for establishing effective disease diagnosis, treatment and prevention strategies.
Introduction to diseases
Disease: an abnormal life state corresponding to health. There is also a sub-health state between disease and health.
Health: not only the absence of disease or infirmity, but a state of complete physical, mental and social well-being
Sub-health: a state of low physiological function between health and disease
Aging: a comprehensive state in which the body's adaptability to the external environment decreases due to morphological changes, functional decline, and metabolic disorders during the aging process.
Brain death: Irreversible and permanent loss of all brain function (including cerebrum, diencephalon and brainstem) and permanent cessation of functioning of the body as a whole
Cause: a causative factor that is essential to cause a disease, confer characteristics on the disease, or determine the specificity of the disease
Water and electrolyte metabolism disorders
dehydration
A group of clinical syndromes in which the human body consumes a large amount of water due to insufficient drinking water or pathological changes and cannot replenish it in time, resulting in a decrease in extracellular fluid and metabolic disorders.
hypotonic dehydration
Loss of Na is greater than water loss, serum Na concentration is <135mmol/L, plasma osmotic pressure is <290mmol/L, and is accompanied by a decrease in extracellular fluid volume.
Causes and Mechanisms
lost through kidneys
Long-term continuous use of diuretics
Adrenocortical insufficiency
parenchymal renal disease
renal tubular acidosis
Extrarenal loss
fluid loss through gastrointestinal tract
Liquid accumulates in the third gap
lost through skin
Effects on the body
Decreased extracellular fluid, prone to shock
Decreased plasma osmolality
Have obvious signs of water loss
Hyponatremic patients with renal sodium loss
hypertonic dehydration
Water loss is greater than sodium loss, serum Na concentration >150mmol/L, plasma osmotic pressure >310mmol/L
Causes and Mechanisms
reduced water intake
Too much water loss
water loss through respiratory tract
Transcutaneous water loss
transrenal water loss
gastrointestinal water loss
Effects on the body
Thirsty
Decreased extracellular fluid
Transfer of intracellular fluid to extracellular fluid
Hemoconcentration
central nervous system dysfunction
isotonic water loss
Water and sodium are lost proportionally, and blood volume is reduced, but serum Na concentration and plasma osmotic pressure are still within the normal range.
Edema
Accumulation of excess fluid in tissue spaces or body cavities
Classification
According to the extent of edema
generalized edema
localized edema
According to the cause of disease
renal edema
hepatic edema
cardiac edema
dystrophic edema
Lymphedema
inflammatory edema
According to the organ tissue where edema occurs
subcutaneous edema
Brain edema
Pulmonary Edema
Pathogenesis
Disorders of fluid exchange inside and outside blood vessels
Increased capillary hydrostatic pressure
Decreased plasma colloid osmotic pressure
Increased microvascular wall permeability
Lymphatic drainage is blocked
Imbalance of fluid exchange inside and outside the body - sodium and water retention
Decreased glomerular filtration rate
Increased reabsorption of sodium and water by the proximal convoluted tubule
Increased reabsorption of sodium and water by the distal convoluted tubule and collecting duct
Characteristics and impact on the body
Features
Characteristics of edema fluid
Leakage
exudate
Edema skin characteristics
pitting edema
Hidden edema
Distribution characteristics of generalized edema
Influence
cell dystrophy
Calcium metabolism disorder
The normal range of serum potassium is 3.5~5.5mmol/L
Hypokalemia
Causes and Mechanisms
Insufficient potassium intake
Too much potassium loss
Potassium loss through gastrointestinal tract
Potassium loss through kidney
Transcutaneous potassium loss
Transfer of extracellular potassium into cells
Alkalosis
excessive insulin use
Increased beta-adrenergic receptor activity
Poisoning by certain poisons
hypokalemic periodic paralysis
Effects on the body
Disorders associated with abnormal membrane potential
Neuromuscular effects of hypokalemia
Effects of hypokalemia on myocardium
Changes in physiological properties of myocardium
Increased excitability
Increased self-discipline
reduced conductivity
Contractile changes
