MindMap Gallery Pharmacology
This is a mind map about pharmacology. The main content includes: Introduction to pharmacology of the efferent nervous system, drugs affecting immune function, chemotherapeutic drugs, endocrine drugs, visceral and blood drugs, cardiovascular drugs, drugs affecting autoactivity, central Neuropharmacology, Efferent Neuropharmacology, General Review.
Edited at 2024-11-27 13:49:52Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Pharmacology
Summary
drug effects
dynamics
Basic rules of drug action
Drug action and pharmacological effects
Drugs can prevent, treat and diagnose diseases
Therapeutic effect
adverse reactions
side effect
Reason: low selectivity
Wide range of action
Effects of a drug at therapeutic doses that occur simultaneously with the therapeutic effect and are unrelated to the therapeutic purpose
predictable
Varies with different treatment purposes
toxic reactions
The dose of the drug is too high or the drug is taken for too long (too much drug accumulates in the body)
allergy
carryover effect
secondary reaction
idiosyncratic reaction
drug dependence
duality
Dosage and effects
Dose-response curve
quantitative response
minimum effective dose
efficacy
Maximum effect a drug can have
potency strength
The dose required for a drug to achieve a certain effect
The dose-effect curve of the drug shifts to the right, indicating that the potency intensity becomes smaller
For drugs of the same potency, the dose-effect curve is further to the right, the smaller the potency intensity.
slope
qualitative reaction
half
effective amount
Toxic dose
Lethal dose LD50
A dose that kills half of all animals
therapeutic index
structure and effect
Main mechanism
receptor pathway
non-receptor pathway
with receptor
concept
Classification
Ligand binding properties
drug interactions
drug-receptor theory of action
Receptor agonists and antagonists
Agonist drugs
Has both affinity and intrinsic activity for the receptor
Intrinsic activity: the ability of a drug to agonize receptors
Antagonist
Affinity but no intrinsic activity
Competitive (reversible)
Competes for the same receptor as an agonist and its binding is reversible
Concomitant use with agonists can shift the dose-effect curve to the right in parallel
Non-rivalrous (irreversible)
Competes for the same receptor as an agonist and its binding is irreversible
partial agonist
modulation of receptors
intracellular signaling pathways
Influencing factors
pharmacokinetics
drug transport across membranes
passive
initiative
internal processes
absorb
Gastrointestinal absorption
Oral administration
Sublingual administration
Rectal administration
skin absorption
injection
respiratory tract absorption
hepatic first pass effect
"First pass elimination"
distributed
biotransformation
excretion
Basic concepts of pharmacokinetics
Blood drug concentration-time curve
rise
drug absorption
slope
Absorption rate
decline
drug elimination
peak time
An indicator of how quickly a drug is absorbed
area under curve
drug absorption process
room model
Drug elimination type
first order kinetics
Constant ratio elimination, the drug elimination rate is directly proportional to the blood drug concentration
Characteristics of drugs eliminated according to first-order kinetics: drug half-life is dose-dependent
zero order dynamics
Constant elimination, a constant amount of medicine is eliminated per unit time
nonlinear dynamics
Basic pharmacokinetic parameters
Absorption Parameters--Bioavailability
Distribution parameters--apparent distribution volume
Reflects the basic distribution of drugs in the body (inside/outside cells, organs)
Elimination parameter--half-life
Empirical value 5´ Half-life = time required to reach steady state plasma
Reference indicators for confirming dosing intervals
Plasma concentration-time curve of multiple doses
Introduction to Pharmacology of the Efferent Nervous System
Efferent nervous system components
type
autonomic nervous system
Sympathy
stress stress
parasympathetic
full food sleep
body motor nerves
effector
Autonomy
cardiac muscle, smooth muscle, glands
sports
skeletal muscle
transmitter
Before the holiday
ACh
After the holiday
ACh
NF
receptor
ACh
receptor that binds acetylcholine
M receptor/muscarinic
Effector cell membranes innervated by parasympathetic postganglionic F
M1
ganglion, gland cell
Nerve excitement Gastric acid secretion
