Pharmacology of antibiotic, corticosteroids, insulin, and

antidiabetic drugs

A report submitted to the

College of Nursing
University of Duhok

Student name: khamlin Hamad abdal

Moodle Email: khamlinnurse@gmail.com
Year: 3rd
Course:2nd
Course code: NUB0718
Instructor: dr.Badran ahmad Saleh
Data: 29/6/2020
Objectives
  Antibiotic (definition ,medical uses, mode of
action, classification, types, side affects,
pharmacokinetics, pharmacodynamics,
contraindications

 Corticosteroids .definition, medical uses , types,

Adverse drug reaction, drug to drug interactions,
mechanism of action , contraindication
 Insulin, definition ,types, medical uses,
administration, side affect, adverse reaction
contraindication
 Antidiabetic drugs, introduction ,types , mechanism
of action, side affects, medical uses, contraindication

An antibiotic is a type of antimicrobial substance

active against bacteria. It is the most important type
of antibacterial agent for fighting bacterial
infections, and antibiotic medications are widely
used in the treatment and prevention of such
infections.[1][2] They may either kill or inhibit the
growth of bacteria. A limited number of antibiotics
also possess antiprotozoal activity.[3][4] Antibiotics
are not effective against viruses such as
the common cold or influenza [5]; drugs which
inhibit viruses are termed antiviral drugs or antivirals
rather than antibiotics.

Sometimes, the term antibiotic—literally "opposing

life", from the Greek roots ἀντι anti, "against" and
βίος bios, "life"—is broadly used to refer to any
substance used against microbes,
Medical uses
A doctor prescribes antibiotics for the treatment of a
bacterial infection. It is not effective against viruses.
Know whether an infection is bacterial or viral helps to
effectively treat it.
If people overuse antibiotics or use them incorrectly, the
bacteria might become resistant. This means that the
antibiotic becomes less effective against that type of
bacterium, as the bacterium has been able to improve its
defenses.
A doctor can prescribe a broad-spectrum antibiotic to treat
a wide range of infections. A narrow-spectrum antibiotic is
only effective against a few types of bacteria.
Some antibiotics attack aerobic bacteria, while others work
against anaerobic bacteria. Aerobic bacteria need oxygen
and anaerobic bacteria do not.
In some cases, a healthcare professional may provide
antibiotics to prevent rather than treat an infection, as
might be the case before surgery. This is the ‘prophylactic’
use of antibiotics. People commonly use these antibiotics
before bowel and orthopedic surgery.
Types of antibiotics
There are hundreds of different types of antibiotics, but
most of them can be classified into 6 groups.

 Penicillin’s (such as penicillin and amoxicillin) –

widely used to treat a variety of infections, including
skin infections, chest infections and urinary tract
infections
 Cephalosporins (such as cephalexin) – used to treat
a wide range of infections, but some are also
effective for treating more serious infections, such
as septicaemia and meningitis
 Aminoglycosides (such as gentamicin and
tobramycin) – tend to only be used in hospital to treat
very serious illnesses such as septicemia, as they can
cause serious side effects, including hearing loss and
kidney damage; they're usually given by injection,
but may be given as drops for some ear or eye
infections
 Tetracycline’s (such as tetracycline and doxycycline)
– can be used to treat a wide range of infections,
but are commonly used to treat acne and a skin
condition called rosacea
 Macrolides (such as
erythromycin and clarithromycin) – can be particularly
useful for treating lung and chest infections, or as an
alternative for people with a penicillin allergy, or to
treat penicillin-resistant strains of bacteria
  Fluoroquinolones (such as ciprofloxacin
and levofloxacin) – are broad-spectrum
antibiotics that were once used to treat a
wide range of infections, especially
respiratory and urinary tract infections.
These antibiotics are no longer used
routinely because of the risk of serious side
effects

Penicillin (PCN or pen) is a group of antibiotics, derived originally

from common moulds known as Penicillium moulds; which
includes penicillin G (intravenous use), penicillin V (use by
mouth), procaine penicillin, and benzathine
penicillin (intramuscular use). Penicillin antibiotics were among
the first medications to be effective against many bacterial
infections caused by staphylococci and streptococci. They are
still widely used today, though many types of bacteria have
developed resistance following extensive use.