changes in electrocardiogram
Impairment of myocardial function
Arrhythmia
Damage associated with cellular metabolic disorders
Skeletal muscle damage
kidney damage
Effect on acid-base balance
hyperkalemia
Causes and Mechanisms
Too much potassium
Decreased potassium excretion
kidney failure
Mineralocorticoid deficiency
Transfer of potassium from intracellular to extracellular
acidosis
Hyperglycemia combined with insulin deficiency
use of certain medications
decomposition of matter
hypoxia
hyperkalemic periodic paralysis
Effects on the body
Neuromuscular effects of hyperkalemia
acute hyperkalemia
chronic hyperkalemia
Effects of hyperkalemia on myocardium
Changes in physiological properties of myocardium
excitability changes
reduced self-discipline
reduced conductivity
reduced contractility
changes in electrocardiogram
Impairment of myocardial function
Acid-base balance and acid-base disorders
Regulation of acid-base balance
blood buffer system
bicarbonate buffer system
Phosphate buffer system
protein buffer system
The regulatory role of the lungs in acid-base balance
central regulation of respiratory movements
Peripheral regulation of intentional movement
The regulatory role of tissue cells in acid-base balance
The regulatory role of the kidney in acid-base balance
Proximal tubule secretion of H and reabsorption of NaHCO3
The external convoluted tubule and collecting duct secrete H and reabsorb NaHCO3
Common indicators of acid-base balance disorders
PH and H concentration
arterial blood CO2 partial pressure
Standard bicarbonate and actual bicarbonate
buffer base
Base remaining
anion gap
simple acid-base balance disorder
metabolic acidosis
A decrease in pH caused by an increase in fixed acid and/or a loss of HCO3, characterized by a primary decrease in plasma HCO3
Causes and Mechanisms
Kidney acid excretion and alkali retention dysfunction
kidney failure
renal tubular dysfunction
Use carbonic anhydrase inhibitors
Too much HCO3 is lost directly
metabolic dysfunction
lactic acidosis
ketoacidosis
other reasons
Excessive intake of exogenous fixed acids
hyperkalemia
Hemoconcentration
body's compensatory adjustments
Buffering of blood and buffering and compensatory regulation of intracellular and intracellular ion exchange
compensatory regulation of the lungs
Compensatory regulation of kidneys
Effects on the body
cardiovascular system changes
ventricular arrhythmias
Decreased myocardial contractility
Decreased responsiveness of the vasculature to catecholamines
central nervous system changes
changes in skeletal system
respiratory acidosis
A decrease in pH caused by CO2 excretion disorder or excessive inhalation, characterized by a primary increase in plasma H2CO3 concentration.
Causes and Mechanisms
Respiratory center depression
airway obstruction
Respiratory muscle paralysis
Thoracic lesions
lung disease
Improper management of artificial respirators
Too much CO2 inhalation
body's compensatory adjustments
Compensatory adjustment of acute respiratory acidosis
Chronic~
Effects on the body
CO2 directly relaxes blood vessels
Effects on central nervous system function
metabolic alkalosis
An increase in pH caused by an increase in extracellular fluid base and/or H loss, characterized by a primary increase in plasma HCO3
Causes and Mechanisms
Too much acid loss
lost through kidneys
Widespread use of diuretics
Adrenocortical hormone excess
Transgastric loss
HCO3 excess load
Hypokalemia
liver failure
body's compensatory adjustments
Buffering of blood and buffering and compensatory regulation of intracellular and intracellular ion exchange
compensatory regulation of the lungs
renal compensatory regulation
Effects on the body
Changes in central nervous system function
Neuromuscular effects
respiratory alkalosis
PaCO2 decrease and pH increase caused by pulmonary hyperventilation, characterized by primary decrease in plasma H2CO3 concentration
Causes and Mechanisms
Hypoxemia and lung disease
Direct stimulation of the respiratory center or psychogenic hyperventilation
Strong body metabolism
Improper use of artificial respirator
body's compensatory adjustments
Ion exchange inside and outside cells and intracellular buffering
renal compensatory regulation
Effects on the body
hypoxia
Hypoxia: A pathological process in which tissue oxygen supply is reduced or oxygen cannot be fully utilized, leading to abnormal changes in tissue metabolism, function, and morphological structure.
