Last zatchot/ Bacteria - viruses - fungai - Plasmudium

Question 1

Explain Classification of Antibiotics drugs ( Cell water inhibitors) , penicillin’s mechanism of action , resistance of Penicillin, pharmacokinetics

Answer 1

—Classification of Cell wall inhibitors
1-Penicillin
2-Cephalosporin
3-Monobactams
4-Carbapenems
5-Glycopeotides

— Penicillin mechanism :
The mechanism is for all penicillins groups is the same , Penicillin bind to (PBP - Penicillin binding protein ) on the bacterial cell wall and inhibits the transpeptidse enzyme which is inhibite the transpeptades reaction , which is synthesis the walls of the cell , then it’s activates the autolytic enzyme called autolysin leading to cell rapture which is result of of cell wall inhibition and autolysis
-NB! The penicillin mechanism requires proliferation microorganisms, have no effect of bacteria that not dividing
—Penicillin resistant:
Enzymatic hydrolysis of the beta-lactam ring results in loss
of antibacterial activity. The formation of beta-lactamases
(penicillinases) by most staphylococci and many Gram-negative
organisms is a major mechanism of bacterial resistance. Inhibitors of these bacterial enzymes (eg, clavulanic acid, sulbactam, tazobactam) are often used in combination with penicillins to prevent their inactivation. Structural change in target PBPs is another mechanism of resistance and is responsible for methicillin resistance in staphylococci and for resistance to penicillin G in pneumococci (eg, PRSP, penicillin resistant Streptococcus pneumoniae)
and enterococci. In some Gram-negative rods (eg, Pseudomonas
aeruginosa), changes in the porin structures in the outer cell wall membrane may contribute to resistance by impeding access of penicillins to PBPs
1-MRSA ( methilin resistant staphylococcus aureus )
2-Some E-Coli
3-Psudomons
4-some streptococci
—- Penicillin Pharmacokinetics:
-Some penicillin should be Givin :
IV , IM , orally
-distribution: penicillin normally is non-ionised but once it reach the blood PH 7,47 become ionised and can’t pass BBB except in case which is meningitis due to tight junction gets dilated duo to inflammation so the Penicillin can reach the BBB
- penicillin can cross placenta but its not tetroginc bcs the fetal tissue has no Transpeptidase enzyme / PBP
-Excretion : mostly renal

Question 2

classification of Penicillin drugs

Answer 2

-Natural :
1- Benzylpenicillin ( Penicillin G) short acting -Parenteral
2-Phenoxymethylpenicillin
(penicillin V) Orally - Short acting
3-Benzathine BenzylPencillin ( long acting per 7d - IM)
-Semi - Synthetic :
1-Anti Staphylococci Penicillin: Oxacilln
2-Extended Spectrum Penicillin:
Ampicillin - Amoxicillin
3-Antipsudomonal Pencillin :
Piperacillin , Ticarcillin

Question 3

Explain BenzylPenicillin , Spectrum , list of bacteria , disadvantage

Answer 3

-Drug : Benzylpenicillin amp 1mlion ED
-Its the original Penicillin
-Spectrum : Narrow spectrum duo to targeting few Gram + bacteria only such as :
1-Streptococci
2-P.Coccai
3-Some staphylococci which is not producing B-Lactamse
4-Gono coccai : Gonnoria : Gram-
5-Treponin pellidum ( Sophylis) gram-
-disadvantage:
1-Cant be orally bcs HCL
2-Half life 2-4h ( shorty acting )
3- B-lactamse enzyme sensitivity
4-Narrow spectrum

Question 4

Explain Phenoxymethylpenicillin ( Penicillin V) , Benzathine Benzylpenicillin ,Anti-Staphylococcal, Drug , spectrum, resistance,

Answer 4

-Drug : Phenoxymethylpenicillin Tab0.25 Penicillin V
-Its the same as Penicillin G , But its acid stable , Also short acting , and narrow spectrum
———————————
-Drug : Benzathine Benzylpenicillin
-Its the same as penicillin G but with modification which makes it last longer 7-14 days
- its most used in prophylaxis and treatment of syphalis during pregnancy
——————————-
-,Anti-Staphylococcal,
-Drug : Oxacillin Tab/Amp 0,25/0,5
-they are effective against B-Lacatmes producing Staphylococci , But they have no effect or low activity against
other Gram- and Gram+ bacteria: Narrow spectrum .
-They most used against MRSA only

