DEPARTMENT OF PHARMACOLOGY

ASSIUT UNIVERSITY-FACULTY OF MEDICINE

LECTURE NOTES
IN

PHARMACOLOGY
FOR NURSING

VOLUME II FIRST EDITION

Editors
Prof. Moustafa Mahmoud Dr. Mahran Shaker

2020
 Analgesic Drugs

- Analgesia means loss of pain sensation therefore analgesic drugs are used to relief
pain.
- There are two types of analgesic drugs :
1- Narcotic analgesic e.g. morphine .
2- Non- narcotic ( = antipyretic = anti-inflammatory) drugs e.g. salicylates.

Narcotic analgesics ( Morphine).

Pharmacological actions
(1)- central nervous system:
a- Analgesia.
Both components of pain ( sensory and emotional ) are suppressed.
b- Euphoria.
A pleasant sensation and freedom of distress and anxiety.
c- Sedation .
The patient will be quiet and calm, drowsy with decreased physical and mental
activities and may proceed to sleep
d- Respiratory depression.
e- Cough suppression.
f- Miosis.
g- Nausea & vomiting by stimulation of CTZ in the brain stem.
h- Truncal rigidity. An increased the tone of the large trunk muscles. This
reduces respiratory movements.
(2)- Gastrointestinal tract.
a- Constipation due to :
- Decreased peristaltic movements.
- Increased intestinal tone.
- Spasm of sphincter.
- Dissication of faeces due to excessive water absorption by the bowel
- The euphoric effect made the patient unaware about defecation
b- Aggravation of biliary colic due to spasm of sphincter of oddi.
(3)- Genitourinary tract.
- Renal function is depressed due to decreased renal perfusion ( Renal blood flow) .
- Urine retention due to spasm of the sphincter.
- Renal colic due to uretric stone due to increased tone of ureteric muscle fibers.
- Labor may be prolonged for unknown cause.
(4)- Endocrine effects.
- Morphine inhibits :- Antidiuretic hormone release. - Prolactin secretion.

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Therapeutic uses of morphine.
(1)- For analegesia.
- During labor (Meperidine is better).
- Cancer and terminal pains.
- Myocardial infarction.
(2)- Acute pulmonary edema associated with left heart failure.
(3)- Treatment of dry cough ( codeine ). Non narcotic cough suppressants ( e.g.
dextromethorphane) is preferable.
(4)- Diarrhea. Non narcotic antidiarrheal agents (e.g. diphenoxylate & loperamide ).
Treatment of infection ( if present ) should be the first line.
(5)- In anaesthesia.
- As preoperative medication for its sedative and analgesic effects.
- As general analgesic ( Fentanyl+ droperidol ).
- Spinal or epidural administration induces long lasting analgesia with fewer
side effects.
Side effects and toxicity .
- Extension of pharmacological effects:
- Nauesa and vomiting.
- Constipation.
- Respiratory depression.
- Tolerance develops to soma effects.
- Analgesia.
- Euphoria.
- Respiratory depression.
- Emetic.
- Hypotensive effect.
- Development of opioid dependence.
- Acute morphine toxicity:
- Diagnosed by the triad of :
a- Coma.
b- Respiratory depression
c- pin point pupils.
- Treatment by morphine antagonists e.g. Naloxone or Naltrexone.
Contraindications and precautions of use.
(1)- Head injuries as it elevates ICT.
(2)- During pregnancy. The fetus may becomes dependent.
(3)- Impaired pulmonary functions e.g. bronchial asthma.
(4)- Impaired hepatic or renal functions.

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 Nan-narcotic analgesics.
Non sleroidal anti-inflammatory drugs ( NSAIDs)
Acetylsalicylic acid ( Aspirin).
Pharmacological actions.
(1)- Anti-inflammatory effect.
- Aspirin inhibits inflammation via:
- Inhibition of prostglandin synthesis.
- Inhibition of migration of leukocytes (i.e polymorph nuclear cells & macrophages).
(2)- Analgesia.
- Aspirin is effective in relief of mild to moderate pain ( e.g. muscular, joint, dental
and postpartum pains ) by two mechanisms :
- Peripheral by reducing the inflammation.
- Central by elevation of pain threshold.
(3)- Antipyresis.
- An elevated body temperature significantly reduced by aspirin (but not
hypothermic). This effect is due to increased loss of body temperature ( not decreased
heat production) due to peripheral vasodilation with profuse sweating. This effect is
accomplished by resitting of the hypothalamic heat control centre down to 37 0c.
Again this is due to inhibition of prostaglandins.
(4)- Blood platelets.
- Platelet aggregation is irreversibly inhibited by aspirin. This effect is due to
inhibition of thromboxaneA2 synthesis that has thrombogenic effect.
Therapeutic uses.
- Analgesia & anti-inflammatory
- Antipyretic.
- Anti-platelet aggregation to prevent arterial thrombosis. This is beneficial
effect to reduce the incidence of acute cardiac is ischaemic attacks.
Side effects.
(1)- Gastrointestinal : gastric upset & gastritis due to :
0- Irritation of gastric mucosa by the undissolved tablets.
0- Absorption of non-ionized aspirin by the stomach.
0- Inhibition of protective PG, by gastric mucosa.
- Nausea & vomiting may occur with large doses due to central effects.
- Bleeding gastritis & erosions. With usual therapeutic doses, the body looses 1ml
of blood 1 day and this increases by increasing the dose.
(2)- Central nervous system
- Using high doses, the patient may suffer from tinnitus, decreased hearing and
vertigo. These can be reversed by dose reduction.
- Higher doses, may produce hyperpnea and respiratory alkalosis (Co2 wash ).
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 - Latter on, metabolic acidosis develops due to accumulation of salicylic acid
derivatives and respiratory depression.
(3)- Aspirin has dual effect on uric acid :
- Doses less than 2g\D increases plasma uric acid.
- Doses more than 5g\ day decreases plasma uric acid ( i.e. uricosuric effect ).
(4)- Hypersensitivity reactions e.g. rash, bronchospasm & shock.
General Anesthetics
Definition
- "General anesthesia" means induction of a state that includes.
- Unconsciousness.
- Loss of sensations ( i.e. analgesia).
- Skeletal muscle relaxation.
- An ideal general anesthetic is the one that is able to produce:
- Smooth induction of anesthesia.
- Rapid recovery after stop of administration.
- Has a wide safety margin.
- Induces full muscle relaxation.
There is no one single drug has all these conditions to a satisfactory degree when
used alone. They only can be obtained by the use of drug combinations.
Types of G. anesthetics.
(1)- Inhalation anesthetics.
a)- volatile liquids e.g.
- Halothane.
- Enflurane.
- Isoflurane.
- Methoxyflurane.
b) Gases e.g.
- Nitrous oxide.
(2)- Intravenous anesthetics
a)- Barbiturates e.g. Thiopental.
b)- Benzodiazepines e.g. Diazepam& midazolam.
c)- Opioids e.g. Fentanyl, sufentanil, alfentanyl and remifentanil.
d)- Propofol.
e)- Ketamine.
Stages of G. anesthesia.
- when a general anesthetic is introduced, the depth of anesthia increases as the
concentration of the anesthetic in the blood increases.
- There are 4 stages anesthesia according to the depth of anesthesia:

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(1)- Stage of analgesia.
- The patient starts to feel analgesia while still conscious.
- It merges into stage 2 when the patient start to be unconsciousness.
(2)- Stage of excitement.
- Inspite of unconsciousness the patient is excited.
- Respiration is irregular (both in depth & rate). Rapid pulse & decreased BP
- Vomiting & excessive salivation.
- Muscle struggle.
N.B. all effort should be made to limit the duration & severity of this stage.
(3)- Stage of surgical anesthesia.
- Starts with recurrence of normal respiratory & cardiovascular functions.
- Extends to complete respiratory arrest.
- Can be subdivided into 4 planes based on :
- Ocular movement (Decreasing).
- Eye reflexes. (Decreasing).
- pupil size. (Increasing).
(4)- Stage of medullary paralysis.
- Starts with complete respiratory arrest.
- Both respiratory and vasomotor centers paralysis.
- These can be reversed by cessation of administration with full respiratory and
cardiovascular support. Otherwise, death is rapid.
N.B - These stages were described as if the patient is taking only ether
inhalation without any other preanesthetic pre-medication or anesthetic adjuvants.
- Intravenous anesthetics have the advantage of inducing surgical anesthesia with
very rapid induction & excitation stages. This means minimal side effects.
- In order to reduce the dangers of general anesthesia the patient should be prepared.
Preanesthetic medication.
Means preparation of the patient before giving anesthetics for the following reasons:
1)- To reduce anxiety and ensure rapid and smooth induction.
2)- To minimize as much as possible side effects e.g. salivation.
3)- To get benefits from drug combinations i.e. synergism.
- The following drugs can be used as preanesthetic medicines:
1)- Sedative hypnotic drugs :
- These drugs induce sedation, hypnosis, anti-arrhythmic, antihistaminic and
antiemetic effects. They include:
- Benzodiazepines (Diazepam & Lorazepam) - Phenothiazines (Promethazine).
2)- Opioid analgesics.
- To reduce the anaesthetic conc. That is needed for induction.
- Reduce the incidence of excitement during recovery from anesthesia.
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 - Pre-operative relief of pain.
- They include morphine & meperidine (Pethidine).
3)- Anticholinergic drugs.
- These are useful to antagonize the autonomic side effects of anesthetics:
- Increased bronchial & salivary secretion.
- Excessive vagal stimulation that can lead to bradycardia & hypotension.
- They include atropine & scopolamine.
4)-Drugs that reduce both volume & acidity of gastric acid secretion:
- H2 receptor blockers e.g. cimetidine , ranitidine, famotidine & nizatidine.
- Prokinetic drugs e.g. metochlopramide. that enhance GI motility with rapid
gastric emptying. This is useful in emergency states that need rapid anesthesia (to
decrease the incidence of vomiting during anesthesia).
5)- Induction of anesthesia using intravenous anesthetic ( rapid induction & short
excitation stages) and then maintain anesthesia by inhalation ( low concentration).