Cyanosis: When the concentration of deoxyhemoglobin in the capillary blood reaches or exceeds 5g/dl, the skin and mucous membranes turn blue-purple
Commonly used blood oxygen indicators
Blood oxygen partial pressure (PO2)
When the partial pressure of oxygen is 150mmHg, the partial pressure of carbon dioxide is 40mmHg, and the temperature is 38°C, the amount of oxygen that can be combined with hemoglobin (Hb) in 100ml of blood outside the body
blood oxygen capacity
blood oxygen content
hemoglobin oxygen saturation
Causes, classification and characteristics of blood oxygen changes of hypoxia
hypotonic hypoxia
Decreased partial pressure of arterial oxygen and decreased blood oxygen content
reason
Inhaled oxygen partial pressure is too low
External respiratory dysfunction
venous blood flows into arteries
Characteristics of blood oxygen changes
PaO2 decreases
Decreased arterial oxygen content
Decreased arterial oxygen saturation
Blood oxygen levels are normal or increased
blood hypoxia
Decreased hemoglobin content, or changes in hemoglobin properties, resulting in lower blood oxygen content
reason
Decreased hemoglobin content
poisoned by carbon monoxide
Methemoglobinemia
Abnormally increased affinity of hemoglobin for oxygen
Characteristics of blood oxygen changes
PaO2 is normal
SaO2 normal or reduced
Reduction in hemoglobin content or changes in properties
circulatory hypoxia
Reduced tissue blood flow reduces tissue oxygen supply
reason
systemic circulatory disorder
local circulatory disorder
Characteristics of blood oxygen changes
PaO2 is normal, arterial oxygen saturation is normal
Blood oxygen volume and blood oxygen levels are normal
Increased difference in arterial and venous blood oxygen content
organizational hypoxia
reason
Drug inhibition of mitochondrial oxidative phosphorylation
Decreased respiratory enzyme synthesis
mitochondrial damage
Characteristics of blood oxygen changes
Functional and metabolic changes
respiratory system
Increased pulmonary ventilation
high altitude edema
circulatory system
Heart function and structural changes
heart rate slows down
weakened myocardial contractility
Decreased cardiac output
Ectopic heart rhythms and conduction blocks
right ventricular hypertrophy
Changes in blood flow distribution
changes in pulmonary circulation
hypoxic pulmonary vasoconstriction
hypoxic pulmonary hypertension
tissue capillary proliferation
blood system
Increased red blood cells and hemoglobin
Increased 2,3-DPG in red blood cells and enhanced oxygen release capacity of red blood cells
fever
Fever: When the body temperature set point moves upward due to the action of pyrogen, causing the regulatory body temperature to rise, exceeding the normal body temperature by 0.5℃
Overheating: Due to body temperature regulation disorders, or heat dissipation disorders and abnormal function of heat-producing organs, etc., the body temperature regulation center cannot control the body temperature at a level compatible with the set point, which is a passive increase in body temperature.
endogenous pyrogen
Endogenous pyrogen cells produce and release substances that can cause an increase in body temperature under the action of heating activators.