Contraindication to penicillin
1. Anaphylaxis
2. Hypersensitivity
Pharmacodynamic of penicillin
When large amounts of penicillin are available, the
enzyme is completely blocked. When small amounts
of penicillin are available, the enzyme resumes normal
function. Thus the bacterial-killing activity
of penicillin changes as drug levels in the body change.
This is considered the “pharmacodynamics” of penicillin.

Pharmacokinetic
There is, however, some hepatic elimination.
The pharmacokinetic advantage to this drug is that high
serum concentrations are achieved rapidly, but the half-life
is approximately 30 minutes, necessitating redoing every
4-6 hours. Penicillin G is poorly absorbed orally, with a
bioavailability of 15-30%.
Antimicrobial agents may also be classified
based on their mechanism of action.
1. Agents that inhibit cell wall synthesis or
activate enzymes that disrupt cell wall, causing
a weakening in the cell wall, cell lysis, and
death. Includes penicillins, cephalosporins,
vancomycin, and imidazole antifungal agents.
2. Agents that act directly on cell wall, affecting
permeability of cell membranes, causing
leakage of intracellular substances. Includes
antifungal agents amphotericin and nystatin,
polymixin, and colistin.
3. Agents that bind to ribosomal subunits,
altering protein synthesis and eventually
causing cell death. Includes aminoglycosides.
4. Agents that affect bacterial ribosome
function, altering protein synthesis and causing
slow microbial growth. Does not cause cell
death. Includes chloramphenicol, clindamycin,
erythromycin, tetracyclines.
5. Agents that inhibit nucleic acid metabolism
by binding to nucleic acid or interacting with
enzymes necessary for nucleic acid synthesis.
Inhibits DNA or RNA synthesis. Includes
rifampin, metronidazole, quinolones (e.g.,
ciprofloxacin).
6. Agents that inhibit specific metabolic steps
necessary for microorganisms, causing a
decrease in essential cell components or
synthesis of nonfunctional analogues of
normal metabolites. Includes trimethoprim and
sulfonamides.
7. Agents that inhibit viral DNA synthesis by
binding to viral enzymes necessary for DNA
synthesis, preventing viral replication. Includes
acyclovir, vidarabine.
Antibiotics should only be prescribed
to treat health problems:
 that are not serious but are unlikely
to clear up without antibiotics – such
as acne
 that are not serious but could spread
to other people if not promptly
treated – such as the skin
infection impetigo or the sexually
transmitted infection chlamydia
 where evidence suggests that
antibiotics could significantly speed
up recovery – such as a kidney
infection
 that carry a risk of more serious
complications – such
as cellulitis or pneumonia
Antimicrobial or antibiotic modes of action

Antibacterial action generally falls within one of four

mechanisms, three of which involve the inhibition or
regulation of enzymes involved in cell wall
biosynthesis, nucleic acid metabolism and repair, or
protein synthesis, respectively. The fourth
mechanism involves the disruption of membrane
structure. Many of these cellular functions targeted
by antibiotics are most active in multiplying cells.
Since there is often overlap in these functions
between prokaryotic bacterial cells and eukaryotic
mammalian cells, it is not surprising that some
antibiotics have also 
Drug interactions to antibiotics

Antibiotics may have interactions with other

prescription and nonprescription medications. For
example, clarithromycin (Biaxin, an antibiotic) should
not be taken with metoclopramide (Reglan,
a digestive system drug).
Be sure a doctor and pharmacist know about all the
other medications a person is taking while on
antibiotics
Side effects
Antibiotics commonly cause the following side effects:
 diarrhea
 nausea
 vomiting
 rash
 upset stomach
 with certain antibiotics or prolonged use, fungal infections of the
mouth, digestive tract, and vagina

Less common side effects of antibiotics include:

 formation of kidney stones, when taking sulphonamides

 abnormal blood clotting, when taking some cephalosporins)
 sensitivity to sunlight, when taking tetracycline’s
 blood disorders, when taking trimethoprim
 deafness, when taking erythromycin and the
aminoglycosides

Some people, especially older adults, may experience

bowel inflammation, which can lead to severe, bloody diarrhea.

