his article is about the science and art of healing.

For medicaments,
see Pharmaceutical drug. For other uses, see Medicine
(disambiguation).
"Academic medicine" redirects here. For the journal, see Academic
Medicine (journal).
Medicine

Statue of Asclepius, the Greek god of

medicine, holding the symbolic Rod of
Asclepius with its coiled serpent
Specialist Physician, medic
Medicine is the science and practice of the diagnosis, treatment, and
prevention of disease. Medicine encompasses a variety of health
care practices evolved to maintain and restore health by the
prevention and treatment of illness. Contemporary medicine applies
biomedical sciences, biomedical research, genetics, and medical
technology to diagnose, treat, and prevent injury and disease,
typically through pharmaceuticals or surgery, but also through
therapies as diverse as psychotherapy, external splints and traction,
medical devices, biologics, and ionizing radiation, amongst others.[1]
Medicine has existed for thousands of years, during most of which it
was an art (an area of skill and knowledge) frequently having
connections to the religious and philosophical beliefs of local culture.
For example, a medicine man would apply herbs and say prayers for
healing, or an ancient philosopher and physician would apply
bloodletting according to the theories of humorism. In recent
centuries, since the advent of modern science, most medicine has
become a combination of art and science (both basic and applied,
under the umbrella of medical science). While stitching technique for
sutures is an art learned through practice, the knowledge of what
happens at the cellular and molecular level in the tissues being
stitched arises through science.
Prescientific forms of medicine are now known as traditional medicine
and folk medicine. They remain commonly used with or instead of
scientific medicine and are thus called alternative medicine. For
example, evidence on the effectiveness of acupuncture is "variable
and inconsistent" for any condition,[2] but is generally safe when done
by an appropriately trained practitioner.[3] In contrast, treatments
outside the bounds of safety and efficacy are termed quackery.
Contents [hide]
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References Etymology[edit]
Medicine (UK: /ˈmɛdsɪn/ ( listen), US: /ˈmɛdɪsɪn/ ( listen)) is the
science and practice of the diagnosis, treatment, and prevention of
disease.[4][5] The word "medicine" is derived from Latin medicus,
meaning "a physician".[6][7]
Clinical practice[edit]

The Doctor by Sir Luke Fildes (1891)

Medical availability and clinical practice varies across the world due
to regional differences in culture and technology. Modern scientific
medicine is highly developed in the Western world, while in
developing countries such as parts of Africa or Asia, the population
may rely more heavily on traditional medicine with limited evidence
and efficacy and no required formal training for practitioners.[8] Even in
the developed world however, evidence-based medicine is not
universally used in clinical practice; for example, a 2007 survey of
literature reviews found that about 49% of the interventions lacked
sufficient evidence to support either benefit or harm.[9]
In modern clinical practice, physicians personally assess patients in
order to diagnose, treat, and prevent disease using clinical judgment.
The doctor-patient relationship typically begins an interaction with an
examination of the patient's medical history and medical record,
followed by a medical interview[10] and a physical examination. Basic
diagnostic medical devices (e.g. stethoscope, tongue depressor) are
typically used. After examination for signs and interviewing for
symptoms, the doctor may order medical tests (e.g. blood tests), take
a biopsy, or prescribe pharmaceutical drugs or other therapies.
Differential diagnosis methods help to rule out conditions based on
the information provided. During the encounter, properly informing the
patient of all relevant facts is an important part of the relationship and
the development of trust. The medical encounter is then documented
in the medical record, which is a legal document in many
jurisdictions.[11] Follow-ups may be shorter but follow the same
general procedure, and specialists follow a similar process. The
diagnosis and treatment may take only a few minutes or a few weeks
depending upon the complexity of the issue.
The major physiologic triggers of adrenaline release center upon stresses, such as physical
threat, excitement, noise, bright lights, and high ambient temperature. All of these stimuli are
processed in the central nervous system.[73]
Adrenocorticotropic hormone (ACTH) and the sympathetic nervous system stimulate the
synthesis of adrenaline precursors by enhancing the activity of tyrosine
hydroxylase and dopamine β-hydroxylase, two key enzymes involved in catecholamine
synthesis.[citation needed] ACTH also stimulates the adrenal cortex to release cortisol, which
increases the expression of PNMT in chromaffin cells, enhancing adrenaline synthesis. This
is most often done in response to stress.[citation needed] The sympathetic nervous system, acting
via splanchnic nerves to the adrenal medulla, stimulates the release of
adrenaline. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts
on nicotinic acetylcholine receptors, causing cell depolarization and an influx
of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of
chromaffin granules and, thus, the release of adrenaline (and noradrenaline) into the
bloodstream.[74]
Unlike many other hormones adrenaline (as with other catecholamines) does not
exert negative feedback to down-regulate its own synthesis.[75]Abnormally elevated levels of
adrenaline can occur in a variety of conditions, such as surreptitious epinephrine
administration, pheochromocytoma, and other tumors of the sympathetic ganglia.
Its action is terminated with reuptake into nerve terminal endings, some minute dilution, and
metabolism by monoamine oxidase and catechol-O-methyl transferase.