Etiology and pathogenesis
Fever is usually caused by a heating activator acting on the body, activating endogenous pyrogen-producing cells to produce and release endogenous pyrogens, and then causing an increase in body temperature through some subsequent steps.
external pyrogen
bacteria
Gram-positive bacteria
Staphylococcus, Streptococcus, Pneumococcus, Diphtheria bacillus
Gram-negative bacteria
Escherichia coli, Typhimurium, Neisseria gonorrhoeae, meningococci
Mycobacteria
Virus
Fungi
spirochetes
protozoa
products in the body
Antigen-antibody complex
Steroid
Extensive destruction of tissue in the body
endogenous pyrogen
interleukin-1
Tumor necrosis factor
Interferon
interleukin-6
macrophage inflammatory protein-1
stress
When the body feels strong stimulation from various factors, in order to meet its coping needs, the adaptive changes and reconstruction of the homeostasis of the internal environment occur
functional metabolism
Changes in the locus coeruleus-sympathetic-adrenomedullary system
central effect
Excited, alert, focused and nervous
Overactivation—anxiety, fear, or anger
peripheral effect
Mainly manifested by rapid increase in plasma levels of catecholamines such as norepinephrine, epinephrine, and dopamine
Enhance heart function
Regulate blood perfusion
Improve respiratory function
Promote energy metabolism
Changes in the hypothalamic-pituitary-adrenocortical hormone system
central effect
A moderate amount of excitement or pleasure
excessive adaptation mechanism disorder
peripheral effect
Helps maintain blood pressure
Helps maintain blood sugar
Conducive to fat mobilization
Fight cell damage
Inhibit inflammatory response
stress ulcer
Acute lesions of the gastric and duodenal mucosa caused by strong stress mainly manifest as erosion, shallow ulcers, bleeding, etc. In severe cases, gastrointestinal perforation and massive bleeding may occur, which are the most characteristic pathological changes of stress.
ischemia reperfusion injury
IRI: Restoring blood perfusion and oxygen supply to some ischemic tissues and organs will actually aggravate tissue damage.
The mechanism
Increased free radicals
free radical generation
Single electron reduction during oxidative phosphorylation
Enzymatic and non-enzymatic reactions
free radical elimination
Antioxidants
Antioxidase
The mechanism by which IRI causes an increase in free radicals
mitochondrial damage
Oxidative phosphorylation dysfunction Decreased antioxidant enzyme activity
Neutrophil recruitment and activation
Catalyzed by NADPH oxidase and NADH oxidase, free radicals are generated
Increased formation of xanthine oxidase catalyzes increased ROS generation
Catecholamine autooxidation manganese plus
Increased free radicals cause damage to the body
membrane lipid peroxidation
protein function inhibition
Nucleic acid damage and DNA fragmentation
calcium overload
Mechanism of calcium overload caused by IRI
Abnormal Na-Ca exchange
Protein kinase (PKC) activation
biofilm damage
Mechanism of body damage caused by calcium overload
energy metabolism disorder
Decomposition of cell membrane and structural proteins
aggravate acidosis
Overactivation of inflammatory response
IRI causing mechanism
Increased production of cell adhesion factors
Increased production of chemokines and cytokines
Mechanisms that cause body damage
Microvascular damage
Hemorrheological changes
Increased permeability
cell damage
shock
Under the influence of severe blood loss, infection, trauma and other strong pathogenic factors, the effective circulating blood volume of the body is sharply reduced, and the tissue blood perfusion is seriously insufficient, causing cell ischemia and hypoxia, which affects the function and metabolism of important life organs. Systemic critical pathological process of disorder or structural damage
The mechanism
microcirculatory mechanism
microcirculatory ischemic phase
Less perfusion and less flow, less perfusion and less flow, and the tissue is in a state of ischemia and hypoxia.