M2
heart
Myocardial contractility and heart rate decrease
M3
endothelium smooth muscle glands
Vasodilation Smooth muscle contraction Glandular secretion
M4 M5
central nervous system
N receptor/nicotinamide
Ganglion, on skeletal muscle cell
Nm
neuromuscular junction N receptor
muscle contraction
Nn
Neural N receptors Central N receptors
Nerve excitation Catecholamine release
NF
Receptor that binds norepinephrine
a receptor
a1
Vascular Urethral Intestinal Smooth Muscle Liver Heart
Contraction Contraction Relaxation Glycogenolysis Gluconeogenesis Enhanced Contraction Arrhythmia
a2
presynaptic membrane
Inhibition of transmitter release
b receptor
b1
heart
Cardiotonic drug···Adrenaline
b2
smooth muscle skeletal muscle liver
Relaxation Glycogenolysis Sodium uptake Glycogenolysis Gluconeogenesis
b3
fat cells
lipolysis
Classification by transmitter
cholinergic nerves
In addition to sympathetic postganglionic fibers
noradrenergic nerves
sympathetic postganglionic fibers
Biological effects
Cholinergic nerve excitation
Decreased reaction, trimming, energy storage
Excitation of M receptors on effectors
M-like effect
Cardiac depression
smooth muscle contraction
Eye
pupillary sphincter contraction
miosis
ciliary muscle contraction
Ciliary zonules relax and lens curvature becomes larger
look close
increased glandular secretion
N receptor stimulation on effectors
N-like effect
Nm receptor stimulation
Autonomic ganglion Increased adrenal medulla secretion
Nn receptor stimulation
motor nerve skeletal muscle contraction
Noradrenergic nerve stimulation
exercise stress
a type effect
Skin, mucosa, and visceral vasoconstriction
The dilator muscle contracts and the pupil dilates
b type effect
b1 excited
Myocardial contraction, heart rate increases
b2 excited
Visceral skeletal muscle coronary vasodilation, bronchial relaxation
efferent nerve drugs
cholinergic drugs
Organophosphorus esters cholinesterase reactivating drugs
anticholinergics
M choline receptor blockers
Atropine alkaloids
atropine
clinical application
Visceral smooth muscle spasm
Inhibit glandular secretion
It is used for administration before general anesthesia to reduce the secretion of the respiratory tract and salivary glands and prevent secretions from blocking the respiratory tract and causing suffocation or aspiration pneumonia.
ophthalmology
iridocyclitis
Check the fundus
Optometry and glasses
Atropine eye drops cause: pupil dilation, increase in intraocular pressure, accommodative paralysis
bradyarrhythmia
sinus block, atrioventricular block
shock
Mechanism: Relieve vasospasm, improve microcirculation, and increase blood flow to important organs
Organophosphate poisoning
Scopolamine
Anisodamine
Outstanding Features: Strong effect on relieving spasm of visceral smooth muscles and small blood vessels
Synthetic and semi-synthetic derivatives
N-choline receptor blockers
Nm choline receptor blockers
Adrenergic drugs
a adrenoceptor agonist
norepinephrine
adverse reactions
local tissue ischemia and necrosis
acute renal failure
Drop in blood pressure after discontinuation of medication
Metahydroxylamine
to get adrenaline
a, b adrenoceptor agonists
Adrenaline AD
clinical application
cardiac arrest
anaphylactic shock
Treat the root cause
Reduce release of allergenic mediators
Treat the symptoms
Shrink arterioles and eliminate mucosal edema
Improve heart function
Relieve bronchospasm
bronchial asthma
Best suited for local anesthesia and local hemostasis
Ephedrine
dopamine DA
Shock with weakened myocardial contractility and decreased urine output
b adrenoceptor agonists
b1, b2 adrenoceptor agonists
isoproterenol
clinical application
bronchial asthma
atrioventricular block
cardiac arrest
b1
Dobutamine
b2
b3
anti-adrenergic drugs
a adrenergic receptor blocking drugs
a1, a2 receptor blocking drugs
Phentolamine
Pharmacological effects
block a1 receptor
relax blood vessels
block a2 receptors
excited heart
Cholinomimetic effect
Increased gastrointestinal smooth muscle tone
Histamine effect
increased gastric acid secretion
clinical application
peripheral vasospastic disease
Leakage of intravenous norepinephrine solution
Acute myocardial infarction and refractory congestive heart failure
Mechanism: dilate arterioles and venules, reduce cardiac pre- and post-load, increase cardiac output,
shock
adrenal pheochromocytoma
adverse reactions