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 Sedative Hypnotics
* Sedative drug : is a drug which causes sedation
* Sedation means → calmness 4 decreases activity
* Hypnotic drug : is a drug which causes hypnosis
* Hypnosis means → a state resembling natural sleep.
They include :
A) Benzodiazepines
B) Barbiturates
C) Others
Benzodiazepines:
This group include
* Diazepam
* Lorazepam
* Flurazepam
* Clonazepam
* Pharmacological actions :
- Sedation in small dose hypnosis in large dose
- Skeletal muscle relaxation
- Anti convuls ant action.
- May produce ↓ in BP and reflex tachycardia
* Side effects.
1) Residual effects in the form of drowsiness and decreased meutal function
2) Tolerance after prolonged vse
3) withdrawal symptoms after prolonged vse. E.g Anxiety and insomnia
Therapeutic vses :
1) Treatment of anxiety
2) Treatment of sleeping problems
3) Treatment of epilepsy and status epilepticvs
4) As I.V anesthetic agents
5) As musele relaxant
6) preanesthetic medication
Barbiturates
* They are now used only as anticonvulsants. E.g Phencbar brutal 20 minute
* The ultra short acting barbiturates ( thiopental ) is used as I.V anesthetic agent
* They have several side effects cause addiction so their uses are restricted
Buspirone
Antianxiety without hypnosis and skeletal muscle relaxant

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 Anticonvulsant
Epilepsy: Chronic disorder characterized by recurrent fits/seizure
Seizure: Episode of brain dysfunction due to abnormal discharge of cerebral neurons
Etiology: -Idiopathic -Trauma -CNS infection
-Brain tumor –Metabolic -Electrolyte disturbance
Classification:
1-Drugs effective in grand mal and focal epilepsy
Phenytoin – Carbamazepine – Valproic – Phenobarbital – Primidone
2-Drugs effective in absence(Petit mal)
Ethosuximide- Valproic acid- Clonazepam
3- Drugs effective in status epileptics:
Diazepam – Phenytoin
1-Diphenyl hydantoin:
Pharmacodynamic:
Block activated Na channel so decrease repetitive neuronal discharge
Therapeutic Uses:
1-Grand Mal Epilepsy – focal epilepsy
2-Status epileptics I.V
3-Cardiac arrhythmia
4-Trigeminal neuralgia
Side effects:
1-I.V high dose induce CVS collapse and CNS depression –nystagmus- diplopia –
vertigo
2-Gingival hyperplasia
3-Hypersensitivity: skin rash
4-Vit D deficiency: adult-osteoprosis
Children-rickettes
2-Carbamazepine
Pharmacodynamic:
Similar to phenytoin
Therapeutic Uses:
1-Generalized tonic-clonic Convulsion
2-Partial Fits
3-Trigeminal neuralgia
4-Mood stabilizer
Side Effects:
1-CNS: ataxia, diplopia and drowsiness
2-GIT: nausea and vomiting
3-Blood: aplastic anemia and agranulocytosis
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3-Valproic acid
Pharmacodynamic:
1-Interaction with voltage sensitive Na Channel
2-Enhance GABA accumulation
Indications:
1-All types of epilepsy
2-Bipolar affective disorder (mood stabilizer)
Side Effects:
1-CNS
2-GIT
3-Skin rash –alopecia
4-Pancreatitis
5-Hepatitis
6-Increase appetite
4-Phenobarbital:
Long acting barbiturate
Pharmacodynamic:
1-Enhance GABA inhibitory action
2-Reduce excitatory effect og glutamate
Uses:
1-Anticonvulsant broad spectrum
2-Status epilepticus
Side effects:
1-CNS depression
2-Tolerance and dependence
3-Nystagmus and ataxia
4-Megaloblastic anemia
5-Primidone:
Prodrug resembles Phenobarbital
Indications:
1-Grand Mal Epilepsy
2-Focal Epilepsy
3-Refractoty Epilepsy
Side effects:
1-Sedation,ataxia and psychotic reaction
2-Skin rash, Blood dyscriasis and lympadenopathy
3-Megaloblasic Anemia

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 CHEMOTHERAPY OF MICROBIAL DISEASES
INTRODUCTION
Antimicrobials are drugs used in the treatment of infectious disease whether bacterial,
viral, fungal or parasitic. They are either kill (-cidal) or inhibit the growth (-static) of
microorganisms with minimal harm to the host (human being). The antimicrobials
obtained from living microorganisms (e.g., fungi) and inhibit or kill other
microorganisms are called antibiotics. However, synthetic antimicrobials (man-mad)
are called chemotherapeutic agents. Development of acquired resistance to
antimicrobial drugs, as a result of misuse, limits the usefulness of these drugs.
I- SULFONAMIDES
Synthetic chemotherapeutic agents,
Table (1): shows different classes of sulfonamides.

Mechanism of action
Folic acid is required for the synthesis of DNA and RNA both in bacteria and
mammals. Mammals get their folic acid in their diet whereas bacteria synthesize
their own folic acid from p-aminobenzoic acid. Sulfonamides, being structural
analogues to p-aminobenzoic acid (PABA), compete with PABA for the enzyme
dihydropteroate synthetase required for bacterial folic acid synthesis and so inhibit
folic acid synthesis.
Antibacterial spectrum
 Sulfonamides are primarily bacteriostatic against many Gram-positive and Gram-
negative bacteria (broad-spectrum).
 Trimethoprim acts synergistically with sulphamethoxazole because it inhibits
dihydrofoolate reductase, which converts folic acid into tetrahydrofolic acid;
produces sequential block. Co-trimoxazole (sulphamethoxazole-trimethoprin
combination) is bactericidal.
 Excessive pus as a source of PABA antagonizes sulphonamide actions.

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Therapeutic uses
1. Urinary tract infections (UTIs): First, previously untreated acute UTIs (Co-
trimoxazole; sulphamethoxazole-trimethoprim).
2. Prostatitis: Co-trimoxazole (sulphamethoxazole-trimethoprim).
3. Meningicoccal meningitis: prophylaxis and treatment (sulphadiazine)
4. Ulcerative colitis: sulfasalazine.
5. Infected burns, bed sores and leg ulcers: silver sulfadiazine topically.
6. Respiratory tract infections: as sinustitis, otitis media, bronchitis, pneumonitis
(Co-trimoxazole (sulphamethoxazole-trimethoprim) or sulphaisoxazole.
7. Chlamydial eye infections: sulphacetamide sodium eye drops.
Adverse effects
1. Hypersensitivity reactions: fever and photosensitivity. Not taken with sulpha-
containing drugs as thiazide and loop diuretics, diazoxide, and sulphonyl urea
because of cross allergy (if present).
2. Blood dyscrasis: due to bone marrow suppression and hemolytic anemia in
paients with G-6-PD.
3. Crystalluria (stone kidney): avoided by plenty of water intake, alkalinization
of urine and/or using triple sulpha..
4. Kernicterus: may occur in the premature newborn due to displacement of
billirubin from plasma protein binding sites by sulphonamides.
5. Drug interaction: Displace warfarin from plasma protein binding 
increasing warfarin levels and so bleeding possibility being high.
CO-TRIMOXAZOLE
(Sulphamethoxazole-Trimethoprim combination)
Advantages over sulphonamides:
 Individually both trimethoprim and sulphamethoxazole are bacteriostatic but the
combination, co-trimoxazole is bactericidal.
 They act synergistically, sequentially block folic acid synthesis.
Therapeutic uses
1. Urinary tract infections (not previously treated with any antibiotics).
2. Typhoid: as an alternative to quinolones or chloramphenicol.
3. Bacterial diarrheas and dysentry caused by shigella.
1. Pneumocystis carinii infections in AIDS patients.
2. Bacterial prostatitis and Respiratory tract infections.
Nursing implications on sulphonamides and cotrimoxazole:
1. The nurse should advise the patient to take plenty of fluids as water to avoid
precipitation of the acetylated metabolites of sulpha drugs in the kidney and hence
protects the kidney from stone formation.

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2. The nurse should advise the patient to avoid using of sulphonamides during late
pregnancy or to neonates to avoid hyperbilirubinemia manifested by physiological
jaundice.
3. Cotrimoxazole is used twice daily i.e., every 12 hours.

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 II- CELL WALL SYNTHESIS INHIBITORS
(BETA-LACTAM ANTIBIOTICS)
(Penicillins, Cephalosporins, Monobactams and Carbapenems)
 All β-lactam antibiotics are bactericidal.
 All β-lactam antibiotics are bacterial cell wall synthesis inhibitors
 All β-lactam antibiotics act by binding with penicillin-binding proteins inhibiting
peptidoglycan formation and/or activation of autolytic enzymes (autolysin) that
result in death of bacterial cells due to inhibition of cell wall synthesis.
 All β-lactam antibiotics are highly selective because human cells don’t contain
peptidoglycan cell wall (target site).
1. Penicillins
Stability:
Penicillin salts are stable for long period in dry crystal form. However, after
dissolution penicillins lose their activity rapidly (after 1-2 weeks).
Resistance to penicillins:
 β-lactamases (penicillinases) produced by some microorganisms as staph &
pseudomonas destroy some penicillins as amoxicillin and ampicillins. Therefore,
these microorganisms are resistant to these types of penicillins.
Classification of Penicillin and their antimicrobial activity:
i. Narrow spectrum penicillins: act mainly against G+ve organisms
except staph
 Short acting (4-6h): Parenteral penicillin G & Oral penicillin V
 Repository (Long-acting): Procaine penicilline G (12-24 h; I.M) &
Benzathine penicilline G (IM injection /21 days).
ii. Penicillinase-resistant penicillins:
 Methicillin: used parenteral only.
 Cloxacillin,dicloxacillin and flucloxacillin: oral and
parenterals.
iii. Broad spectrum penicillins: act against both G+ve and G-ve:
1. Ampicillin (6h intervals), used before meal because it is
affected by protein diet (drug-food interaction).
2. Amoxicillin (8h intervals, no drug-food interactions).
iv. Antipseudomonal penicillins: Carbencillin & piperacillin.
Beta Lactamase Inhibitors
 e.g., clavulanic acid, sulbactam and tazobactam.
 They have no antibacterial activity but prevent penicillins decomposition by beta
lactamases-producing microrganisms and so extend the spectrum of penicillins.