Question 5

Explain Extended Spectrum penicillin , antibiotic drugs , B-Lcatamse inhibitors drugs , Spectrum, List of bacteria , ROA , resistance, Combination with B-Lcatamse inhibitors, , mechanism of Gram- , difference between Ampicillin and Amoxicillin

Answer 5

-Antibiotic drugs : , B-Lctms inhbt
1-Ampicillin + Sulbactam Amp 0,5/0,25
2-Amoxicillin + Clavulanic Acid Tab 0,25/0,6
-Spectrum : they are narrow/moderate spectrum duo to coverage of G+,G- Such as :
1-Slamonila
2-H.influenza
3-Protus
4-Shigella
-ROA : they are acid stable so they can be orally
-resistant: they are sensitive to B-Lactamse , and thats why we give them in combination with B-Lactamse inhibitors
-Mechanism of acting on Gram- :
The ampicillin/Amoxicillin have NH2 group : Amino acid,so it can pass the pores of the outer membrane as nutrients, and destroy the Cell wall and activate Autolysin
———————————
-Ampicillin:
1-oral absorption: +
2-distribution :+
3-Diarrhoea : +++ bcs its not absorbed 100% so it kills the bacteria in the GI
4-Spectrum : shigella , H.influenza
———
Amoxicillin :
1-oral absorption: ++
2-distribution :++ more in lung
3-Diarrhoea :+
4-Spectrum : Salmonila/typhoid fever ,
H,Pylori , Streptococcus pneumonia

Question 6

Explain Anti-Pesudmonal penicillin, Drugs , spectrum, resistance

Answer 6

-Drugs :
1-piperacillin , Ticarcillin Amp
-Spectrum: they are targeting pseudomonal (Mainly) , Also G+ and G- also anaerobic bacteria, so they are broad spectrum
-resistant: they are B-Lactamase sensitive thats why we should combine it with Sulbactam ( b lactamse inhibitor )

Question 7

What are the uses of Penicillin

Answer 7

1-Streptococcal infection: wound spesis , tonsillitis, sub endocrdaitis
2-P.Coccoi : pneumonia
3-Syphalis , Gonnoria
4-Minigialcoccai : meningitis
5-Typhoid fever
6-Pesudomons
7-Actinomycosis ,Anthrax , H.Influenza

Question 8

Explain side effect of penicillin and drug interactions

Answer 8

—Side effect :
1-Allergic reaction : it occurs with all types of penicillin, and its not duo to penicillin it self but to degradation products common to all penicillin it more commonly in parental

2-Diarrhea: disruption of the balance of intestinal
microorganisms. It occurs to a greater extent with those
agents that are incompletely absorbed and have an
extended antibacterial spectrum. Pseudomembranous
colitis from Clostridium difficile may occur with penicillin use
3-Nephritis
4–Neurotoxicity: The penicillins can provoke seizures if injectedintrathecally or if very high blood levels. Epileptic patients are particularly at risk due to the ability of penicillins to cause GABAergic inhibition
– Drug intractions :
1-bactriostatics : bcs the penicillin need prolofration to act
2-Anti-pesudomonal with aminoglycosides : bcs they are diffreant in charge puting them in one syrngist they will make complex and antagonise each other

Question 9

Explain the cephalosporin, structure,generation,,Pharmacokinetics,

Answer 9

-Cephalosporin Also a B-lactamse ring have similar mechanism of action As penicillin
-Each newer generation increasingly resistant to B-Lactamse .
-Pharmacoinatic :
-Distribution:They are widely distributed,But 3rd ,4th,5th generation can Penetrate CSF
-Ceftriaxone 3rd gen , are mainly excreted by bile