The sympathoadrenal medullary system is excited, causing a large amount of catecholamines to be released into the blood
Compensatory significance
Helps maintain arterial blood pressure
Increased blood return volume
increased cardiac output
Increased peripheral resistance
Helps blood supply to the heart and brain
microvascular congestion phase
There is less flow during irrigation, more flow during irrigation, and the tissue is in a state of congestion and hypoxia.
microvascular dilation mechanism
Acidosis reduces vascular smooth muscle responsiveness to catecholamines
Increased production of blood vessel dilating substances
blood pressure stasis mechanism
White blood cells adhere to venules
Hemoconcentration
Decompensation and vicious cycle
The amount of blood returned to the heart decreases sharply
autotransfusion stopped
Decreased blood perfusion of the heart and brain
Microcirculatory failure stage
No perfusion, no flow, microthrombus formation, no reflow phenomenon
microvascular paralytic dilation
DIC formation
hemodynamic changes
coagulation system activation
TAX2-PGI2 imbalance
Persistent hypoperfusion of systemic organs
cellular molecular mechanisms
changes in cell membrane
The earliest site of change during shock
Mitochondrial changes
The earliest organelle to change during shock
changes in lysosomes
cell death
Activation of inflammatory cells and increased expression of inflammatory mediators
Disturbances in the balance between coagulation and anticoagulation
Abnormality of blood coagulation system
Activation of the coagulation system
Abnormalities in coagulation factors
Abnormalities in coagulation factors associated with bleeding tendencies
hereditary plasma coagulation factor deficiency
Decreased acquired plasma coagulation factors
Abnormalities in coagulation factors associated with thrombophilia
Inherited clotting factor abnormalities
Acquired increase in plasma coagulation factors
Abnormal function of the anticoagulant system and fibrinolytic system
Anticoagulant system dysfunction
Decreased or deficient antithrombin III
Protein C or protein S deficiency
Hereditary deficiencies or abnormalities and APC resistance
acquired lack
Fibrinolytic system dysfunction
Activation and inhibition of fibrinolytic system
Bleeding tendency caused by hyperfibrinolytic function
Decreased fibrinolytic function and thrombosis tendency
Disseminated intravascular coagulation (DIC)
Under the action of certain pathogenic factors, a large amount of procoagulant substances enter the blood, coagulation factors and platelets are activated, causing an increase in thrombin, and extensive microthrombi are formed in the microcirculation, which in turn causes secondary complications due to a large amount of consumption of coagulation factors and platelets. Fibrinolytic function is enhanced, and the body develops a pathophysiological process characterized by hemostasis and coagulation dysfunction.
Cause
Pathogenesis
Tissue factor is released, exogenous coagulation function is activated, and the coagulation process is initiated.
Damage to vascular endothelial cells, disorders of coagulation and anticoagulation regulation
Massive destruction of blood cells and activation of platelets
Massive destruction of red blood cells
Destruction or activation of white blood cells
activation of platelets
Procoagulant substances enter the blood
Pathophysiological basis of clinical manifestations
Bleeding
Blood clotting substances are consumed and reduced
fibrinolytic system activation
Fibrin(ogen) degradation product formation
organ dysfunction
shock
anemia
cardiac insufficiency
Changes in the structure and function of the heart caused by various reasons are pathophysiological processes in which the ventricular pumping volume and/or filling function are low, so that the heart cannot meet the needs of material metabolism. Clinically, it manifests as dyspnea, edema, and increased venous pressure. syndrome of congestion and reduced cardiac output
Common causes
Common triggers
body compensation
Activation of neurohumoral regulatory mechanisms
Sympathoadrenal medullary system activation
Increased myocardial contractility and increased heart rate