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Preparations: Unasyn (ampicillin + sulbactam), Augmentin (amoxicillin +
clavulanate) and Tazocin (Piperacilliln + Tazobactam)
.Pharmacokinetics of penicillins:
 Penicillins that are resistant to hydrolysis by gastric fluids (acid-resistant) are
taken orally while acid labile penicillins are taken parenterally. Parental
penicillins can be given by intramuscular or intravenous injection. Only clear
aqueous solution used I.V.
 The drugs are widely distributed in the body fluids. They do not cross the blood-
brain barrier unless the meninges are inflamed.
 Elimination of penicillins occurs rapidly, mainly through the kidneys by tubular
secretion (blocked by probenecid) and lesser amount by glomerular filtration.
Therapeutic uses of penicillins:
1. Penicillin G: I.V. used in bacterial meningitis, pneumonia, bacterial
endocarditis, follicular tonsillitis, and some UTI.
2. Penicillin V: orally in pharyngitis.
3. Repository penicillins (procaine penicillin and benzathine penicillin) are used
mainly in the prophylaxis from rheumatic fever, and syphilis.
4. Antistaph penicillins (Flucloxacillin): Different staph infections (bone and joint
infections and skin and soft tissue infections and abscess.
5. Broad-spectrum penicillins (amoxicillin, ampicillin, etc): used in:
a) Upper respiratory tract infections: as sinusitis, and bronchitis (amoxicillin).
b) UTI (Augmentin)
c) Bacterial meningitis (I.V ampicillin + chloramphenicol)
d) Salmonella infection as typhoid (amoxicillin)
e) H. Pylori in peptic ulcer: Amoxycillin 500 mg TID for 2 weeks included in
triple antibiotic therapy.
6. Piperacillin I.V. and other antipseudomonal penicillins: Serious G-ve infections,
bacteremias, pneumonias, infections following burns and some UTI infections.
Adverse effects
i) Allergic reactions, range from rash to fatal anaphylactic reaction. Therefore
every patient is routinely asked about previous history of penicillin allergy. A
skin test is also performed.
ii) GI disturbances: as diarrhea with broad spectrum penicillins given orally.
iii) Nephritis: Methicillin has the potential to cause nephritis.
iv) Neurotixicity: as seizures with intrathecal penicillins (in epileptic patients).
Nursing implications for penicillins:
1. Sensitivity tests are essential prior administration of parenteral penicillins.
Intradermal injection of one drop of penicillin-polylysine conjugated or very diluted
penicillins can be used for this purpose (1:50 dilution).
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 2. Patient monitoring: The nurse should monitor and observe all patients for signs of
allergic reactions (fever, rash, bronchospasm, hypotension, etc.), especially after first
dose of penicillin.
3. Management of anaphylactic reactions: The nurse should be ready for prompt
management of penicillin allergy, especially anaphylactoid reactions by the S.C
epinephrine (life-saving drug) at once, I.V corticosteroids as hydrocortisone and O2
therapy (but under medical supervision).
4. Oral ampicillin should be given every 6 h and before meals to avoid drug-food
interactions, while amoxicillin given each 8 hourly and after meal.
5. Never give procaine penicillin or benzathine penicillin I.V. because they are in
suspension dosage-form.
2. Cephalosporins
Classification: Four generations based on antibacterial spectrum.
Properties CEHALOSPORIN GENERATIONS
FIRST SECOND THIRD FOURTH
PARENTERA Cephalothin Cefuroxime* Cefotaxime* Cefepime*
L Cephazolin Cefoxitin Ceftriaxone* Cefpirome
Cefamandole Ceftazidime
Cefoperazone
ORAL Cephalexin* Cefachlor Cefixime -
Cefadroxil Cefuroxime
Pass BBB Not pass BBB Only cefuroxime Pass BBB Pass BBB
Spectrum Active against More active More active Similar to
G+ve/weak against G-ve / against G-ve / third-
against G-ve less against less against generation
G+ve G+ve but highly
resistant to β-
lactamases.
* Frequently used
N.B. Cephalosporins activities against G-ve infections, their passage across blood
brain barriers and their costs are increased from first to second to third/fourth
generations.
Therapeutic uses
1. Infections resistant to penicillins (not MRSA).
2. Pneumonia: 3rd generation e.g., cefotaxime.
3. Meningitis: 3rd generation e.g., ceftriaxone, cefotaxime i.v.
4. URTIs as sinusitis: Cefadroxil orally.
5. Urinary tract infection, especially in pregnancy or in resistant cases.

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6. Pre-and post operative surgery: first or second generation
7. Typhoid fever (ceftriaxone).

Adverse effects
1. Allergy: including rash, fever and even anaphylaxis may occur. Partial cross-
allergy may occur with penicillins; about 10% of people allergic to penicillins
may be allergic to cephalosporins.
2. GI upset & superinfections manifested by Diarrhea.
3. Nephrotoxicity: Cephradine may cause nephrotoxicity.
4. Intolerance to alcohol also occurs (disulfiram like reactions) .
3- Carbapenems
e.g., Imipenem:.
 The broadest spectrum β-lactam antibiotics (active against G+ve, G-ve, aerobic
and anerobic).
 It is resistant to most β-lactamases.
 It is rapidly inactivated by renal tubular enzyme dihydropeptidase forming
nephrotoxic metabolite. Cilastatin inhibits this dihydropeptidase enzyme and so used
in fixed dose combination with Imipenem under the trade name of “Tienam”
 Imipenem may cause seizures (high doses in predisposed patients).
e.g., Meropenem:
 Not metabolized by dihydropeptidase enzyme.
 Less liable to produce seizure.
4- Monobactams
Aztreonam is a new β-lactam antibiotic in which the other ring is missing, hence
monobactam. It is effective against Gram-negative organisms. Its positive feature is
its lack of cross-sensitivity with other β-lactam antibiotics. Therefore, it can be used
in patients who are allergic to penicillins or cephalosporins.

III- Protein synthesis inhibitors

1. Aminoglycosides. 3. Chloramphenicol
2. Tetracyclines 4. Macrolides
1- AMINOGLYCOSIDES
Members: Streptomycin, Kanamycin, Gentamicin, Tobramycin, Amikacin and
neomycin
Aminoglycosides properties:
 Aminoglycosides share the following properties, which are as follows:
 All aminoglycosides are stable water-soluble solutions (c.f. penicillins).

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 They ionize in solution; are not absorbed adequately after oral administration,
inadequate concentrations being found in cerebrospinal fluid.
 All are excreted unchanged, relatively rapidly, by glomerular filtration, by the
normal kidney.
 All are bactericidal and more active at alkaline pH.
 They act by interfering with bacterial protein synthesis.
 All are active primarily against aerobic Gram-negative bacilli.
 Have narrow margin of safety.
 Serious toxicity limits the usefulness of the aminoglycosides, and all members of
the group share the same spectrum of toxicity (nephrotoxicity and ototoxicity),
Mechanism of action
 The bactericidal activity of aminoglycosides may be mediated by inhibiting protein
synthesis resulting from binding with 30 S subunits of ribosomes.
Spectrum of action:
 Aminoglycosides are active mainly against most aerobic Gram-negative bacilli
and some Gram-positive bacteria. Anaerobic bacteria are resistant because
aminoglycoside transport into cells is oxygen-dependent.
A postantibiotic effect:
 Residual bactericidal activity persisting after the serum concentration falls below
the minimum inhibitory concentration.
 This post-antibiotic effect of aminoglycosides probably account for the efficacy of
the once-daily dosing regimens of aminoglycosides despite long periods during
which antibiotic is not present.
Adverse Effects:
1. Ototoxicity: Damage of 8th cranial nerves irreversible and progressive
destruction of vestibular or cochlear sensory cells  loss of equilibrium and deafness
respectively.
2. Nephrotoxicity: due to marked accumulation of aminoglycoside in the proximal
tubular cells.
3. Neurotoxicity: An unusual toxic reaction of acute neuromuscular blockade and
apnea has been attributed to the aminoglycosides.
4. Rare hypersensitivity reactions: including skin rashes, eosinophilia, fever, blood
dyscrasias, angioedema, stomatitis, and anaphylactic shock, have been reported.
Therapeutic uses:
1. STREPTOMYCIN:
Tuberculosis: Streptomycin combined with other drugs is used as a second line
therapy to treat tuberculosis (TB). In some cases, strains with multi-drug resistant
TB (MDRTB) are susceptible to streptomycin containing regimen.