History[edit]
Main article: History of catecholamine research
Extracts of the adrenal gland were first obtained by Polish physiologist Napoleon Cybulski in
1895. These extracts, which he called nadnerczyna("adrenalin"), contained adrenaline and
other catecholamines.[76] American ophthalmologist William H. Bates discovered adrenaline's
usage for eye surgeries prior to 20 April 1896.[77] Japanese chemist Jokichi Takamine and his
assistant Keizo Uenaka independently discovered adrenaline in 1900.[78][79] In 1901,
Takamine successfully isolated and purified the hormone from the adrenal glands of sheep
and oxen.[80] Adrenaline was first synthesized in the laboratory by Friedrich Stolz and Henry
Drysdale Dakin, independently, in 1904.[79]

Society and culture[edit]

Adrenaline junkie[edit]
See also: Novelty seeking
An adrenaline junkie is somebody who engages in sensation-seeking behavior through "the
pursuit of novel and intense experiences without regard for physical, social, legal or financial
risk".[81] Such activities include extreme and risky sports, substance abuse, unsafe sex, and
crime. The term relates to the increase in circulating levels of adrenaline during
physiological stress.[82] Such an increase in the circulating concentration of adrenaline is
secondary to activation of the sympathetic nerves innervating the adrenal medulla, as it is
rapid and not present in animals where the adrenal gland has been removed.[83] Although
such stress triggers adrenaline release, it also activates many other responses within the
central nervous system reward system which drives behavioral responses, so while the
circulating adrenaline concentration is present, it may not drive behavior. Nevertheless,
adrenaline infusion alone does increase alertness[84] and has roles in the brain including the
augmentation of memory consolidation.[82]:147–8
Strength[edit]
Main article: Hysterical strength
Adrenaline has been implicated in feats of great strength, often occurring in times of crisis.
For example, there are stories of a parent lifting part of a car when their child is trapped
underneath.[85][86]