renin angiotensin aldosterone system activation
Increase renal perfusion pressure
Natriuretic peptide system activation
Natriuresis, dilation of blood vessels, and inhibition of renin and aldosterone
The heart's own compensation
increased heart rate
baroreceptor
volume receptor
chemoreceptors
cardiac tensogenic dilation
Increased myocardial contractility
ventricular remodeling
cardiomyocyte remodeling
Changes in non-myocardial cells and extracellular matrix
extracardiac compensation
increase blood volume
blood flow redistribution
The mechanism
Decreased myocardial contractile function
Myocardial contraction-related protein changes
Myocardial energy metabolism disorder
myocardial excitatory coupling disorder
myocardial diastolic dysfunction
Reduced active diastolic function
passivity
Uncoordinated diastolic and systolic activities of various parts of the heart
clinical manifestations
Decreased cardiac output
Reduced heart pumping ability
Redistribution of blood flow to organs
venous congestion
systemic congestion
Venous congestion and increased venous pressure
Hepatomegaly and liver function damage
Changes in gastrointestinal function
Edema
Pulmonary circulation congestion
Difficulty breathing
pulmonary insufficiency
Respiratory failure: Severe impairment of pulmonary ventilation and/or ventilation function caused by various reasons, resulting in hypoxemia (lowering of PaO2) with or without carbon dioxide retention (reduced PaO2) during resting breathing state. Increased PaCO2), causing a series of pathophysiological changes and clinical manifestations of the syndrome
Etiology and pathogenesis
Pulmonary ventilation dysfunction
Alveolar hypoventilation
restrictive hypoventilation
Limited alveolar expansion during inspiration
Respiratory muscle activity disorder
Decreased thoracic compliance
Reduced lung compliance
Pleural effusion and pneumothorax
obstructive hypoventilation
Ventilation disorders caused by airway narrowing or obstruction
central airway obstruction
Obstruction outside the chest - inspiratory dyspnea
Blockage in the chest - expiratory dyspnea
peripheral airway obstruction
Inspiratory dyspnea
Blood gas changes during alveolar hypoventilation
PO2 decreases and PCO2 increases PaCO2 is the best indicator of alveolar ventilation
Pulmonary ventilation dysfunction
diffusion disorder
Common causes
Reduced alveolar membrane area
Increased alveolar membrane thickness
Blood gas changes
PaO2 decreases, PaCO2 does not increase
Alveolar ventilation and blood flow imbalance
Partial alveolar hypoventilation
Partial alveolar blood flow is insufficient
Increased anatomical shunting
Mechanisms of respiratory failure caused by common respiratory diseases
acute respiratory distress syndrome
chronic obstructive pulmonary disease
Changes in metabolic function
Acid-base balance and electrolyte balance
metabolic acidosis
respiratory acidosis
respiratory alkalosis
changes in respiratory function
Hypoxia has a direct inhibitory effect on the respiratory center
Circulatory system changes
Excitable cardiovascular motor centers to a certain extent
Severe direct inhibition of cardiovascular center and heart activity
central nervous system changes
pulmonary encephalopathy
Hypercapnia, acidosis, cerebral edema due to hypoxia, neuronal dysfunction
changes in kidney function
gastrointestinal changes
Liver insufficiency
Various factors that cause liver damage damage liver cells and cause dysfunction in synthesis, degradation, detoxification, storage, secretion, and immunity. The body may develop clinical syndromes such as jaundice, bleeding, infection, renal dysfunction, and hepatic encephalopathy.
Reduced diffusion time
hepatic encephalopathy
A spectrum of severe neuropsychiatric syndromes secondary to liver dysfunction, when other known brain disorders have been excluded.
Pathogenesis
ammonia poisoning theory
Elevated blood ammonia
Insufficient ammonia removal
Guanylate cycle disorders
Insufficient energy
Severe impairment of enzyme systems
Missing various substrates
Collateral circulation is formed and portosystemic shunt allows DNA to bypass the liver and enter the blood.