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1. GENTAMICIN, TOBRAMYCIN, AMIKACIN, AND NETILMICIN:
 For most indications, gentamicin is the preferred agent because of long experience
with its use and it’s relatively low cost.
 These drugs are used interchangeably for the treatment of the following
infections.
a. Urinary tract infections b. Pneumonia
c. Meningitis d. Peritonitis
e. Sepsis f. Topical use: skin infections (burns).
2. NEOMYCIN:
 Topically neomycin is used for skin and mucous membrane infections.
 Orally, it is used for preparation of the bowel for surgery and hepatic coma.
2. TETRACYCLINES
 Broad-spectrum bacteriostatic antibiotics. The group includes tetracycline,
oxytetracycline, doxycycline and minocycline.
Mechanism of action
 Tetracyclines are bacteriostatics.
 Protein synthesis inhibitors; act by binding to 30 S subunits of ribosomes.
Antibacterial spectrum
 Broad spectrum (affect both Gram-positive and Gram-negative bacteria,
Chlamydia, and some protozoa as amoebae).
 Minocycline is also effective against Neisseria meningitidis and has been used to
eradicate this organism from the nasopharynx of carriers; it does not cross the
blood-brain barrier and is not used to treat meningitis.
Absorption of tetracyclines:
 Tetracyclines are usually given orally and the absorption of most preparations is
irregular and incomplete.
 Absorption is better in the absence of food.
 Tetracyclines chelate metal ions (calcium, magnesium, iron, and aluminium),
forming non-absorbable complexes. Therefore, their absorption decreased in the
presence of milk, certain antacids and iron preparations except minocycline and
doxycycline; almost completely absorbed.
Therapeutic uses
1. They are highly effective & useful in the following infectious disease:
a. Cholera (doxycycline)
b. Bacillary dysentery caused by shigella or salmonella.
c. Chlamydial infections e.g., inclusion conjunctivitis and trachoma.
d. Brucellosis and tularemia (streptomycin added)
e. Skin infections as acne vulgaris.
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 f. Eye infections (topical tetracyclines).
g. Intestinal amoebiasis.
h. Sexually transmitted diseases (e.g., syphilis & gonorrhea).
2. They are also useful in mixed infections of the respiratory tract.
Adverse effects (side effects and toxicity):
1. Gastrointestinal irritantion: nausea & vomiting are common.
2. Suprainfection and diarrhea: due to development of pseudomembranous colitis
as a result of inhibition of intestinal flora by broad spectrum antibiotics. This can
be treated by metronidazole or vancomycin orally.
3. Teeth and bone abnormalities:
 If tetracyclines are taken during pregnancy & early childhood, they chelate
calcium and deposited in growing bones and teeth leading to bone deformity
and yellow-brown teeth discoloration.
 So, tetracyclines should be avoided during pregnancy, lactation and children
up to 8 years.
4. Phototoxicity may occur, particularly with demeclocycline.
5. Teratogenicity and growth retardation.
6. Hepatotoxic with large doses.
7. Nephrotoxicity: expiry trtracyclines may cause “Fanconi syndrome”
characterized by azoturia, glucosuria, polyuria and acidosis)
3. CHLORAMPHENICOL
Mechanism of action:
Chloramphenicol act by inhibition of protein synthesis through binding to 50 S
subunit of the bacterial ribosome, just like erythromycin and clindamycin.
Antibacterial spectrum:
 Broad-spectrum of antimicrobial activity, including Gram-negative and Gram-
positive organisms and rickettsiae.
 Bacteriostatic for most organisms but bactericidal for H. influenzae.
Therapeutic uses
 Serious adverse effects limit the usefulness of chloramphenicol.
 It is reserved for serious infections; used only when benefit is greater than the
risk. It may be used for:
1. Meningitis caused by H. influenza- resistant to other drugs (ampicillin added).
2. Bacterial conjunctivitis and other eye infections.
3. Typhoid fever but is not preferred because of serious adverse effects.
Ciprofloxacin, amoxycillin and co-trimoxazole are effective and less toxic.

19
Adverse effects
1. Bone marrow depression: reversible bone marrow suppression and
irreversible aplastic anemia are the most dangerous adverse effect and can be
fatal. Therapy should therefore be monitored.
2. Grey baby syndrome: In newborn babies which includes vomiting, diarrhea,
flaccidity, low temperature and ashen-grey color.
3. Hypersensitivity reactions
4. Gastrointestinal disturbances can also occur.
5. Liver microsomal enzyme inhibitors.
6. MACROLIDES
Members:
Erythromycin Clarithromycin Azithromycin
Spiramycin Roxithromycin.
Mechanism of action:
 The macrolides inhibit bacterial protein synthesis by binding to the 50 S subunit
of the bacterial ribosome, just like chloramphenicol and clindamycin.
 The action may be bactericidal or bacteriostatic, depending on the dose and the
organism.
Antimicrobial spectrum:
 Erythromycin has similar activity of penicillin G and so approved to be a safe and
effective alternative for penicillins in penicillin-allergic patients. It is effective
against Gram-positive bacteria and some Gram-negatives. It is used every 6 h for
several days (3-7 days).
 Azithromycin is less active against Gram-positive bacteria than erythromycin, but
more active against H. influenzae and Legionella. It has excellent action against
Toxoplasma gondii, killing the cysts. It is used once daily for three doses.
 Clarithromycin: It is more active against H. influenza, leprosy, and Helicobacter
pylori. It is used twice daily for several days.
N.B. Both Clarithromycin and azithromycin have longer duration of action than
erythromycin and less side effects. In addition, more effective against G-ve including
H. pylori , mycoplasma and H. influenza.
Therapeutic uses
Macrolides are used in:
a. Pharyngitis, tonsillitis and most respiratory infections caused by
Pneumococci or H. influenza (All).
b. Prophylaxis against rheumatic fever (Eryhthromycin).
c. Atypical pneumonia caused by Mycoplasma pneumoniae (Azithromycin).
d. Corynobacterial diphtheria (Erythromycin with antitoxin).

21
 e. Chlamydia trachomatis infection of the urogenital tract (Azithromycin).
f. Peptic ulcer (Clarithromycin)
Adverse effects
1. GI disturbances: are common (Erythromycin more than others).
2. Cholestatic jaundice: with high doses (most probably due to estolate ester).
3. Hypersensitivity reactions: may be seen.
4. Enzyme inhibitors: with erythromycin and clarithromycin, but not azithromycin
and so drug-interactions are high with them.
IV- Quinolones & Fluoroquinolones
The quinolones are synthetic antimicrobials having a quinolone structure recently
introduced into clinical practice. These are classified as:
1. Quinolone: e.g., Nalidixic acid (Negram)
2. Fluoroquinolones: Floxacin derivatives of quinolones classified into 4 generations
based on antibaterial spectrum:
i- First generation fluoroquinolones:
 More potent than quinolone (about 60 times).
 Active against G-ve organisms including pseudomonas that cause UTI.
 e.g., Norfloxacin (Noroxin) effective in UTI
ii- Second generation fluoroquinolones:
 Wider spectrum than 1st generation (G+ve, G-ve and mycobacteria, and
mycoplasma pneumonia).
 e.g., Ciprofloxacin (Ciprobay, Ciprofar, Cipro) & Ofloxacin (Tarivid)
iii- Third generation: (new fluoroquinolones):
 Wider spectrum than second generation, especially against G +ve Strept.
pneumonia, MRSA and against enterococci.
 e.g., Levofloxacin (Tavanic) Gatifloxacin (TEQUIN)
iv- Fourth generation: The most recent generation:
 The broadest spectrum fluoroquinolones with enhanced activity (G+ve, G-
ve and anerobes).
e.g., Trovafloxacin e.g., Cinfloxacin

Mechanism of action:
These bactericidal agents act by inhibiting topoisomerase II (DNA gyrase) and thus
interfere in DNA rejoining step, replications and finally inhibiting DNA synthesis.
Pharmacokinetics
Given orally, these agents are well absorbed. Aluminium and magnesium antacids
interfere in their absorption. They distribute well into body tissues except the brain.
Elimination is partly by hepatic metabolism and partly by renal excretion.

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Therapeutic uses
Flouroquinolones are used in the following:
1. Acute and recurrent UTIs: norfloxacin.
2. Bacterial prostatitis: norfloxacin, ciprofloxacin.
3. Typhoid carrier: Norfloxacin, ciprofloxacin.
4. Bronchitis caused by H. Influenza: Lomefloxacin.
5. Multi-drug resistant T.B.: Ciprofloxacin.
6. Invasive external otitis caused by P. aeruginosa (Ciprofloxacin).
7. Soft tissue infections (bone and joint infections) as Gram-negative bacillary
osteomyelitis: Ciprofloxacin.
8. Sexually- transmitted disease e.g., Ciprofloxacin and Ofloxacin.
Adverse effects
 Allergy and photosensitivity: skin rashes.
 Chondrolytic effect (Arthropathy) has been reported in young individuals up to 18
years. Rupture tendons were also reported.
 CNS toxicity: Headache, dizziness, and seizures in epileptics.
 Drug interactions: e.g., Ciprofloxacin increases the blood level of theophylline
and can lead to theophylline toxicity.
V- DRUGS USED FOR TUBERCULOSIS
 Tuberculosis is caused by Mycobacterium tuberculosis. For many centuries,
tuberculosis was a major killer disease. About 40-50 years ago, drugs were
developed and it became a curable disease.
 Recently, the problem of T.B. increased again because of Development of
multidrug-resistant T.B. and Increasing immunocompromized patients e.g., HIV.
 Classification of anti T.B.

Figure (1): classification of antimycobacterial agents.

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Fluoroquinolones include: Ciprofloxacin, Ofloxacin
Macrolides include: Clarithromycin, zithromycin,
 The second-line drugs are used when first-line agents cannot be used due to
adverse effects or because organisms are resistant to the first-line drugs.
 To decrease the possibility of resistance development, multidrug therapy
(polytherapy) is used as follows:
 A first phase of about 2 months consisting of three (or four) drugs, used
concomitantly: isoniazid, rifampicin, pyrazinamide (plus ethambutol or
streptomycin if the organism is suspected to be resistant).
 A second phase, continuation phase, of 4 months, consisting of two drugs:
isoniazid and rifampicin. This is the usual short-term or six-month course. Long-
term therapy for immunocompromised patients applied for longer periods (9-12
months).

Figure (2): protocol of short-term treatment of T.B.

ISONIAZID
Mechanism of action:
 It inhibits mycolic acid synthesis (unique to mycobacteria) producing inhibition of
cell wall synthesis. It has Tuberculocidal (in active dividing cells) or
tuberculostatic effect (in non-dividing cells).
Pharmacokinetics:
INH is readily absorbed from the gastrointestinal tract and is widely distributed. It
penetrates well into tuberculous lesions. Metabolism (acetylation) is genetically
determined and may be slow of rapid in different people. Slow acetylators have a
better therapeutic response. INH is excreted in urine, partly unchanged and partly
acetylated.