In less common instances, penicillin’s, cephalosporins, and

erythromycin can also cause inflamed bowels
antibiotics use during pregnancy and lactation
There was no teratogenic potential for penicillins G and V potassium (V-
Cillink); unlikely potential for amoxicillin, chloramphenicol
(Chloromycetin), ciprofloxacin (Cipro), doxycycline (Vibramycin),
levofloxacin (Levaquin), and rifampin (Rifadin); and undetermined
potential for clindamycin (Cleocin), vancomycin, and gentamicin (see
accompanying table). All agents were FDA Pregnancy Category B
(amoxicillin, clindamycin, penicillin G, penicillin V potassium, and
vancomycin) or C (chloramphenicol, ciprofloxacin, gentamicin,
levofloxacin, and rifampin), except for doxycycline, which was category
D.
Evidence suggested that increased maternal dose or shorter dosing
intervals should be considered for amoxicillin, gentamicin, and penicillins
G and V potassium. However, information on pharmacokinetics during
pregnancy was inadequate for the other antibiotics. There were limited
data on several other aspects of antibiotic use during pregnancy, but the
authors stress that conducting studies in this area would be challenging.
Despite the lack of scientific evidence, the authors conclude that
physicians should make balanced judgments about the well-being of the
mother and her child before making decisions about antibiotic use during
pregnancy and lactation.
View/Print Table
Relative Risk of Human Teratogenic Risk Associated with Antibiotic
Use in Pregnancy and Lactation
FDA
PREGN
TERATOGENIC ANCY
ITY RISK/DATA CATEG
ANTIBIOTIC AVAILABLE ORY

Amoxicilli Unlikely/fair B
n

Chloramp Unlikely/fair C
 FDA
PREGN
TERATOGENIC ANCY
ITY RISK/DATA CATEG
ANTIBIOTIC AVAILABLE ORY

henicol
(Chloromy
cetin)

Ciprofloxa Unlikely/fair C
cin (Cipro)

Clindamy Undetermine B
cin d/limited
(Cleocin)

Doxycycli Unlikely/fair D
ne
(Vibramyc
in)

Gentamici Undetermine C
n d/limited

Levofloxa Unlikely/fair C
cin
(Levaquin
)

Penicillin None/good B
G

Penicillin None/good B
V
 FDA
PREGN
TERATOGENIC ANCY
ITY RISK/DATA CATEG
ANTIBIOTIC AVAILABLE ORY

potassium
(V-Cillink)

Rifampin Unlikely/limit C
(Rifadin) ed to fair

Vancomy Undetermine B
cin d/very limited

FDA = U.S. Food and Drug Administration.

Corticosteroids
Corticosteroids are class of drug that lowers inflammation in the body.
They also reduce immune system activity.

Because corticosteroids ease swelling, itching, redness, and allergic

reactions, doctors often prescribe them to help treat diseases like:

 asthma
 arthritis
 lupus
 allergies
Corticosteroids resemble cortisol, a hormone naturally produced
by the body’s adrenal glands. The body needs cortisol to stay
healthy. Cortisol is a major player in a wide range of processes
in the body, including metabolism, immune response, and stress.

 types
Glucocorticoids such as cortisol affect carbohydrate, fat, and
protein metabolism, and have anti-
inflammatory, immunosuppressive, anti-proliferative,
and vasoconstrictive effects. Anti-inflammatory effects are
mediated by blocking the action of inflammatory
mediators (transrepression) and inducing anti-inflammatory
mediators (transactivation). Immunosuppressive effects are
mediated by suppressing delayed hypersensitivity reactions by
direct action on T-lymphocytes ,Anti-proliferative effects are
mediated by inhibition of DNA synthesis and epidermal
cell turnover Vasoconstrictive effects are mediated by inhibiting
the action of inflammatory mediators such as histidine.
MOA, GC causes their affect by binding to the Glucocorticoid
receptor GR . The activated of GR complex , in turn ,
up -regulates the the expression of anti-inflammatory proteins
in the nucleus (transactivation) and represses the expression of
proinflamatory proteins in the cytosol by preventing the
translocation of other transcription factors from the cytosol into
the nucleus (transrepression)

 Adverse reactions
Related to route of administration
Systematic use is associated with endocrine disorders
Drug to drug interaction
1. Increase in drug when given with erythromycin,
ketoconazole, or troleandomycin
2. Decrease in dose when given with salicylates, barbiturates,
phenytoin, or rifampin

 Mineralocorticoids such as aldosterone are primarily

involved in the regulation of electrolyte and water balance
by modulating ion transport in the epithelial cells of
the renal tubules of the kidney.