vary by tissue type and tissue expression of adrenergic receptors. For

example, high levels of epinephrine causes smooth muscle relaxation
in the airways but causes contraction of the smooth muscle that lines
most arterioles.
Epinephrine acts by binding to a variety of adrenergic receptors.
Epinephrine is a nonselective agonist of all adrenergic receptors,
including the major subtypes α1, α2, β1, β2, and β3.[59] Epinephrine's
binding to these receptors triggers a number of metabolic changes.
Binding to α-adrenergic receptors inhibits insulin secretion by the
pancreas, stimulates glycogenolysis in the liver and muscle,[60] and
stimulates glycolysis and inhibits insulin-mediated glycogenesis in
muscle.[61][62] β adrenergic receptor binding triggers glucagon secretion
in the pancreas, increased adrenocorticotropic hormone (ACTH)
secretion by the pituitary gland, and increased lipolysis by adipose
tissue. Together, these effects lead to increased blood glucose and
fatty acids, providing substrates for energy production within cells
throughout the body.[62]
Its actions are to increase peripheral resistance via α1 receptor-
dependent vasoconstriction and to increase cardiac output via its
binding to β1 receptors. The goal of reducing peripheral circulation is
to increase coronary and cerebral perfusion pressures and therefore
increase oxygen exchange at the cellular level.[63] While epinephrine
does increase aortic, cerebral, and carotid circulation pressure, it
lowers carotid blood flow and end-tidal CO2 or ETCO2 levels. It
appears that epinephrine may be improving macrocirculation at the
expense of the capillary beds where actual perfusion is taking
place.[64]
Measurement in biological fluids[edit]
Epinephrine may be quantified in blood, plasma or serum as a
diagnostic aid, to monitor therapeutic administration, or to identify the
causative agent in a potential poisoning victim. Endogenous plasma
epinephrine concentrations in resting adults are normally less than
10 ng/L, but may increase by 10-fold during exercise and by 50-fold
or more during times of stress. Pheochromocytoma patients often
have plasma adrenaline levels of 1000–10,000 ng/L. Parenteral
administration of epinephrine to acute-care cardiac patients can
produce plasma concentrations of 10,000 to 100,000 ng/L.[65][66]
Biosynthesis and regulation[edit]
 The biosynthesis of adrenaline involves a series of enzymatic reactions.
In chemical terms, epinephrine is one of a group of monoamines
called the catecholamines. It is produced in some neurons of the
central nervous system, and in the chromaffin cells of the adrenal
medulla from the amino acids phenylalanine and tyrosine.[67]
Epinephrine is synthesized in the medulla of the adrenal gland in an
enzymatic pathway that converts the amino acid tyrosine into a series
of intermediates and, ultimately, epinephrine. Tyrosine is first oxidized
to L-DOPA, which is subsequently decarboxylated to give dopamine.
Oxidation gives norepinephrine. The final step in epinephrine
biosynthesis is the methylation of the primary amine of
norepinephrine. This reaction is catalyzed by the enzyme
phenylethanolamine N-methyltransferase (PNMT) which utilizes S-
adenosyl methionine (SAMe) as the methyl donor.[68] While PNMT is
found primarily in the cytosol of the endocrine cells of the adrenal
medulla (also known as chromaffin cells), it has been detected at low
levels in both the heart and brain.[69]
For noradrenaline to be acted upon by PNMT in the cytosol, it must first be shipped out
of granules of the chromaffin cells. This may occur via the catecholamine-
H+ exchanger VMAT1. VMAT1 is also responsible for transporting newly synthesized
adrenaline from the cytosol back into chromaffin granules in preparation for release.[46]
In liver cells, adrenaline binds to the β adrenergic receptor, which changes conformation and
helps Gs, a G protein, exchange GDP to GTP. This trimeric G protein dissociates to Gs alpha
and Gs beta/gamma subunits. Gs alpha binds to adenyl cyclase, thus converting ATP into
cyclic AMP. Cyclic AMP binds to the regulatory subunit of protein kinase A: Protein kinase A
phosphorylates phosphorylase kinase. Meanwhile, Gs beta/gamma binds to the calcium
channel and allows calcium ions to enter the cytoplasm. Calcium ions bind to calmodulin
proteins, a protein present in all eukaryotic cells, which then binds to phosphorylase kinase
and finishes its activation. Phosphorylase kinase phosphorylates glycogen phosphorylase,
which then phosphorylates glycogen and converts it to glucose-6-phosphate.[citation needed]