Question 10

Explain 1st-5th generation of Cephalosporin, Spectrum,Resistance,BBB,allergy

Answer 10

1St Gen
-Drugs :
1-Cefazolin amp 0.5 2-Cefalexine tab
-Spectrum: narrow spectrum, duo to covering G+ same as Penicillin G with some G- ( E coli klebsiella )
-resistant: Sensitive to B-Lactamse
-BBB : Dont pass
-Allergy : Cross allergy with Penicillin
—————————–
2nd Gen
-Drugs : Cefuroxime Tab/Amp
-Spectrum : Covering G+ and some G- such as ( H.Influenza,Neaseria , Proteus ) but not Pesudomons , Narrow spectrum
-Resistant : Reletavly resistant to B-Lactamse
-BBB: only Cefuroxime Can pss
-Allergy : Cross allergy with penicillin
————————————–
3rd Gen
-Drugs :
1-Oral :
-Cefixime
-Ceftibutene
2-Parenteral :
-Cefotaxime
-Ceftriaxone
-Ceftazidime
—Spectrum: mainly Gram- and also a few of Gram+ ,Also active aginst psudomonas , And anaerobic , Moderate spectrum
-Resistant: Resistant to B-Lactramse
-BBB : Pass BBB
-Allergy: No cross allergy with Penicillin
————————————————-
4th Gen
-Drugs : Cefepime Amp 0.5
—Spectrum: Coverse G+,G- , Pusdomonas , Also anaerobic , Broad spectrum
-Resistant: highly resistant to B-Lactamse
-BBB : Pass BBB
-Allergy: No cross allergy with Penicillin
————————————————————
5th Gen
-Drugs : Ceftaroline Amp 0.5
—Spectrum: Coverse G+,G- , Pusdomonas , Also anaerobic ,MRSA, Broad spectrum
-Resistant: highly resistant to B-Lactamse
-BBB : Pass BBB
-Allergy: No cross allergy with Penicillin
————————————————————

Question 11

mechansim of resistance for cephalosporins

Answer 11

Structural differences from penicillins render cephalosporins
less susceptible to penicillinases produced by staphylococci, but many bacteria are resistant through the production of other betalactamases that can inactivate cephalosporins. Resistance can also result from decreases in membrane permeability to cephalosporins and from changes in PBPs. Methicillin-resistant staphylococci are also resistant to cephalosporins.

Question 12

Uses of Cephalosporin + Side effect

Answer 12

-Most urgent :
1-Meningitis -ve
2-Osteomyelitis
3-Skin infection
4-Typhoid fever
5- UTI : E-Coli -Ve
6-Rsp infection
7-Gannoria
8-ENT
9-intestinal infection
10-Topical
——————————————————-
-Side effect :
1-Nephrotoxince : Most of them is 1gen
-VIP-2-Disulferam like action : normally alcohol > Acetyldhayed > Co2 and H2o, by the help of Aldahyed dehydrogenase , so these drugs inhibit aldehyide dehydrogenase which results of bad mood and nause and vomiting is also ( Drug interaction)
-VIP-3-Prothrombin : 3rd generation inhibt the enzyme Vit k exopidese lead to hypoprothrombinemia

Question 13

Explain Monobactams , Drug , structure , Spectrum, Allergy

Answer 13

-Drug : Aztreonam amp 0.5
-Structure : B-lactam ring similar to Penicillin
-Spectrum: Narrow spectrum, Only Gram-
-resistant: highly resistant
-Allergy: no allergy at all

Question 14

Explain Carbapenems,Drugs ,Structure , spectrum , resistance , Side effect ,

Answer 14

-Drugs :
1-imipenem/Cilastatin Amp 0,5
2-Ertapenem 0,5 amp
-Structure : uniq changes in the structure, Containing B-Lcatamse ring
-Spectrum: broad spectrum duo to :
1-Gram +
2-Gram -
3-Pusdomonas
4-Anearobic
—Resistant : highly resistant
-Side effect : the imipenem alome cause nephrotoxcicty from its products by enzyme Dyhdryopeptedase , So we administered with Cilastatin inhibits the renal dyhdryopeptadese to prevent formation of toxic formation
-Etrapenem : its without this effect so administered alone

Question 15

Explain glycopeptides ,Drug , mechanism,spectrum,Pharmcokintics ,side effects uses

Answer 15

-Drug : Vancomycin Amp 0,5 iVI
-mechanism: inhibits cell wall synthesis by binding to D-Ala-D-Ala terminal of growing peptide chain during cell wall synthesis resulting inhibitions of the transpeptdese reaction , Prevent further elongation and cross - linking of peptidoglycan
-Spectrum : narrow spectrum duo to :
Only gram + such as :
1-Staphylococci MRSA
2-P.Cocci
3-Entra cocci
4-Anearobic infeaction
-Pharmcokintics:
1-Not absorbed orally
2-Not metabolise in liver
3-Execreted by kidney
-Side effect :
1-Red man syndrome: Histamine reales
2-Nephrotoxcicty
3-Ototoxicity
4-Vein thromphlitis
—Uses :
1-MRSA
2-Culstrirudum diffucel colitis

Question 16

classification of protines synthisis antibiotics

Answer 16

a) Antibiotics targeting the 50S ribosomal subunit
macrolides
lincosamides
chloramphenicol
б) Antibiotics targeting the 30S ribosomal subunit
aminoglycosides
tetracyclines

Question 17

Explain The Proteins synthesis Inhibitors ( Aminoglycosieds ) Drugs , chemistry , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 17