Cellular Mechanism of Action

Aldosterone and other

synthetic mineralocorticoids bind to cytoplasmic
mineraolocorticoid receptors (MR), and activated
receptors affect gene transcription. The cellular
mechanism of action is similar to that of
glucocorticoid receptors, but affecting different
genes

 Adverse reaction

Increase fluid volume

Allergic reactions
 Drug to drug interaction
Decrease effectiveness salicylates, barbiturates,
hydantoins, rifampin, and anticholinesterases

What are corticosteroids used for?

Corticosteroids are mainly  used to reduce inflammation
and suppress the immune system.
They are used to treat conditions such as:
 asthma
 allergic rhinitis  and hay fever
 urticarial (hives)
 atopic eczema
 chronic obstructive pulmonary disease (COPD)
 painful and inflamed joints, muscles and tendons
 lupus
 inflammatory bowel disease (IBD) including Crohn's
disease and ulcerative colitis
 giant cell arteritis and polymyalgia rheumatica
 multiple sclerosis (MS)
Corticosteroids can also be used to replace certain
hormones that are not being produced by the body
naturally for example, in people with Addison's disease.
Potential side effects of long-term treatment include:
 increased appetite“ potentially leading to weight
gain
 acne
 thinned skin  that bruises easily
 increased risk of infections
 mood changes, mood swings and  depression
 diabetes
 high blood pressure
 osteoporosis (weak and brittle bones)
 withdrawal symptoms caused by suppression of the
adrenal glands
If you have troublesome side effects after taking
corticosteroids, don't stop taking your medication until
your doctor says it's safe to do so, because of the
possibility of these unpleasant withdrawal effects.
Your dose may need to be reduced slowly over a few
weeks or months, and you may have to have tests to
ensure that your adrenal glands are still working properly
before stopping corticosteroids altogether, if you have
been taking them for a long time.
Contraindication to corticosteroids
1. Peptic ulcer
2. Diabetes mellitus
3. Hypertension
4. Viral and fungal infections
5. Tuberculosis and other infections
6. Osteoporosis
7. Herpes simplex keratitis
8. Psychosis
9. Epilepsy
10. CHF
11. Renal failure
Insulin
 ( from Latin insula, 'island') is a peptide hormone produced
by beta cells of the pancreatic islets; it is considered to be the
main anabolic hormone of the body. It regulates
the metabolism of carbohydrates, fats and protein by promoting
the absorption of glucose from the blood
into liver, fat and skeletal muscle cells. In these tissues the
absorbed glucose is converted into
either glycogen via glycogenesis or fats (triglycerides)
via lipogenesis, or, in the case of the liver, into
both. Glucose production and secretion by the liver is strongly
inhibited by high concentrations of insulin in the blood. Circulating
insulin also affects the synthesis of proteins in a wide variety of
tissues. It is therefore an anabolic hormone, promoting the
conversion of small molecules in the blood into large molecules
inside the cells. Low insulin levels in the blood have the opposite
effect by promoting widespread catabolism, especially of reserve
body fat.

 Medical uses
Insulin is used to treat a number of diseases
including diabetes and its acute complications such as diabetic
ketoacidosis and hyperosmolar hyperglycemic states. It is also
used along with glucose to treat high blood potassium
levels. Insulin was formerly used in a psychiatric treatment
called insulin shock therapy
 The five types of insulin are:
 rapid-acting insulin
 short-acting insulin
 intermediate-acting insulin
 mixed insulin
 long-acting insulin.

Rapid-acting insulin

Rapid-acting insulin starts working somewhere between 2.5 to 20 minutes after

injection. Its action is at its greatest between one and three hours after injection and can
last up to five hours. This type of insulin acts more quickly after a meal, similar to the
body's natural insulin, reducing the risk of a low blood glucose (blood glucose below 4
mmol/L). When you use this type of insulin, you must eat immediately after you inject. 