Pathology[edit]
Increased epinephrine secretion is observed in pheochromocytoma, hypoglycemia,
myocardial infarction and to a lesser degree in benign essential familial tremor. A general
increase in sympathetic neural activity is usually accompanied by increased adrenaline
secretion, but there is selectivity during hypoxia and hypoglycaemia, when the ratio of
adrenaline to noradrenaline is considerably increased.[47][48][49] Therefore, there must be some
autonomy of the adrenal medulla from the rest of the sympathetic system.
Myocardial infarction is associated with high levels of circulating epinephrine and
norepinephrine, particularly in cardiogenic shock.[50][51]
Benign familial tremor (BFT) is responsive to peripheral β adrenergic blockers and β2-
stimulation is known to cause tremor. Patients with BFT were found to have increased
plasma epinephrine, but not norepinephrine.[52][53]
Low, or absent, concentrations of epinephrine can be seen in autonomic neuropathy or
following adrenalectomy. Failure of the adrenal cortex, as with Addisons disease, can
suppress epinephrine secretion as the activity of the synthesing
enzyme, phenylethanolamine-N-methyltransferase, depends on the high concentration of
cortisol that drains from the cortex to the medulla.[54][55][56]
Terminology[edit]
Epinephrine is the pharmaceutical's United States Adopted Name and International
Nonproprietary Name, though the name adrenaline is frequently used. The
term epinephrine was coined by the pharmacologist John Abel (from the Greek for "on top of
the kidneys"), who used the name to describe the extracts he prepared from the adrenal
glands as early as 1897.[57] In 1901, Jokichi Takamine patented a purified adrenal extract,
and called it "adrenalin" (from the Latin for "on top of the kidneys"), which
was trademarked by Parke, Davis & Co in the U.S.[57] In the belief that Abel's extract was the
same as Takamine's, a belief since disputed, epinephrine became[when?] the generic name in
the U.S.[57] The British Approved Name and European Pharmacopoeia term for this drug is
adrenaline and is indeed now one of the few differences between the INN and BAN systems
of names.[58]
Among American health professionals and scientists, the term epinephrine is used
over adrenaline. However, pharmaceuticals that mimic the effects of epinephrine are often
called adrenergics, and receptors for epinephrine are called adrenergic receptors or
adrenoceptors.

Emotional response[edit]
Every emotional response has a behavioral component, an autonomic component, and a
hormonal component. The hormonal component includes the release of epinephrine, an
adrenomedullary response that occurs in response to stress and that is controlled by
the sympathetic nervous system. The major emotion studied in relation to epinephrine is
fear. In an experiment, subjects who were injected with epinephrine expressed more
negative and fewer positive facial expressions to fear films compared to a control group.
These subjects also reported a more intense fear from the films and greater mean intensity
of negative memories than control subjects.[41] The findings from this study demonstrate that
there are learned associations between negative feelings and levels of epinephrine. Overall,
the greater amount of epinephrine is positively correlated with an arousal state of negative
feelings. These findings can be an effect in part that epinephrine elicits physiological
sympathetic responses including an increased heart rate and knee shaking, which can be
attributed to the feeling of fear regardless of the actual level of fear elicited from the video.
Although studies have found a definite relation between epinephrine and fear, other
emotions have not had such results. In the same study, subjects did not express a greater
amusement to an amusement film nor greater anger to an anger film.[41] Similar findings were
also supported in a study that involved rodent subjects that either were able or unable to
produce epinephrine. Findings support the idea that epinephrine does have a role in
facilitating the encoding of emotionally arousing events, contributing to higher levels of
arousal due to fear.[42]
Memory[edit]
It has been found that adrenergic hormones, such as epinephrine, can produce retrograde
enhancement of long-term memory in humans. The release of epinephrine due to
emotionally stressful events, which is endogenous epinephrine, can modulate memory
consolidation of the events, ensuring memory strength that is proportional to memory
importance. Post-learning epinephrine activity also interacts with the degree of arousal
associated with the initial coding.[43] There is evidence that suggests epinephrine does have a
role in long-term stress adaptation and emotional memory encoding specifically. Epinephrine
may also play a role in elevating arousal and fear memory under particular pathological
conditions including post-traumatic stress disorder.[42] Overall, "Extensive evidence indicates
 that epinephrine (EPI) modulates memory consolidation for emotionally arousing tasks in
animals and human subjects.”[44] Studies have also found that recognition memory involving
epinephrine depends on a mechanism that depends on β adrenoceptors.[44]Epinephrine does
not readily cross the blood–brain barrier, so its effects on memory consolidation are at least
partly initiated by β adrenoceptors in the periphery. Studies have found that sotalol, a β
adrenoceptor antagonist that also does not readily enter the brain, blocks the enhancing
effects of peripherally administered epinephrine on memory.[45] These findings suggest that β
adrenoceptors are necessary for epinephrine to have an effect on memory consolidation.