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 Figure (3) rapid and slow actylators of INH
Therapeutic uses a) Treatment of tuberculosis b) Prophylaxis of
tuberculosis
Adverse effects (dose-dependent):
1. Peripheral neuritis: Common in slow acetylators. INH is structural analogue to
pyridoxine, increasing its excretion with a result of pyridoxine deficiency leading
to parethesiae, numbness of hands & feet. Overcome by giving Vit B6.
2. Hepatitis: Common in rapid acetylators (1 %) because acetylated isoniazid is
responsible for this effect. Drug must be stopped only if liver transaminase
becomes 5 fold higher than normal.
3. Hemolysis: in patients with with G-6-PD.
4. Drug-interactions: INH is an enzyme inhibtor to phenytoin → increasing
phenytoin toxicity (nystagmus & ataxia). Rifampicin and phenytoin are enzyme
inducers to INH → increase INH hepatitis.
RIFAMPICIN
 Rifampicin is a semisynthetic macrocyclic antibiotic drug.
 It is bactericidal for M. tuberculosis, leprosy and many Gram-positive and Gram-
negative bacteria.
 It acts by inhibiting DNA-dependent RNA polymerase that results in inhibition of
RNA synthesis.
Pharmacokinetics: Rifampicin is well absorbed orally and widely distributed. It
gives an orange color to body secretions (saliva, sputum, tears, sweat and urine). It is
metabolized in liver and excreted in bile and urine. It is strong liver microsomal
enzyme inducer. So, it is a substrate for drug-drug interaction.

24
 
Figure (4): Drug interactions with rifampicin
Therapeutic uses:
i. Treatment of T.B. (first line with other drugs)
ii. Treatment of Leprosy
iii. Prophylaxis of meningitis: (600 mg/day orally for 4 days).
iv. Resistant staph. Infections: Combined with vancomycin in endocarditis or
osteomyelitis. Also, it is used in MRSA in patients allergic to beta-lactam
antibiotics combined with Co-timoxazole.
v. Treatment of Brucellosis combined with doxycycline.
Adverse effects
1. Harmless orange red-discoloration of secretions: as urine, saliva, sweat, tears
& sputum.
2. Strong enzyme-inducer (drug interactions): Rifampicin increases the metabolism
of oral anticoagulants, oral hypoglycemics, oral contraceptives, corticosteroids,
digitoxin and so decreasing their effects.
3. Impaired liver function & jaundice (hepatotoxicity).
4. Flu-like syndrome:
• If rifampicin is given intermittently (less than twice weekly) or regularly in a
dose of 1200 mg daily or more.
• Manifested by fever, chills, myalgia, headache, acute tubular necrosis,
thrombocytopenia, haemolytic anaemia or shock.

VI- ANTIFUNGAL DRUGS

Fungal infections are called mycoses and in general can be divided into
A. Superficial Infections infections affecting skin, nails, scalp, mucous membranes.
1. Dermatomycoses: Infections of the skin, hair and nails caused by
dermatophytes e.g., Tinea
2. Candidiasis: Infection of the mucus membrane of the mouth (thrush), vagina,
or skin, by candida albicans.

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 B. Systemic Infections: Affecting internal tissues and organs.
Incidence: Fungal infections increased recently because of:
a. Increased use of broad-spectrum antibiotics, leading to suprainfections.
b. Decreased immunity because of either disease, e.g., AIDS or because of drugs,
e.g., immunosuppressants or anticancer drugs.
DRUGS USED FOR FUNGAL INFECTIONS
Classification (based on clinical uses):
A) Systemic Antifungal Drugs:
i) Amphotericin B* ii) Flucytosine
iii) Griseofulvin iv) Azoles * e.g., ketoconazole
B) Topical Antifungal Drugs:
i) Nystatin ii) Natamycin
iii) Salicylic & benzoic acids iv) Azoles * e.g., Miconazole
* Used in both systemic & topical fungal infections.
1. AMPHOTERICIN B ((Fungizone)
Amphotericin B is a macrolide polyene antibiotic.
Mechanism of action: It binds to the ergosterol in the cell membrane of the fungi
and forms pores in it. This disturbs the permeability and transport function of the
membrane. It may act as fungistatic or fungicidal depending on conc & organisms.
Relative selective toxicity is due to presence of ergosterol only in fungal cell
membranes but cholesterol found in mammalian cell membranes.

Figure (4) mechanism of action of amphotericine

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Pharmacokinetics:
• Poorly absorbed from GIT. So, used orally only for local GIT fungal infections.
• For systemic infections, amphotericin is given I.V.
• Long half- life ’’about 15 days’’ because of strongly binding to plasma proteins
and slow excretion in urine over several days.
• Distributed widely to the body tissues BUTonly 2-3 % of amphotericin blood
levels can reach CSF and so intrathecal administration is needed in fungal
meningitis.
Therapeutic indications:
1. I.V. infusion is the drug of 1st choice in:
a) Most systemic fungal infections.
b) Highly indicated in life-threatening fungal infections (in AIDS & cancer
patients on immunosuppressants).
2. Intrathecal amphotericin B: used in fungal meningitis.
3. Topical amphotericin preparations: used in:
a) In superficial fungal infections.
b) Cutaneous & mucocutaneous fungal infections e.g., oral or vaginal candidiasis.
Adverse effects:
1. Initial febrile reactions: Shivering, chills, fever, wheezing, hypotension with
initial doses. Using steroids & antipyretics is necessary concurrently or before
therapy to control these severe febrile reactions.
2. Nephrotoxicity:
• In over 80 % of patients  irreversible renal damage due to increased intra-
renal vascular resistance resulting in Azotemia & renal failure.
• Hospitalization with close medical supervision.
• Renal function should be monitored.
• Renal failure needs termination of drug therapy.
• Should not be used with nephrotoxic drugs as aminoglycosides & cisplatin.
3. Hypochromic normocytic anemia: due to reduction in hemopoietic growth
factor (erythropoietin) production by the kidney.
4. Hypokalemia: due to distal renal tubular acidosis.
5. Bone marrow suppression: anemia & thrombocytopenia.
6. Thrombophlebitis due to I.V.
7. GI upset: nausea & vomiting at initial therapy.

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 2. Ketoconazole (Nizoral)
Uses:
1. Systemic fungal infections: Single daily dose is useful in systemic fungal
infections. Needs long period of therapy so not preferred against systemic
infections.
2. Topical infections: Lotion, creams and even tablets are used in topical fungal
infections & dandruff. Also, it is effective in oral & oropharyngeal candidiasis. It
is also useful in acute candida vulvovaginitis and tinea in the skin.
3. Hormonal indications: Ketoconazole tablets is useful in androgen-dependent
prostatic cancer & Cushing syndrome because it Inhibits adrenal steroids &
testosterone synthesis.
Adverse effects of ketoconazole
1. Blocking testosterone synthesis  gynecomatia & impotence in male.
2. Blocking steroid synthesis  Cortisone deficiency → allergy & inflammation.
3. GI upset: nausea & vomiting are common.
4. Hepatotoxicity: increased liver enzymes.
Nystatin (Mycostatin)
It is polyene antibiotic.
Mechanism of action: similar to amphotericin B; binds to ergosterol in the cell
membrane  disruption in cell membrane permeability.
Uses: Treatment of topical candidiasis of skin & mucous membranes (Oral
candidiasis (monilia) & vaginitis treated by creams; Intestinal candidiasis &
oropharngyeal treated by oral nystatin. Not used in systemic fungal infections
because it is not absorbed and not reach systemic sites. In addition, it is too toxic for
systemic administration as I.V.

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 HORMONES FOR NURSING
Introduction
Hormones are specific organic substances secreted by the endocrine glands and exert
important physiological functions on various tissues of the body. The endocrine
glands are many including thyroid, parathyroid, adrenals, pancreatic islets, ovaries,
testes, hypothalamus; anterior and posterior pituitary. This chapter will spotlight on
the pharmacology of drugs frequently used in commonly hormonal disorders.
I- INSULIN AND DIABETES MELLITUS
Objectives: By the end of this lecture, students will be able to:
1. Differentiate between different types of diabetes mellitus.
2. Describe the pharmacology of drugs used in diabetes mellitus.
3. Recognize the main adverse effects of antidiabetic drugs and how to overcome.
4. Discuss nursing implications and role of nurse in the management of diabetic
patients.
Diabetes mellitus: Life-long metabolic disorder characterized by hyperglycemia as a
result of absolute or relative lack of insulin or insulin resistance.
Types of diabetes mellitus:
a) Type I diabetes: Formerly known as insulin-dependent diabetes mellitus
(IDDM). It is characterized by absolute deficiency of insulin caused by
massive ß-cell destruction as a result of autoimmune disorders triggered by an
invasion of viruses or the action of chemical toxins. Type I diabetes must be
treated by insulin.
b) Type II diabetes: Formerly known as non-insulin-dependent diabetes mellitus
(NIDDM). It is characterized by insulin resistance, -cells dysfunctions and
common in obese patients. Type II diabetes can be treated by oral antidiabetics
in early stage and insulin in advanced stage.
Management of diabetes mellitus:
A. Non-pharmacological approaches:
1- Patient education and monitoring.
2- Diet (the cornerstone of therapy for all patients)
3- Exercise / physical activity
B. Pharmacological approach:
1- Insulin 2- Oral antidiabetics.
Insulin
 Human insulin is chemically identical to endogenous insulin but it is not derived
from the human pancreas; it is manufactured by biotechnology. On the other hand,
animal insulin obtained from Beef or Pork pancreas; use is obsolete now due to
their antigenic properties and availability of human insulin.
 Insulin administered parenterally because it is destroyed in the GIT.
29
Types of Insulin preparations:
Insulins differ in onset and duration; classified into short, intermediate and long
acting:
a) Short acting insulins:
 e.g., Insulin Lispro (Humalog), Insulin Aspart (Novolog) and Regular
Insulin.
 Onset is 15 min, peaks in 1-2 h and duration is 3-5 h.
 All insulin preparations are given by S.C. injection except regular insulin
which is the only insulin that can be given by I.V. injection in diabetic coma or
diabetic ketoacidosis.
b) Intermediate-acting Insulins:
 e.g., Isophane Insulin suspension (NPH, Humulin N, Novolin N), Lent
Insulin, Neutral Protamine Lispro (NPL).
 Onset is 1-1.5 h, peaks in 8-12 h and duration is 18-24 h.
 Administered by S.C. injection only.
c) Long-acting insulins:
 e.g., Insulin Glargine (Lantus) and Insulin Detemir (Levemr).
 Like the other insulins, they must be given subcutaneously.
 Duration: about 24 h with delayed onset.
Routes of Insulin Administration
Because insulin is a polypeptide, it is degraded in the GIT, if taken orally. Insulin is
generally administered by:
a) Parenteral Injections:
 S.C.: for most preparations and almost all patients
 I.V.: In a hyperglycemic emergency, regular insulin is the only insulin
injected intravenously.
 Usually disposable plastic syringes or pen injection device are used for
injection.
b) Nasal Spray & Inhalation: Under investigational trials.
Indications of Insulins:
1- All cases of Type-I diabetes
2- Advanced cases of Types-II diabetes; after failure of diet regulation plus
exercise plus oral hypoglycemic.
3- Type II diabetes (temporary) during stress periods e.g. infection, surgery or
pregnancy
4- Emergency treatment of diabetic ketoacidosis & hyperglycemic coma
5- Hyperkalaemia due to renal failure.