Orthostatic hypotension (orthostatic hypotension)
Gastrointestinal symptoms; abdominal pain, diarrhea, vomiting
phenoxybenzamine
a1
Prazosin
a2
Yohimbine
bAdrenoceptor blocking drugs
propranolol
Contraindications
bronchial asthma
severe atrioventricular block
sinus bradycardia
local anesthetic
central nervous system drugs
general anesthesia
sedation hypnosis
Sleep and sleep disorders
benzodiazepines
Mechanism of action
Closely related to the GABAA receptor, a subtype of the transmitter GABA receptor in the brain
Seven families: a, b, g, d, e, q, r
Promote the binding of GABA to GABAA receptors, leading to Cl- influx
Classification
Long acting type
diazepam
For pre-anesthetic administration rather than induction of anesthesia
Medium effect type
Short-acting
adverse reactions
"Hangover": dizziness, drowsiness, fatigue, dry mouth, constipation
respiratory and circulatory depression
Rescue with flumazenil
Ataxia
tolerance dependence addiction
Withdrawal reaction
barbiturates
Other sedative-hypnotics
Antiepileptic convulsions
Antipsychotic
Treat central nervous system degeneration
Antipyretic, analgesic, anti-inflammatory and anti-gout
Antipyretic, analgesic and anti-inflammatory drugs
Salicylates
aspirin
adverse reactions
gastrointestinal reactions
Bleeding and coagulation disorders
salicylic acid reaction
allergic reaction
'Aspirin Asthma'
'allergy"
Reye syndrome
Other antipyretic, analgesic and anti-inflammatory drugs
Anilines
Acetaminophen
Fever patients with peptic ulcer
propionic acid
ibuprofen
Rheumatoid and rheumatoid arthritis, general pain
Acetic acid
Indomethacin
Selective cyclooxygenase-2 inhibitors
celecoxib
Nimesulide
Meloxicam
parecoxib
Antipyretic and analgesic compound reagent
antigout medicine
analgesia
opiate alkaloids
morphine
Morphine hydrochloride
Contraindications
labor pain relief
Pain relief for breastfeeding women
Morphine can cross the placental barrier and cause respiratory depression in the fetus
bronchial asthma
pulmonary heart disease
Patients with increased intracranial pressure caused by craniocerebral injury
Morphine crosses the blood-brain barrier
Patients with severely reduced liver function
Semisynthetic derivatives of morphine
Naloxone
Synthetic
Morphinans
butorphanol
Phenylpropanoids
Pentazocine
Piperidines
Pethidine
clinical application
analgesia
Combined with atropine to treat biliary colic
Relieve morphine-induced ballistic sphincter spasm
When giving pain relief during labor, it should not be used within 2 to 4 hours before delivery.
Neonates are particularly sensitive to the respiratory depression of pethidine
cardiogenic asthma
Not for use in cor pulmonale
Pre-anesthetic administration
artificial hibernation
Fentanyl
Aminoketones
Methadone
opioid receptor antagonists
Naloxone
Naltrexone
central excitement
Drugs that affect their own activity
cardiovascular drugs
Drugs that act on ion channels in the cardiovascular system
Drugs to treat chronic heart failure
Pathophysiological mechanisms and action links of commonly used clinical drugs
positive inotropes
cardiac glycosides
Pharmacological effects
Enhance myocardial contractility
slow heart rate
Effects on conductive tissue and cardiac electrical properties of myocardium
Yifang
Decreased sinus node automaticity
Affects Purkinje fiber self-discipline
Inhibit sodium potassium ATPase
Young room
Slow down atrioventricular node conduction velocity
The subject of shortening the effective refractory period of the atrium
Effect on electrocardiogram
subtopic
clinical application
chronic cardiac insufficiency
It is most effective for patients with chronic cardiac insufficiency accompanied by atrial fibrillation and fast ventricular rate.
Arrhythmia
Atrial fibrillation (atrial fibrillation)
Mechanism: Slows down atrioventricular conduction (increases covert conduction)
atrial flutter
paroxysmal supraventricular tachycardia
Poisoning prevention and treatment
prevention
treat
Phenytoin
non-glycoside inotropes
Renin-angiotensin-aldosterone system inhibitors
vasodilators
b receptor blocking drugs
antihypertensive drugs
Classification
Commonly used medicines
diuretics
Hydrochlorothiazide
Mechanism of action
Early days
Natriuretic, diuretic, lower blood volume
long
Affects the sodium-calcium exchange mechanism, reducing intracellular calcium and reducing the responsiveness of vascular smooth muscle cells to vasoconstrictor substances.