he adrenal medulla is a minor contributor to total circulating catecholamines(L-DOPA is at a

higher concentration in the plasma),[11] though it contributes over 90% of circulating
epinephrine. Little epinephrine is found in other tissues, mostly in scattered chromaffin cells.
Following adrenalectomy, epinephrine disappears below the detection limit in the blood
stream.[12]
The adrenal glands contribute about 7% of circulating norepinephrine, most of which is a spill
over from neurotransmission with little activity as a hormone.[13][14][15] Pharmacological doses of
epinephrine stimulate α1, α2, β1, β2, and β3 adrenoceptors of the sympathetic nervous system.
Sympathetic nerve receptors are classified as adrenergic, based on their responsiveness to
adrenaline.[16]
The term "adrenergic" is often misinterpreted in that the main sympathetic neurotransmitter is
norepinephrine (noradrenaline), rather than epinephrine, as discovered by Ulf von Euler in
1946.[17][18]
Epinephrine does have a β2 adrenoceptor-mediated effect on metabolism and the airway,
there being no direct neural connection from the sympathetic ganglia to the airway.[19][20][21]
The concept of the adrenal medulla and the sympathetic nervous system being involved in
the flight, fight and fright response was originally proposed by Cannon.[22] But the adrenal
medulla, in contrast to the adrenal cortex, is not required for survival. In adrenalectomized
patients hemodynamic and metabolic responses to stimuli such as hypoglycemia and
exercise remain normal.[23][24]
Exercise[edit]
One physiological stimulus to epinephrine secretion is exercise. This was first demonstrated
using the denervated pupil of a cat as an assay,[25] later confirmed using a biological assay
on urine samples.[26] Biochemical methods for measuring catecholamines in plasma were
published from 1950 onwards.[27] Although much valuable work has been published using
fluorimetric assays to measure total catecholamine concentrations, the method is too non-
specific and insensitive to accurately determine the very small quantities of epinephrine in
plasma.

FDA Orange Book

1. Prescription Drug Products
<="" div="" style="box-sizing: border-box; padding: 1em 1px 0.2em; width:
598.59375px; overflow-x: auto; max-width: 100%;">
Prescription Drug Products: 1 of 12 (RX Drug Ingredient)
 Prescription Drug Products: 1 of 12 (RX Drug Ingredient)

Drug Ingredient EPINEPHRINE

Proprietary Name EPIPEN

MYLAN SPECIALITY LP (Application Number: N019430.

Applicant
Patents: 7449012, 7794432, 8048035, 8870827, 9586010)

from FDA Orange Book

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598.59375px; overflow-x: auto; max-width: 100%;">
Prescription Drug Products: 2 of 12 (RX Drug Ingredient)

Drug Ingredient EPINEPHRINE; LIDOCAINE HYDROCHLORIDE

LIDOCAINE
Proprietary Name
HYDROCHLORIDE AND EPINEPHRINE

1. EASTMAN KODAK (Application

Number: A040057)
2. HOSPIRA (Application Number: A078772)
3. HOSPIRA (Application Number: A088571)
Applicant 4. HOSPIRA (Application Number: A089635)
5. HOSPIRA (Application Number: A089644)
6. HOSPIRA (Application Number: A089645)
7. HOSPIRA (Application Number: A089646)
8. HOSPIRA (Application Number: A089651)
from FDA Orange Book
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598.59375px; overflow-x: auto; max-width: 100%;">
Prescription Drug Products: 3 of 12 (RX Drug Ingredient)