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Adverse effects of Insulins:
a) Hypoglycemia c) Allergic reactions
b) Lipodystrophy d) Others as seizures and coma

Figure (6): symptoms of hypo-and hyperglycemia.

Oral Antidiabetic Drugs

Classification of Oral Antidiabetics:
1. Insulin Secretagogues ( insulin secretion): e.g., sulphonylureas
2. Insulin sensitizers (sensitivity of cells to insulin): e.g., thiazolidindiones and
biguanides.
3. Inhibitors of glucose absorption from GIT: e.g., acarbose
4. Inhibitors of glucose production by the liver:
– Depeptidyl peptidase inhibitors
– Biguanides.

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 Sulfonylureas:
 The oldest drugs, increase release of insulin from functioning beta islets of
pancreas.
1- First generation: e.g., Tolbutamide: it is not used now.
2- Second generation: Glibenclamide (Daonil), Glipizide (Minidiab), Gliclazide
(Diamicron) and Glyburide (DIABETA, Micronase).
3- Third generation: e.g. Glimepiride (Amaryl)
Notes:
 2nd and 3rd generations are:
o More potent & less toxic than first generation
o Commonly used now because most of them used once daily (3rd
generation) or twice daily (2nd generation).
o Can be used only in type II diabetes either alone or combined with
insulin sensitizers.
Adverse drug reactions:
a) Hypoglycemic reactions: especially with overdosage, elderly patients, hepatic
or renal dysfunctions.
b) Teratogenicity and so, not used in pregnancy.
c) Weight gain: due to appetite stimulant effect.
d) Failure to therapy: secondary (due to beta cells exhaustion). These drugs
produce squeezing effects on beta cells and so exhausted.
Insulin sensitizers: Biguanides & Thiazolidindiones
a) Biguanides:
Metformin (Glucophage):
• It increases the use of glucose by muscle and fat cells, decreases hepatic
glucose production, and decreases intestinal absorption of glucose.
• It does not cause hypoglycemia.
• Metformin may be used alone or in combination.
• Lactic acidosis is the main adverse effect with large dose of metformin.
• Metformin is ontraindicated in liver or renal impairment, therefore, nurse must
check renal function before beginning this medication
b) Glitazones:
Pioglitazone (Actos) and rosiglitazone (Avandia):
• They are insulin sensitizers: decrease insulin resistance, stimulate receptors on
muscle, fat, and liver cells. These effects results in increased uptake of glucose
in periphery and decreased production by the liver.
• May be used as monotherapy or in combination with insulin, metformin
(Glucophage) or a sulfonylurea

32
ADRs:
• Troglitazone  Hepatotoxic  Obsolete.
• Weight gain (↑S.C.fat & Fluid retention)
• Bone fractures
• Hepatic microsomal enzyme induction   Metabolism of contraceptives.
• Contraindicated in patients with liver disease or who have ALT levels > 2.5 of
normal.
Inhibitors of glucose absorption from GIT: e.g., Acarbose
• Acarbose inhibits alpha-glucosidase enzymes (amylase) in GI tract and so
delays absorption of complex CHO and simple sugars.
• Advantages: It does not cause hypoglycemia or weight gain.
• Contraindicated in cirrhosis, malabsorption, severe renal impairment.
New drugs
a) Sitagliptin (Januvia)
• It is an oral anti- diabetic drug.
• Indirectly, it potentiates the secretion of insulin and suppress the release of
glucagon by the pancreas.
b) Sodium Glucose Cotransporter 2 Inhibitors (SGLT-2):
• e.g., Empagliflozin, Dapagliflozin, serglifozin
• These drugs inhibit glucose reabsorption in the proximal tubules of the kidney
and so exert their effects by causing the kidneys to excrete glucose into the
urine. Their effects are independent on insulin availability in pancreas.
Nursing implications:
a) When mixing insulins, nurse should draw up the regular insulin first.
b) Nurse should rotate sites of injection of insulin to avoid development of
lipodystrophy.
c) Absorption of injected insulin in abdomen is not uniform with injections in
arms or legs.
d) Glucose monitoring is highly recommended for diabetic patients because tight
glycemic control can reduce the complications of diabetes.
e) Switch from oral into short acting insulin therapy in diabetics undergoing
surgery.
f) For elective surgery, nurse must schedule patient early to avoid prolonged
fasting.
g) Use ACE inhibitors to delay nephropathy & limit dietary intake of protein
h) Patients on glitazones, nurse must suspect hepatotoxicity and monitor liver
functions.
i) Metformin is used cautiously with liver and renal impairment to avoid lactic
acidosis.
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 j) For patients with diabetic ketoacidosis, management should include:
• IV fluids to rehydrate
• I.V. insulin drip with gradual lowering of blood sugars with potassium
supplementation to avoid hypokalemia.
• Judicious administration of sodium bicarbonate
k) Nurse should be familiar with hypoglycemic reactions (palpitations,
tachycardia, tremors and drowsiness) and warn the patients on insulin therapy
or sulphonylurea from these reactions and teach how to manage.

II. CORTICOSTEROIDS

Figure (7): Site of formation of corticosteroids

A) Glucocorticoids
Adrenal glands: the Inner zone (adrenal medulla) secretes epinephrine &
norepinephrine while the outer zone (adrenal cortex) secretes corticosteroids from
cholesterol. Corticosteroids include glucocorticoids e.g., hydrocrortisone and
mineralcorticoids e.g., aldosterone.
Adrenal Cortex (steroid hormones secreted)
Corticosteroids actions:
• Actions of glucocorticoids e.g., hydrocortisone:
– Powerful, magic, strong anti-inflammatory activity.
– Effects on carbohydrate metabolism (Hyperglycemia & glucosuria), fat
metabolism (abnormal fat redistribution; moon face buffalo hump) and
protein metabolism ( proteins catabolism resulting in osteoporosis and
Muscle wasting).
– Immunosuppressives.
– Antiallergic
– Mineralocorticoidal activity: Na/H2O retention & K loss resulting in
edema, hypokalemia & weight gain.

34
• Mineralcorticosteroids e.g., aldosterone:
– Regulates electrolytes in the body, maintains a normal level of sodium in
the blood; causes sodium reabsorption from urine; blood pressure control;
regulates potassium and PH of the blood.
Therapeutic uses of glucocorticoids:
1) Replacement therapy (small doses):
- In acute primary Addison’s syndrome (Addison crisis) due to destruction of
adrenal glands
- In secondary (chronic) adrenal insufficiency due to structural or functional
lesions of the anterior pituitary or hypothalamus (lacking ACTH).
2) Antiinflammatory uses (large doses): Cerebral edema & encephalitis, arthritis
(osteoarthritis, rheumatoid arthritis & gouty arthritis), autoimmune hepatitis,
bronchial asthma (chronic asthma: inhaler) and status asthmaticus (I.V. steroids) and
ocular inflammation as conjuncitivitis.
3) Immunosuppressive uses (large doses):
a) Autoimmune disease: e.g., SLE (systemic lupus erythematosus), polyarthritis,
rheumatoid arthritis, myasthenia gravis, autoimmune haemolytic anaemia,
psoriasis, multiple sclerosis, interstitial pulmonary fibrosis, etc.
b) Inflammatory bowel syndrome: e.g., ulcerative colitis & crown syndrome.
c) Organ transplantation to prevent rejection.
4) Other uses:
a) Antiallergics: skin allergies (dermatitis) & eye allergies (conjuncitivitis).
b) Anticancer: inhibit cell reproduction and are cytotoxic to lymphocytes
c) Antiemetics in chemotherapy-induced emesis
d) Antishock: anaphylactic shock and bee stings.
e) Hypercalcemia: causes hypocalcemia.
f) Nephrotic syndrome & nephritis (large doses).
Preparations:
Systemic:
 Prednisone (Deltasone) or prednisolone
 Betamethasone (Celeston)
 Dexamethasone (Decadron)
 Methylprednisolone (Solucortef)
Topical: Hydrocortisone
Inhalers: Beclomethasone and fluticasone used in COPD, bronchial asthma or
allergic rhinitis.