The three rapid-acting insulin types currently available in Australia are: 

 Fiasp and NovoRapid® (insulin aspart)

 Humalog® (insulin lispro)
 Apidra® (insulin glulisine)..

Short-acting insulin
Short-acting insulin takes longer to start working than the rapid-acting insulins.

Short-acting insulin begins to lower blood glucose levels within 30 minutes, so you need
to have your injection 30 minutes before eating. It has its maximum effect two to five
hours after injection and lasts for six to eight hours. 

Short-acting insulins currently available in Australia are:

 Actrapid®
 Humulin® R.
 Intermediate-acting insulin

Intermediate-acting and long-acting insulins are often termed background or basal

insulins.

The intermediate-acting insulins are cloudy in nature and need to be mixed well.

These insulins begin to work about 60 to 90 minutes after injection, peak between 4 to
12 hours and last for between 16 to 24 hours. 

Intermediate-acting insulins currently available in Australia are:

 Humulin® NPH (a human isophane insulin)

 Protaphane® (a human isophane insulin).

Long-acting insulin

The long-acting insulins currently available in Australia are:

 Lantus® (glargine insulin) – slow, steady release of insulin with no apparent peak action.
One injection can last up to 24 hours. It is usually injected once a day but can be taken twice
daily.
 Toujeo (glargine insulin) – this insulin has a strength of 300 units per ml so is three times
the concentration of other insulin in Australia. It is given once a day and lasts for at least 24
hours. It should not be confused with regular Lantus which has a strength of 100 units per ml.
Toujeo is given for safety by a disposable pen only. Toujeo gives a slower, steadier glucose
profile especially during the night. 
 Levemir® (detemir insulin) –slow, steady release of insulin with no apparent peak action
and can last up to18 hours. It is usually injected twice daily. 

Although these insulins are long-acting, they are clear and do not need mixing before
injecting.

Mixed insulin

Mixed insulin contains a pre-mixed combination of either very rapid-acting or short-

acting insulin, together with intermediate-acting insulin. 

The mixed insulins currently available in Australia are:

 rapid-acting and intermediate-acting insulin  

o Ryzodeg 70:30 (70% long acting Degludec, 30% rapid Aspart)
o NovoMix® 30 (30% rapid, 70% intermediate Protaphane)
o Humalog® Mix 25 (25% rapid, 75% intermediate Humulin NPH)
o Humalog® Mix 50 (50% rapid, 50% intermediate Humulin NPH)
 short-acting and intermediate-acting insulin  
o Mixtard® 30/70 (30% short, 70% intermediate Protaphane)
o Mixtard® 50/50 (50% short, 50% intermediate Protaphane)
o Humulin® 30/70 (30% short, 70% intermediate Humulin NPH).
  Insulin administration
Sites
 Abdomen (fattest absorption, most preferred)
 Buttocks
---( intermediate )
 Upper arm
 Thigh-lateral &anterior aspect (slowest)
 Rotate the site of injection around a selected
area
 Common side affects of insulin therapy
1. Hypoglycemia
2. Allergic reaction
3. Insulin resistance
4. Insulin lipohypertrophy
5. Insulin Edema , weight gain

 Contraindications to insulin
 If patient has hypersensitivity to any ingredient
in the product (older preparation made with
beef and pork) and if the patient is
hypoglycemic
Antidiabetic drugs (with the exception of insulin) are all
pharmacological agents that have been approved
for hyperglycemic treatment in type 2 diabetes mellitus (DM). If
lifestyle modifications (weight loss, dietary modification, and
exercise) do not sufficiently reduce A1C levels (target level: ∼
7%), pharmacological treatment with antidiabetic drugs should
be initiated. These drugs may be classified according to their
mechanism of action as insulinotropic or
 non-insulinotropic. They are available as monotherapy or
combination therapies, with the latter involving two (or, less
commonly, three) antidiabetic drugs and/or insulin. The exact
treatment algorithms are reviewed in the treatment section
of diabetes mellitus. The drug of choice for all type 2 diabetic
patients is metformin. This drug has beneficial effects
on glucose metabolism and promotes weight loss or at least
weight stabilization. In addition, numerous studies have
demonstrated that metformin can reduce mortality and the risk
of complications. If metformin is contraindicated, not
tolerated, or does not sufficiently control blood glucose levels,
another class of antidiabetic drug may be administered. Most
antidiabetic drugs are not recommended or should be used
with caution in patients with moderate or severe renal failure
or other significant comorbidities. Oral antidiabetic drugs are
not recommended during pregnancy or breastfeeding
 Class Mechanism of Side effects Contraindications
action