-Drugs :
1-Streptomycin Pwdr 1st gen
2-Gentamicin amp 2gen
3-Amikacin pwdr 3 gen ( synthetic drug)
-Chemistry : Consists of NH2+ amino group and glycoside : sugar , And hydroxyle group which is mean ita water sulable
-Pharmacokinetics:
1-Absorption: not orally duo to inozed charge
2-Distribution:
2-1 Not Pass BBB , but pass placenta and its tetaroginic , breast milk Pass ( and its not tetarogenic ) bcs its not absorbed orally
3-Metabolism: in liver
4-Excretion : kidney, high concentration and unchanged and increases alkalinity of urine , Normally Ph of urine is 5.8 so the drug are more used in alklain urine which is needed to treat UTI
—Mechanism of action :
-its inhibit the protein synthesis by binding irriverasbly in the 30s subunit ribosome , which lead to error in the mRNA reaching and formation of functional abnormal proteins
-In details it consists of 3 phases :
1-Attachment: which the amino group NH2+ have positive charge , there will be attraction (Electrostatic Attraction ) bcs the outer membrane of the gram - its consist of negative charge
2-open pores : the outer membrane pores will open only incase of needed of nutrients and the aminoglycosides are similar to the nutrients so the pores will open and the drug molecules will enter
3-irreversible bond : once the drug reached the nucleus there is the ribosomes 30s subunit and it will bind to it irreversibly and inhibit mRNA translation
-Spectrum: they are bactriocidal ( broad spectrum shifted towards Gram -) duo to :
1-Mainly gram - : Entrobactria , Pusdomonas (2gen ,3gen ) , mycobacteria ( 1gen , amikacin )
2- few gram + : staphylococcus
3-TB
-Resistant:
1-P,Coccai
2- Anearobic and intercellular pathogen such as. (Calm my leg )
3-Cant be used for acquired
resp infection
-Uses :
1-Gram - infection: E coli UTI
3-Resp infection
4-Gram - spetecymi
5-TB : Streptomycin , Amikacin
-Side effect :
1-Neohrotoxcity : duo to exacration of this drug in renal , and bcs has + charge and can bind to Kidneys proteins
-VIP-2-Nerve toxicity 8th cranial : the molecule of this drug enters the inner ear and cause toxicity to the 8th cranial nerve ( vitebular and auditory ) and cause deafness duo to accumulate in the endolymph of the inner ear
-VIP-3-NMB : muscle weakness, we can reverse it with Neostagmine
—Dosage : 5mg per kg and its concentration killing dependent

Question 18

Explain The Proteins synthesis Inhibitors ( tetracycline) Drugs , chemistry , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 18

-Drugs :
1-Tetracycline Tab
2-Doxycycline tab/pwder
—Chemistry : there MW less then 500 , and they consist of hydroxyl group which is mean they are water sulable
-Pharmcokintics:
1-Absorpation : incomplete duo to water sulablety , food decrease teh absorption and they are make complex with the metals ( doxycycline is more absorbed)
2-Distribution:
2.1 BBB : not pass
2.2 Placenta / breast milk :pass and its teratogenic
2.3 body fluids :reach
3-metabolism: liver , and exctinssive metabolism , duo to entrohepato circulation
4-Execration : mainly kidney , but they cant Treat UTI duo to extansive metabolism in liver and the drug becomes inactive , but doxycycline’s 50% renal and 50% bilary which can use with patient with renal impairment, but in the same time they are hepatotoxic duo to entroheptaic circulation
-mechanism of action :they are binding reversiblly to 30s subunyand inhibiting the binding of Aminoacyl-tRNA to The Aminoacyl-Centre which is lead to disrupting the early stage of translocation-imitation
-spectrum: broad spectrum/ bacteriostatic
1-most G+ but not Staph
2-most G- but not pausdomonas
3-most of Anearobic bacteria ( CL difesil )
4-Atypical organisms ( Calm my leg ) + borrlia , Reckissia , Coxilla
5-Protozoa : malaria , Toxoplasma ( bind to 40s )
-Resistant: Cross resistant easily and rapid
-uses :
1-Sexual transmitted infections : in patients who has tolerance to B lactamse
2-Pneumophil ( Ligunla )
3-peptic ulcer
4-dangerous infection; Plague , cholera , Antha
4-Zoomases ( loptosorosis , bracellosis )
5-Intracellular pathogens: such as lyma disease, Ricksosis , Q fever )
6-Acne
-Advera effect :
1-GIT upset
-VIP-2-teeth and bone : ditrubunce of skeleton formation deposition in bone and teeth leading leading to ( Colouring the enamel in yellow-Brown color )
-VIP-3-Cholistatic hepatitis: liver cell injury, hepatotoxic, Hypertophy of the hepatocyte
-VIP-4-Photosensitivity
-C.I :
1-Allergies from tetracycline
2-Children under 8 years
3-Pregnancy
4-Liver impairment