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Nursing implications:
1) Nurse should perform a physical assessment to determine baseline weight,
height, vital signs (especially BP), hydration status, immune status.
2) Obtain baseline laboratory studies (blood glucose and CBC).
3) Assess for edema and electrolyte imbalances
4) Sudden stop of steroids after prolonged therapy may be associated with risk of
adrenal insufficiency (Addison syndrome) caused by a sudden drop in serum
levels of cortisone. Therefore, gradual withdrawal is necessary after prolonged
treatment.
5) Nurse should be knowledgeable that patients on steroids for long period
should be treated with anabolics to avoid wasting & osteoporosis.
6) Nurse should advise the patients on inhaler steroids to shake the bottle before
each use.
7) After using an inhaled corticosteroid, instruct patients to rinse their mouths to
prevent possible oral fungal infections.
8) Assess for contraindications to adrenal drugs, especially the presence of peptic
ulcer disease, hypertension and viral infections.
9) Assess for drug allergies and potential drug interactions (prescription and
OTC).
10) Systemic forms may be given by oral, IM, IV, or rectal routes (not SC)
11) Oral forms should be given with food or milk to minimize GI upset
12) Be aware that these drugs may alter serum glucose and electrolyte levels.
13) Clear nasal passages before giving a nasal corticosteroid.
14) Teach patients on corticosteroids to avoid contact with people with infections
and to report any fever, increased weakness, lethargy, or sore throat.
15) Patients should be taught to take all adrenal medications at the same time
every day, usually in the morning, with meals or food.
16) Monitor for adverse drug reactions.
Adverse effects of glucocorticoids:
Unwanted effects occur especially if these drugs are used in high doses and/or for
long time. The adverse effects can be divided into 4 categories:
a. Adverse effects related to immunosuppression (increase infection or injury):
Glucocorticoids suppress the immune response and so infections occur easily and can
be serious. Infections already present in the body, e.g., tuberculosis, can spread.
Wound healing is also impaired. With inhaler steroids, oropharyngeal candidiasis
may be encountered.
b. ADRs due to sudden withdrawal of large doses:
Acute adrenal insufficiency (Addison’s crisis) manifested by anorexia, nausea,
vomiting, malaise, dehydration, hypotension & arthralgia, etc.
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c. Metabolic side effects:
Long-term uses of corticosteroids or using high doses for short time may result in
diabetes mellitus, abnormal fat distribution (moon face, buffalo hump, fat abdomen),
osteoporosis, etc.
d. Other side effects: as hypertension, weight gain, glaucoma, cataract, ulcer,
psychosis, depression etc.
Contraindications (C/I) of glucocorticoids:
A) Absolute C/I:
– Viral conjunctivitis or viral keratitis: Immunosuppressant of
corticosteroids stimulate spreading viral activity  corneal perforation
& iris prolapse.
B) Relative C/I:
– Diabetes Mellitus. - Peptic Ulcer -Osteoporosis
– Psychosis - CHF - HTN
– Acute & chronic infections.
Glucocorticoid antagonists
1. Synthesis inhibitors:
Used in the treatment of Cushing’s syndrome and adrenal carcinoma
Examples: - Aminoglutethimide - Ketoconazole
- Metyrapone - Trilostane
2. Receptor antagonists:
Mifepristone: used in Inoperable patients with ectopic ACTH syndrome.

Figure (8): glucocorticoid antagonists

B) Mineralocorticoids
1. Natural e.g. Aldosteron: acts in collecting tubules of the kidney leading to Na +
/water reabsorption and exchanges of Na + with K + and H + in distal & collecting
tubules producing:
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 – Hypokalemia.
– Metabolic alkalosis
– Edema & hypertension.
2. Synthetic: e.g., Fludrocortisone: Has both glucocorticoid and mineralocorticoid
activity and widely used in adrenal-cortical insufficiency
Side effects: (rare) Headaches, hypertension, dizziness, edema of lower extremities,
tingling, muscle cramps, CHF
Nursing Implications: Monitor electrolytes (baseline then frequently), monitor blood
pressure and weight to assess fluid retention/loss.

Mineralocorticoid receptor antagonists

Spironolactone: It is a competitive antagonist to aldosterone at its receptor.
Uses:
– Primary hyperaldosteronism: as in adenoma of adrenal gland.
– Secondary hyperaldosteronism: as in HF or liver cirrhosis, nephritic
syndrome.
– Heart failure: spironolactone has antiremodeling effect and was found to
reduce morbidity and mortality.
III. FEMALE HORMONES AND CONTRACEPTIVES
Estrogen and progesterone are the endogenous female sex hormones. In addition to
participation in secondary sex character development at puberty in girls, estrogen
have important actions on bone (prevent osteoporosis), cognitive function (balanced
behavior) and regulation of menstrual cycle. Also, female hormones (estrogen either
alone or combined with progestins) are frequently used as contraceptives. In this part
we will discuss the role of female hormones particularly in contraception.
Physiological background:
1- Hypothamus release Gonadotrophin releasing hormones (GnRH)
2- GnRH stimulates anterior pituitary.
3- Anterior pituitary release LH & FSH.
4- Both FSH & LH stimulate gonads to form testosterone, spermatozoa, ova,
estrogen & progesterone.
5- These hormones (testosterone, estrogen & progesterone) when their levels
increased in the blood  their synthesis & secretion are inhibited by negative
feed back mechanism.
A. Estrogens:
Natural estrogen: e.g., estradiol (not effective orally and used topically or
parenterally).
Semisynthetic estrogens: e.g., ethinyl estradiol (Most effective oral estrogen).
Synthetic estrogens: e.g., diethyl stilbosterol (useful orally and parenterally).

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 Therapeutic uses of estrogens:
1- As a hormonal replacement therapy to prevent menopause syndrome,
postmenopausal osteoporosis, senile atrophic vaginitis and also to
correct under-developed female secondary sex characters.
2- Alone or with progestins as hormonal contraceptives.
3- Treatment of amenorrhea: to induce an artificial cycle by withdrawal
bleeding (because abrupt withdrawal of estrogen at the end of an
anovulatory cycle is the cause of menstruation).
4- Treatment of dysmenorrhea & dysfunctional uterine bleeding.
5- To suppress postpartum lactation (low dose estrogen, bromocriptine is
preferred).
Common side effects of estroogens:
1) Nausea and rarely vomiting.
2) Sodium and water retention  edema, weight gain, headache and
nervous tension as well as enlarged tender breast.
3) Intravascular thrombosis.
B. Progesterons:
Natural progesterone: not effective orally due to extensive first pass metabolic
effect and short duration after injection.
Synthetic progestins: resistant to hepatic metabolism, effective orally and long
duration of action. They include: Hydroxyprogesterone caproate (Primolut-dept),
Medroxyprogesterone (provera), Norethisterone (Primolut N), Norgestrel and
levonorgestrel.
Therapeutic uses of progestins:
a. Alone or with estrogens as hormonal contraceptives.
b. Maintenance of pregnancy.
c. Treatment of amenorrhea, dysmenorrhea or dysfunctional uterine
bleeding.
d. Treatment of endometriosis, endometrial carcinoma and premenstrual
tension.
Side effects of progestins:
a. Nausea c) Weight gain,
b. Drowsiness d) Hirsutism and acne
CONTRACEPTION

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1. Hormonal: oral, injectable, S.C. implant and intrauterine device (IUD) loaded
hormones.
2. Chemicals: spermicidal agents (e.g., phenyl mercuric acetate), pessary
(inserted into vagina 30 min before intercourse).
3. Mechanical: male condom, cervical cap and vaginal diaphragm (better
lubricated by spermicidal agents).
4. Intrauterine contraceptive devices “Loop”: T-shaped loops: are
impregnated with barium to render them radiopaque and appear in ultra-
sonography. Two long threads are attached to the loop and extended into the
vagina.
Types of loops:
1- Loops cover by coper (Cooper loop).
2- Loops impregnated with progesterone (loaded loop)
Mechanism of action of loop:
• Histo-biochemical changes in endometrium that decrease implantation of
fertilized ovum in the uterus.
• Increase tubal and uterine motility and so expel ovum.
• Attract macrophages causing phagocytosis of sperms and ovum

.
Figure (9): Loop loaded with medication

5. Physiological methods: safety period

6. Sterilization of male and/or female (vasectomy/ tuber ligation or hysterectomy).
HORMONAL CONTRACEPTION
Injectable contraceptives:
1- Progesterons: Medroxyprogesterone acetate (Depo-provera) I.M./3 months.
ADRs: Irregular bleeding or amenorrhea (may cause permanent infertility).
2- Estrogen + Progestin: Estradiol + Norethisterone (Mesigyna) I.M./month.
More effective than progestins alone but affecting lactation as a side effect
(due to estrogen).
S.C. Implant: Levo-norgestrel (Norplant). It is effective over several years and does
not affect lactation.

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Oral contraceptives:
 Natural hormones are ineffective orally “due to extensive hepatic first pass
metabolism”, therefore, synthetic preparations are used as oral contraceptives.
 Four major types of oral contraceptives including:
A: Combination oral contraceptives B: Sequential pills
C: Minipills (small dose of progestin alone)
D: Post-coital or morning after pills.
A: Combination oral contraceptive pills:
 Every pill contains estrogen + progestin.
 It starts by the 5th day of the menses for 21 days, then rest for 7 days or take iron
during this week.
 COCs are subdivided into 3subtypes:
1- Monophasic pills:
 Each pill contains the same amount of estrogen and progestin.
 According to the amount of estrogen or progestin, subdivided into three types:
a) High dose estrogen (0.5 mg ethinyl estradiol) + High dose progestin (0.5 mg
Norgestrel (Primovlar). High dose estrogen may cause nausea, edema and
thrombosis. Efficacy 100 %. Forgetting one pill can be compensated by taking
two pills next night but not loose protection.
b) Low dose estrogen (0.03 mg ethinyl estradiol) + Low dose progestin (0.15
mg levonorgestrel (Microvlar). Efficacy 100 %. Low estrogen make the drug
with less side effect. Forgetting one pill loss protection.
c) Low dose estrogen (0.03 mg ethinyl estradiol) + high dose progestin (1. 5
mg Norethindrone (Loestrin). Low dose estrogen renders the drug to be with
less side effects but the efficacy is 100 %. High dose progestin make the drug
with less spotting and break through bleeding. Forgetting one pill loss
protection.
2- Biphasic pills.
 Days 1-10: Ethiyl estradiol (0.035 mg) + Norethindrone (0.5 mg)
 Days 11-21: Ethiyl estradiol (0.035 mg) + Norethindrone (1.0 mg)
Advantages:
 Less estrogen with side effects.
 Increasing progestin less spotting or break through bleeding.
3- Triphasic pills (Triovlar):
 First 6 days (brown pills) contain low estrogen (ethinyl estradiol 30 ug + low
progestin (levonorgestrel 50 ug).
 Then 5 days (white pills) contain estrogen 40 ug + more progestin 75 ug
 Then 10 days yellow pills contain less estrogen (30 ug) + still more progestin.