Biguanide (metformin Enhances Lactic acidosis Chronic kidney

) the effect of insuli Weight loss disease
n Gastrointestina Liver failure
l complaints are Metformin must be
common (e.g. diarrhe paused before
a, abdominal cramps) administration of
Reduced vitam iodinated contrast
in B12 absorption medium and major surger
y.

Increase  Risk Severe

Sulfonylureas (e.g., glyburi
insulin secretio of hypoglycemia cardiovascular
de, glimepiride)
n Weight gain comorbidity 
from pancreatic  Hematological Obesity
β-cells changes: agranulocyto Sulfonamide alle
sis, hemolysis rgy (particularly long-
acting substances)

Reduce intestinal Gastrointestin Any

Alpha-glucosidase glucose absorption al complaints preexisting
inhibitors (acarbose) (flatulence, diarrhea, intestinal
feeling of satiety) conditions
(e.g., inflamm
atory bowel
disease)
Severe
renal failure

Thiazolidinediones (piogl Reduce insulin Weight gain Conge

itazone) resistance through the Edema stive heart
stimulation of PPARs Cardiac failure failure
(peroxisome proliferator- Increased risk Liver f
activated receptors) of ailure
Increase transcripti bone fractures (osteo
on of adipokines porosis)
 Amylin Reduce glucagon re Risk Gastro
analogs (pramlintide) lease of hypoglycemia paresis
Reduce gastric Nausea
emptying
Increase satiety

Common contraindications of antidiabetic agents

 Type 1 diabetes mellitus: Patients require insulin therapy (see

principles of insulin therapy).
 Pregnancy and breastfeeding (also see gestational
diabetes): All antidiabetic agents are
contraindicated. Antidiabetic drugs should be substituted with
human insulin as early as possible (ideally prior to
the pregnancy). 

 Renal failure : Antidiabetic drugs that may be administered

if GFR < 30 mL/min include DPP-4 inhibitors, incritin mimetic
drug , meglitinides, and thiazolidinediones. 

 Morbidity and surgery 

 Pause antidiabetic treatment in the following cases:

 Major surgery performed under general anesthesia

 Acute conditions requiring

hospitalization (infections, organ failure)

 Elective procedures associated with an increased

risk of hypoglycemia (periods of fasting, irregular food intake)
Sulfonylureas are associated with the highest risk of hypoglycemia.
All other substances do not carry a significant risk
of hypoglycemia when used as a monotherapy. Combination
therapy, particularly with sulfonylurea, significantly increases the
risk of hypoglycemia!
  Insulinotropic agents
 Mechanism: stimulate the secretion
of insulin from pancreatic β-cells
 Glucose-independent: Insulin is secreted regardless of
the blood glucose level, even if blood glucose levels are low
→ risk of hypoglycemia
 Sulfonylurea, meglitinides
 Glucose-dependent: Insulin secretion is stimulated by
elevated blood glucose levels (postprandially). These antidiabetic
agents depend on residual β-cell function.
 GLP-1 agonists, DPP-4 inhibitors
 Non-insulinotropic agents
 Mechanism
 These agents do not depend on
residual insulin production.
 Effective in patients with nonfunctional
endocrine pancreatic β-cells
 Biguanides (metformin), SGLT-2 inhibitor, thiazolidinedione
s, alpha-glucosidase inhibitors

Biguanides (metformin)
Active agent

 Metformin

Clinical profile

 Mechanism of action: enhances the effect of insulin

 Reduction in insulin resistance via modification of glucose metabolic
pathways
 Inhibits mitochondrial glycerophosphate
dehydrogenase (mGPD)
 Decreases hepatic gluconeogenesis and intestinal
glucose absorption
 Increases peripheral insulin sensitivity
 Lowers postprandial and fasting blood glucose levels

 Reduces LDL, increases HDL

 Indications: drug of choice in all patients with type 2 diabetes

 Clinical characteristics

 Glycemic efficacy: lowers HbA1c by 1.2–2% over 3 months

 Weight loss or weight stabilization
 No risk of hypoglycemia

 Beneficial effect on dyslipidemia

 Studies show metformin reduces the risk of macroangiopathic

complications in diabetic patients. 