Drug Ingredient EPINEPHRINE; LIDOCAINE HYDROCHLORIDE

Proprietary Name XYLOCAINE W/ EPINEPHRINE

FRESENIUS KABI USA (Application

Applicant
Number: N006488)

from FDA Orange Book

View All 12 Prescription Drug Products
2. Discontinued Drug Products
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Discontinued Drug Products: 1 of 21 (DISCN Drug Ingredient)

EPINEPHRINE BITARTRATE; PRILOCAINE

Drug Ingredient
HYDROCHLORIDE

Proprietary Name CITANEST FORTE

Applicant ASTRAZENECA (Application Number: N014763)

from FDA Orange Book

<="" div="" style="box-sizing: border-box; padding: 1em 1px 0.2em; width:
598.59375px; overflow-x: auto; max-width: 100%;">
Discontinued Drug Products: 2 of 21 (DISCN Drug Ingredient)

Drug Ingredient EPINEPHRINE; LIDOCAINE HYDROCHLORIDE

Proprietary Name LIDOCAINE HYDROCHLORIDE W/ EPINEPHRINE

1. ABBOTT (Application Number: A083154)

2. BEL MAR (Application Number: A080757)
3. BEL MAR (Application Number: A080820)
4. DELL LABS (Application Number: A083389)
Applicant 5. DELL LABS (Application Number: A083390)
6. INTL MEDICATION (Application
Number: A086402)
7. WATSON LABS (Application Number: A080377)
8. WATSON LABS (Application Number: A085463

Epinephrine is the active sympathomimetic hormone from the ADRENAL MEDULLA.

It stimulates both the alpha- and beta- adrenergic systems, causes systemic
VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and
dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC
FAILURE and to delay absorption of local ANESTHETICS.
from MeSH
Epinephrine is an alpha-Adrenergic Agonist, and beta-Adrenergic Agonist, and
Catecholamine. The mechanism of action of epinephrine is as an Adrenergic alpha-
Agonist, and Adrenergic beta-Agonist. The chemical classification of epinephrine is
Catecholamines.
FDA Pharmacology Summary from FDA Pharm Classes
Epinephrine Hydrochloride is the hydrochloride salt of the naturally occurring
sympathomimetic amine with vasoconstricting, intraocular pressure-reducing, and
bronchodilating activities. By stimulating vascular alpha-adrenergic
receptors, epinephrinecauses vasoconstriction, thereby increasing vascular resistance and
blood pressure. When administered in the conjunctiva, this agent binds to alpha-
adrenergic receptors in the iris sphincter muscle, resulting in vasoconstriction, a decrease
in the production of aqueous humor, and a lowering of intraocular pressure. Through its
beta1 receptor-stimulating actions, epinephrine increases the force and rate of myocardial
contraction and relaxes bronchial smooth muscle, resulting i