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 Advantages:
- Low estrogen less side effects.
- Increasing progestins to reduce spotting and break through bleeding.
B) Sequential pills:
- Start by estrogen alone for 15 days, then combination of estrogen + progestin for
one 6 days.
- Resemble physiological changes but success rate not more than 98 %.
C) Minipills:
- Small dose of progestin alone e.g., 30 ug levonorgestrel or 350 ug norethindrone.
- Pills are taken every day without interruption.
Advantages:
- No estrogen and so almost with no side effects.
- Does not inhibit lactation (preferred for lactating mother).
- Does not inhibit ovulation (success rate about 97 %)
D) Post-coital pills or Morning-After pills:
- They are used rarely (after rape) and start therapy within 72 h after rape.
- Large dose of estrogen only as diethyl stilbosterol (25 mg) BID for 5 days.
- Or large dose of progestin only
- Or large dose of ethinyl estradiol (100 ug) + Norgestrel (1 mg) two doses in 12 h.
Mechanism of action of hormonal contraception:
Combination of estrogen and progesterone inhibit ovulation
Action of estrogen:
i. Estrogen exert a –ve feedback on the release of LH and FSH by pituitary gland
ii. FSH   Follicle growth   ovulation.
iii. In post coital pills, large dose increase motility of oviduct and decrease
fertilization and implantation.
Action of progestins:
• Withdrawal of the progestin stimulates menstrual bleeding during free week.
• Decrease LH secretion and so reduce ovulation.
• Increase thickness of cervical mucus and so decrease penetration of sperms.
• Alteration of the movement and secretions of the fallopian tubes
• Very large dose of progestin causes atrophy in both ovary and endometrium.

Figure (10): Contraceptives and pituitary gland

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Adverse effects of hormonal contraceptives:
Most adverse effects are due to estrogen.
1. CNS side effects :
• Migraine headache - irritability
• Loss of Libido - Depression.
2. CVS side effects:
• Thromboembolic disorders and DVT
• Fluid retention, edema, weight gain and hypertension.
3. Endocrinal side effects:
• Hyperglycemia
• Uterine bleeding:
o Spotting (minimal bleeding during pill treatment)
o Break-through bleeding (Menstruation during pill)
• Amenorrhea: treated by stopping pills and taking antiestrogen.
• Inhibition of lactation
• Enlarged tender breast
4. Production of tumors:
 High dose oestrogen may cause vaginal, uterine, and breast carcinomas
5. GIT side effects:
 Nausea, dizziness, vomiting
Contraindications - never give oral contraceptives to:
1. Women with previous history of thromboemolic disorders
2. Women with previous history of cardio vascular disorders
3. Uncontrolled hypertensive female.
4. Patients with malignancy of the breast/genital tract
Nursing implications:
• Do NOT massage site after injection with depo provera. It can accelerate
absorption, and shorten period of effectiveness.
• Contraceptives increases the risk for osteoporosis and so calcium intake is
necessary in addition to vitamin D intake and weight-bearing exercise.
• Nurse should be alert with contraindications and cautions of hormonal
contraceptives as: woman with history of: a) Thrombophlebitis and
thromboembolic disorders, b) Cerebrovascular or Cardiovascular diseases, c)
Estrogen-dependent cancer or Breast cancer, d) Benign or malignant liver
tumors, e) Hypertension, Diabetes with vascular involvement.
• The nurse should teach the breastfeeding woman it is BEST to avoid estrogen-
containing contraceptive pills and use either IUD or male contraceptives.

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 IV- THYROID HORMONES AND ANTITHYROIDS

• Thyroid glands secretes three hormones essential for proper regulation of

metabolism
 Thyroxine (T4)
 Triiodothyronine (T3)
 Calcitonin
Thyroid disorders:
A- Hypothyroidism: Deficiency in thyroid hormones.
 Primary: abnormality in the thyroid gland itself
 Secondary: results when the pituitary gland is dysfunctional and does not
secrete TSH
 Tertiary: results when the hypothalamus gland does not secrete TRH, which
stimulates the release of TSH

Forms of hypothyroidism:
Cretinism: Hyposecretion of thyroid hormone during youth leads to cretinism
characterized by low metabolic rate, retarded growth and sexual development,
possibly mental retardation.
Myxedema: Hyposecretion of thyroid hormone during adulthood characterized by
decreased metabolic rate, loss of mental and physical activity, weight gain, loss of
hair, firm edema, yellow dullness of the skin.
Goiter: Enlargement of the thyroid gland results from overstimulation by elevated
levels of TSH; TSH is elevated because there is little or no thyroid hormone in
circulation.

Figure (11): Goiter

Thyroid Preparations:
• Levothyroxine (Levothyroidl): Synthetic thyroid hormone T4
• Liothyronine (Cytomel): Synthetic thyroid hormone T3
• Liotrix (Thyrolar): Synthetic thyroid hormone T3-T4 combined
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Management of hypothyroidism:
• Thyroid preparations are used to treat all three forms of hypothyroidism.
• Levothyroxine is the preferred drug because its hormonal content is
standardized; therefore, its effect is predictable.
• Also, thyroid preparations are used for thyroid replacement in patients whose
thyroid glands have been surgically removed or destroyed by radioactive
iodine in the treatment of thyroid cancer or hyperthyroidism.
Adverse effects of thyroid hormones:
• Cardiac dysrhythmia is the most significant adverse effect.
• Tachycardia, palpitations, angina, hypertension, insomnia, tremors,
headache, anxiety, weight loss, appetite suppression, heat intolerance may
encountered by the patients using levothyroxine for long time.
B- Hyperthyroidism: Excessive thyroid hormones and caused by several diseases:
a. Graves’ disease Plummer’s disease (toxic nodular disease)
b. Multinodular disease Thyroid storm (induced by stress or
infection)

Figure (): Diffuse thyroid goiter

Figure (12): Symptoms of hyperthyroidism

45
Treatment of Hyperthyroidism:
• Antithyroid drugs
• I131 ( radioactive iodine) to destroy the thyroid tissue
• Iodine preparations.
• Surgical subtotal thyroidectomy
1. Antithyroid Drugs:
Thionamides:
• Propylthiouracil (PTU) P.O.
• Methimazole (tapazole) P.O.
Actions:
• Impair synthesis of T3 and T4 in the thyroid gland
• Initial treatment of choice before irradiation or throidectomy
• Effects delayed several weeks until stores of T3 and T4 are
depleted
Uses/ADRs:
• Used to palliate hyperthyroidism and to prevent the surge in thyroid hormones
that occurs after the surgical treatment or during radioactive iodine treatment for
hyperthyroidism
• May cause liver and bone marrow toxicity.
2. Iodine and Iodide therapy:
K+ iodide, Lugol’s iodine: ↓ size and vascularity of thyroid gland
Uses:
 Rarely used as monotherapy (Response ↓ with time)
 In thyroid storm (K+ iodide)
 Before thyroidectomy (lugol’s): to ↓ size, vascularity of the gland
Adverse effects:
Sore mouth and throat, rashes, ulcerations of mucus membrane, metallic taste
Radioactive Iodide (I-131 (P.O.)
Destroys small amount of thyroid tissue.
Uses
1. Patients unresponsive to antithyroid medication (over 30 years age).
Side Effects:
2. Soreness in neck/pain swallowing, increase amount causes increase side effects.
Nausea, vomiting, thin hair, bone marrow depression. Symptoms of
hypothyroidism – patient will usually need replacement treatment.
Thyroid storm’s management:
 Beta blockers :without sympathomimetics activity (propranolol), control
cardiovascular symptoms and prevent conversion of T4 to T3
 If BB is contraindicated diltiazem can be used
46
 K+ iodide to inhibit release of thyroid hormones
 Propylthiouracil: High-dose propylthiouracil (PTU) is preferred because of its
early onset of action and capacity to inhibit peripheral conversion of T4 to T3
Nursing implications for thyroid drugs:
A- For hypothyoid patients:
a. Assess for drug allergies, contraindications, potential drug interactions
b. Obtain baseline vital signs, weight
c. Cautious use advised for those with cardiac disease, hypertension, palpitation
and pregnant women.
d. During pregnancy, treatment for hypothyroidism should continue
e. Fetal growth may be retarded if maternal hypothyroidism is untreated during
pregnancy
f. Adjust dosage every 4 weeks to keep TSH at the lower end of the normal
range.
g. Teach patient to take thyroid drugs once daily in the morning to decrease the
likelihood of insomnia if taken later in the day.
h. Teach patient to take the medications at the same time every day and not to
switch brands without physician approval.
i. Teach patients to report any unusual symptoms, chest pain, or heart
palpitations.
j. Teach patients not to take OTC medications without physician approval.
k. Teach patients that therapeutic effects may take several months to occur.
B- For antithyroid drugs:
a. Better tolerated when given with food.
b. Give at the same time each day to maintain consistent blood levels.
c. Never stop these medications abruptly.
d. Avoid eating foods high in iodine (seafood, soy sauce, tofu, and iodized salt).
e. Monitor for therapeutic response
f. Monitor for adverse effects

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