 Cost-effective
 Important side effects
 Metformin-associated lactic acidosis 

 Incidence: ∼ 8 cases/100,000 patient years

 Clinical features: frequently nonspecific
 Gastrointestinal prodromal symptoms: nausea,
vomiting, diarrhea, abdominal pain
 Severe symptoms: muscle
cramps, hyperventilation, apathy, disorientation, coma
 High-risk groups
 Elderly individuals 

 Patients with cardiac or renal insufficiency

 Diagnostics
  Arterial blood gas (ABG): metabolic
acidosis and anion gap

 ↑ Serum lactate

 Treatment: discontinue metformin and treat acidosis

 Gastrointestinal complaints are common: nausea, diarrhea,

flatulence 

 Vitamin B12 deficiency 

 Metallic taste in the mouth (dysgeusia)

 Contraindications
 Renal failure (if creatinine clearance < 30 mL/min)

 Severe liver failure 

 Intravenous iodinated contrast medium 

 Pause metformin prior to surgery

 Chronic pancreatitis, starvation ketosis, ketoacidosis, sepsis 
 Heart failure (NYHA III and IV), respiratory
failure, shock, sepsis 

 Alcoholism

 Important interactions: sulfonylureas 

Metformin treatment must be paused prior to the administration of a

contrast medium or scheduled surgery to reduce the risk of lactic
acidosis!

Because of its favorable risk-benefit ratio, metformin is the drug of

choice for monotherapy and combination therapy in all stages of type 2
DM!
Sulfonylureas
Active agents

 Glyburide: the standard substance of this class with a relatively

long half-life 
 Glipizide: a short-acting agent

Clinical profile

 Mechanism of action
 Sulfonylureas block ATP-sensitive potassium channels of
the pancreatic β-cells → depolarization of the cell
membrane → calcium influx → insulin secretion 

 Extrapancreatic effect: decreases

hepatic gluconeogenesis and increases
peripheral insulin sensitivity 

 Indications: particularly suitable for patients who are not

overweight, do not consume alcohol, and adhere to a
consistent dietary routine

 Clinical characteristics

 Glycemic efficacy: lowers HbA1c by 1.2% over 3 months

 Long-term experience

 Low-cost

 Important side effects

  Life-threatening hypoglycemia 
 Increased risk in patients with renal failure
 Weight gain

 Hematological changes: granulocytopenia, hemolytic
anemia

 Allergic skin reactions

 Alcohol intolerance 

 Compared to metformin, sulfonylureas are associated

with more cardiovascular (macrovascular) complications.

 Contraindications

 Severe cardiovascular comorbidity 

 Obesity

 Sulfonamide allergy (particularly long-acting substances)

 Severe liver failure

 Severe kidney failure

Beta-blockers may mask the warning signs

of hypoglycemia (e.g., tachycardia) and decrease serum glucose
levels even further (→ see hypoglycemia). Since sulfonylureas also
increase the risk of hypoglycemia, the combination of these two
substances should be avoided!
Reference
 https://books.google.iq/books/about
/Antibiotics.html?
id=4TWyAAAAQBAJ&printsec=frontc
over&source=kp_read_button&redir_
esc=y

 https://books.google.iq/books/about
/Insulin_Resistance.html?
id=WkKuBgAAQBAJ&printsec=frontco
ver&source=kp_read_button&redir_e
sc=y
 https://books.google.iq/books?
id=Em7dCgAAQBAJ&pg=PA220&dq=a
ntidiabetic+drug+book&hl=en&sa=X&
ved=0ahUKEwjF392U6qnqAhXBPOwK
HdzUBF0Q6wEIEjAC#v=onepage&q=a
ntidiabetic%20drug%20book&f=false

 https://books.google.iq/books/about
/Corticosteroids.html?
id=kWiQDwAAQBAJ&printsec=frontc
over&source=kp_read_button&redir_
esc=y