Induces the arterial wall to produce vasodilator substances
adverse reactions
Summary: "Four highs and three lows" "Three liters" (raising blood sugar, raising blood and raising uric acid)
Electrolyte imbalance: hypokalemia, sodium, chloride, hypercalcemia
Affects glucose metabolism and lipid metabolism
Not suitable for patients with diabetes and hypertension
hyperuricemia
aggravate renal dysfunction
Renin-angiotensin-aldosterone system inhibitors
Captopril
adverse reactions
Usually there is a hypotensive reaction, so start taking the medicine with a small dose (hypotension after the first dose)
Irritating dry cough, angioedema
Hyperkalemia, hypoglycemia
fetal calvarial hypoplasia
Long-term medication may result in decreased blood zinc, loss of sense of smell, and hair loss.
Losartan
Valsartan
Remi Gillen
calcium channel blockers
adrenoceptor blocking drugs
b receptor blocking drugs
propranolol
clinical application
mild to moderate hypertension
Hypertension with high cardiac output or high plasma renin levels
Hypertensive patients with tachyarrhythmia (fast heart rate)
adverse reactions
Influence, increase blood lipids and lipid metabolism
Hyperlipidemia is prohibited
Affects blood sugar recovery speed
Not suitable for patients with diabetes, fasting, and anesthesia
Aggravate the hypoglycemic reaction caused by insulin in diabetic patients
Contract bronchial smooth muscle and vascular smooth muscle
Contraindicated in patients with bronchial asthma and peripheral vasospasm
Depress the heart
Contraindicated in patients with heart failure, conduction block, and sinus bradycardia
Reduce renal vascular flow and glomerular filtration rate
Contraindicated in patients with renal insufficiency
Sudden discontinuation of medication causes "discontinuation syndrome"
Metoprolol
atenolol
a1 receptor blockers
Prazosin
adverse reactions
Can cause first dose phenomenon in half of patients
Halve first dose for prevention
Terazosin
labelore
ab receptor blocking drugs
other
Sympatholytic drugs
central sympatholytic drugs
clonidine
clinical application
Hypertensive and renal hypertension patients with ulcer disease
moxonidine
ganglion blocking drugs
Sympathetic nerve ending inhibitors
vasodilators
Reasonable application
Stable blood pressure reduction and long-term treatment
Choose 1 drug according to the degree of high blood pressure
Select drugs based on complications and adverse reaction characteristics
Combination medication
Individualized treatment plan
antianginal drugs
Nitrates
e.g.
Nitroglycerin
adverse reactions
Flushing face
lower blood pressure
Very easy to develop tolerance
Isosorbide dinitrate and pentylenetetranitrate
Isosorbide mononitrate
Mechanism of action
NO production in vascular smooth muscle cells and vascular endothelial cells
bAdrenoceptor blocking drugs
e.g.
propranolol
Contraindications
Asthma, bradycardia, hypotension, severe cardiac insufficiency, chronic obstructive pulmonary disease
calcium channel blockers
Significantly relieves coronary artery spasm
e.g.
nifedipine
The drug of choice for variant angina pectoris
Verapamil
diltiazem
Other anti-angina pectoris
Combined use of angina pectoris drugs
antiarrhythmic drugs
Anti-atherosclerosis
Visceral and blood drugs
Diuretics and dehydration drugs
diuretics
Renal physiological basis and site of action of diuretics
Classification and mechanism of action of commonly used diuretics
Commonly used diuretics
Furosemide
Hydrochlorothiazide
subtopic
Spironolactone
clinical application
Patients with edema with elevated aldosterone have better outcomes
Diuresis is related to aldosterone levels in the body
subtopic
dehydration medicine
Mannitol
adverse reactions
It is contraindicated for those with chronic cardiac insufficiency and those with urinary obstruction.
Increased circulating blood volume worsens heart failure patients
Causes high uric acid
Digestive system medicine
Respiratory system medications
uterine stimulants
anti-anemia drugs
Drugs that act on the coagulation system
endocrine drugs
Adrenocortical hormone drugs
Glucocorticoids
Pharmacological effects
Effect on substance metabolism
Anti-inflammatory
Immunosuppression and anti-allergy
Anti-endotoxin
Improve the body's tolerance to bacterial endotoxins
Does not have antibacterial effect
Anti-shock
toxic shock
High-dose surprise intravenous administration
Affects blood and hematopoietic system
Other functions
clinical application
severe infection
Relieve symptoms and help patients get through the dangerous period
Taboo
Contraindications
non-contraindications
nonspecific keratitis
mineralocorticoid drugs
Corticotropin and corticosteroid inhibitors
adrenocorticotropic hormone
corticosteroid inhibitors
Thyroid hormones and thyroid medicine
hypoglycemic drugs
Sex hormone drugs and contraceptive pills
chemotherapeutic drugs
Drugs that affect immune function