MIZENÍ HERCE BENDY

Druhého září zmizel herec Benda, mistr Jan Benda, jak se mu říkalo od té doby, co jediným
rozběhem vystoupil na jednu z nejvyšších příčlí herecké slávy. Totiž druhého září se nestalo
docela nic; posluhovačka, která v devět hodin ráno přišla poklidit Bendův byt, našla zválenou
postel a celý ten kančí nepořádek, který obyčejně Bendu obklopoval, jenom pan mistr nebyl
doma; ale jelikož na tom nebylo nic neobvyklého, dala byt svým sumárním způsobem do
pořádku a šla zase po svém. Dobrá. Ale od té doby nebylo po herci Bendovi ani památky.
Paní Marešová (totiž ta posluhovačka) se nepodivila příliš ani tomu; prosím vás, tihle herci, to
vám je jako cikáni; kdopak ví, kam zas jel hrát nebo flámovat. Ale desátého září se strhla po
herci Bendovi sháňka; měl přijít do divadla, kde se začínaly zkoušky na Krále Leara; když
Benda nepřišel ani na třetí zkoušku, vzbudilo to přece jen nepokoj a z divadla telefonovali
doktoru Goldbergovi, Bendovu příteli, neví-li, co se děje s Bendou.
Ten doktor Goldberg byl chirurg a vydělával ukrutné peníze na slepých střevech; to už je
taková židovská specialita. Jinak to byl tlustý člověk s tlustými zlatými brýlemi a tlustým
zlatým srdcem; hořel pro umění, měl byt od podlahy po strop ověšený samými obrazy a
oddaně miloval herce Bendu, který k němu choval přátelské opovržení a s jistou
blahosklonností mu dovoloval, aby za něj platil; což, mezi námi, nebyla zrovna maličkost.
Tragická maska Bendova a zářící obličej doktora Goldberga (který pil jenom vodu), to už
patřilo k sobě při všech těch sardanapalských flámech a divokých výtržnostech, které byly
druhou stránkou proslulosti velkého mima.
Tedy tomu doktoru Goldbergovi telefonovali z divadla, co prý se děje s Bendou. Odpověděl, že
nemá ponětí, ale že se po něm podívá; co neřekl, bylo, že už ho sám po celý týden shání po
všech nočních lokálech a výletních hotelech s rostoucím znepokojením; měl tísnivou
předtuchu, že se něco Bendovi stalo. To bylo totiž tak: Doktor Goldberg byl, pokud mohl
zjistit, poslední, kdo Jana Bendu viděl. Někdy koncem srpna s ním ještě podnikl triumfální
tažení noční Prahou; ale pak už Benda nepřišel na žádnou obvyklou schůzku. Snad stůně, řekl
si konečně doktor Goldberg a zajel si jednou večer do Bendova bytu; bylo to právě prvního
září. Zvonil u dveří; nikdo nešel otevřít, ale uvnitř bylo slyšet nějaký šramot. Tu drnčel doktor
dobrých pět minut na zvonek; najednou zazněly kroky a dveře se otevřely; stál v nich Benda
zahalený v županu, a doktor Goldberg se ho zděsil: tak zdivočele vypadal slavný herec s
rozcuchanými a slepenými vlasy a vousy dobrý týden neholenými; zdál se přepadlý a špinavý.
“A, to jste vy,” řekl nevlídně, “co chcete?”
“Proboha, copak se s vámi stalo?” vyhrkl doktor užasle.

Diabetologie, endokrinologie, metabolismus

1. Mezi typické příznaky hypotyreózy nepatří:
hmostnostní přírůstek
zácpa
bradykardie
snížení TSH
2. Bílkovinný komplex s klíčovým významem pro endocytózu se nazývá
Klarithin
Karnitin
Klathrin
Keratin

3. Co nepatří pod diagnózu prediabetes?

hraniční glykemie nalačno (HGL, angl. IFG) jako důsledek inzulinové rezistence
postihující játra
úzký vztah k metabolickému syndromu
nenápadný diabetes v mládí, který hrozí zhoršením ve vyšším věku
porušená glukózová tolerance (PGT, angl. IGT) jako důsledek inzulinové
rezistence postihující kosterní svalstvo

4. Pro energetický metabolismus kosterního svalstva má význam

keratin (ve formě difosfátu)
kreatinin
karnitin
kreatin (ve formě fosfátu)

5. Metabolický syndrom je charakterizován především

zvýšenou činností štítné žlázy
patologickou aktivací mikrozomálních enzymů P450 v důsledku dlouhodobého
metabolizování léků nebo toxinů
inzulinovou rezistencí
sníženou činnosti štítné žlázy

6. Metabolická paměť
je jiný termín pro dlouhodobou paměť (její podstatou je metabolismus bílkovin)
je přetrvávání poškození buněk u diabetu i po normalizaci glykemie
je pojem z evoluční biologie označující funkci starých proteinových domén v
enzymech spojených s evolučně mladými metabolickými cestami
je souhrnný pojem pro imunologickou paměť a další podobné formy v protikladu
k paměti v běžném slova smyslu