Urea elimination disorder, ammonia secretion disorder
Increased production of ammonia
Protein produces ammonia under the action of amino acid oxidase released by intestinal bacteria Ammonia is produced under the action of urease released by bacteria
Increased intestinal ammonia production
Protein components are retained in the intestines
Active gut bacteria
Decreased urea elimination
Increased muscle adenosine catabolism
Toxic effects of ammonia on the brain
Ammonia changes neurotransmitters in the brain
Ammonia interferes with brain cell energy metabolism
Effects of ammonia on nerve cell membranes
GABA theory (γ-aminobutyric acid theory)
pseudoneurotransmitter theory
amino acid imbalance theory
Hepatorenal syndrome
Refers to reversible functional renal failure secondary to liver failure in decompensated liver cirrhosis or acute severe hepatitis.
renal insufficiency
When severe renal dysfunction occurs due to various causes, a variety of metabolites, drugs and poisons will accumulate in the body, water, electrolyte and acid-base balance will be disturbed, as well as renal endocrine dysfunction, resulting in a series of symptoms and signs.
acute renal failure
It refers to the acute short-term impairment of renal urinary function caused by various reasons, resulting in the rapid accumulation of metabolites in the body, disturbance of water, electrolyte and acid-base balance, the occurrence of azotemia, hyperkalemia and metabolic acidosis, and is caused by This clinical syndrome occurs when the internal environment of the body is seriously disturbed.
Pathogenesis
Renal vascular and hemodynamic abnormalities
Decreased renal perfusion pressure
renal vasoconstriction
Sympathoadrenal medullary system excitement
renin-angiotensin system activation
Imbalance in the release of contraction and relaxation factors in the kidney
Renal capillary endothelial cell swelling
Renal intravascular coagulation
tubular damage
tubular obstruction
Original urine leakage
Dysregulation of tube-ball feedback mechanism
Decreased glomerular filtration coefficient
Functional metabolic changes
oliguric acute renal failure
oliguric phase
changes in urine
Oliguria (<400ml/d) or anuria (<100ml/d)
low specific gravity urine
High urine sodium
Hematuria, proteinuria, cast urine
water intoxication
Hyponatremia
hyperkalemia
metabolic acidosis
azotemia
Transition period
Urine output increases to more than 400ml per day
polyuria period
Daily urine output reaches 3000ml or more
recovery period
non-oliguric acute renal failure
chronic renal failure
Various chronic kidney diseases cause chronic progressive and irreversible destruction of nephrons, so that the remaining nephrons are not enough to fully excrete metabolic waste and maintain a constant internal environment, leading to disorders of water, electrolyte and acid-base balance, accumulation of metabolites in the body, and kidney disease. Endocrine dysfunction, a pathological process accompanied by a series of clinical symptoms
Pathogenesis
The role of primary disease
secondary progressive glomerulosclerosis
Changes in hemodynamics of surviving nephrons
Increased mesangial cell proliferation and extracellular matrix production
tubulo-interstitial injury
chronic inflammation
chronic hypoxia
tubular hypermetabolism
Functional metabolic changes
changes in urine
changes in urine output
nocturia
polyuria
Oliguria
Late stage of CRF
Changes in urine osmolarity
Hypotonic urine
In the early stage of CRF, the renal concentrating ability is reduced but the diluting ability is normal.
isotonic urine
In the late stage of CRF, both the concentrating and diluting functions of the kidneys are lost.
changes in urine composition
proteinuria
hematuria
Cast urine
azotemia
plasma urea nitrogen
plasma creatinine
Plasma urate nitrogen
Water, electrolyte and acid-base balance disorders
Water and sodium metabolism disorder
potassium metabolism disorder
Magnesium metabolism disorder
Calcium and phosphorus metabolism disorder
metabolic acidosis
renal osteodystrophy
secondary hyperparathyroidism
Vitamin D3 activation disorder
acidosis
Aluminum accumulation
renal hypertension
sodium and water retention
Excessive secretion of renin
bleeding tendency
renal anemia
Uremia
In the most severe stage of the development of various kidney diseases, due to massive destruction of nephrons, metabolic end products and toxic substances are retained in the body, accompanied by severe disturbances in water, electrolyte and acid-base balance, as well as certain endocrine dysfunction, resulting in A syndrome of symptoms of autotoxicity
Common uremic toxins
parathyroid hormone
Guanidine compounds
Urea
Polyamines
medium molecular weight substances