Question 19

Explain The Proteins synthesis Inhibitors ( macrolides ) Drugs , chemistry , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 19

-Drugs :
1-Erythromycin tab/pwdr 1gen
2-Clarithromycin tab/pwdr 2gen
3-Azithromycin tab 2gen
—Chemistry : consists of macrolacton ring , and sugar and its MW more then 500
-Pharmcokintics:
1-Absorpation : poor and deceased by food
2-Distribution:
2.1 BBB : not pass
2.2 Placenta / breast milk : pass and they are not teratogenic
2.3 body fluids : they reach most body fluids with good concentration ( they have selective distribution to neutrophils and phagocytes
3-metabolism: in liver
4-Execration : they are execrated through liver billary and entrohepatic circulation, thats why they are heptao toxic,
-NB! 1gen is not stable in acid stomach so low bioavailability and short half life , 2nd generation is the opposite
-mechanism of action : they bind reversible to 50s subunits of the ribosomes and inhibit peptide transferase , and inhibit elongation of proteins, which block the translocation of ribosomes to the next Codon on the mRNA
-Spectrum: Bacteriostatic / Concentration dependent, Spectrum:
1-Mainly G +
2-Intercellular pathogens: Calm my leg
3-H.Pylori : Clarithromycin
-Resistant: in the case id macrolides the bacteria becomes resistant in approximately 10 days by changing the 50s binding site
-uses :
1- Gram +
2-Atypical organisms
3-otaits media
4-sinuses
-Advera effect :
1-GIT upset
-VIP-2-Cholistatic hepatitis: duo to accumulation in liver entrohepatic circulation, inhibitory of CYP450
-VIP-3- Ototoxcity
-VIP-4-Prolongation of QT interval : which could cause a ventricular arrhythmia
-C.I : combination of macrolides and penicillins

Question 20

Explain The Proteins synthesis Inhibitors ( Lincosamides ) Drugs , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 20

-Drugs :
1-Lincomycin Tab/amp ( prototype)
2-Clindamycin tab/amp (synthetic drug )
-Pharmcokintics:
1-Absorpation : complete
2-Distribution:
2.1 BBB : yes / Can treat CNSI
2.2 Placenta / breast milk :pass but mo teratogenic
2.3 body fluids :reach , and has selective distribution on bone and joints ( osteomyelitis)
3-metabolism: liver
4-Execration : through bile
-mechanism of action : its bind in the same site of microlieds in the 50s subunits and inhibits piptiedly transferase which is lead to decrease peptide elongation
-spectrum: bacteriostatic
1-gram + Aerobic bacteria : strepto , stephy , P.cocci
2-gram - Anearobic
3-Protosa : malria , Toxoplasma
-Resistant: easy and rapid and if the bacteria get resistant from macrolids it will be resistant to lincosamides also
-uses :
-VIP-1-Dental infection: because most of oral infections its Anearobic bacteria and duo to selectively bone and joints
-VIP-2-Osteomyelitis
-VIP-3-Toxic shock syndrome : such as staphylococcus produce Exotoxins, we cant use bactriocidal bcs it will spread the Exotoxins
-Advera effect :
1-Clostridium defissil

Question 21

Explain The Proteins synthesis Inhibitors ( chloramphenicol ) Drugs , chemistry , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 21

-Drugs :
1-Chloramphenicol
—Chemistry :consist of OH group which mean its very lipid suable, also its MW its less then 500 , Consist of 2 Molecules of Chloride which increase the activity against bacteria and increase toxicity
-Pharmcokintics:
1-Absorpation : Complete and the food doesn’t effect
2-Distribution:
2.1 BBB : Pass and can treat CNSI
2.2 Placenta / breast milk :pass and teratogenic ( gray beby syndrome)
2.3 body fluids :reach with high concentrations
3-metabolism: in liver by Glucronic transferase , Cant be given to child under 2 years bcs unwill development of Glucrinc transferase enzyme
4-Execration : bilary 90%
-mechanism of action :bind to 50s subunit and inhibit peptidyl transferase enzymes and decrease peptides elongation
-Resistant: cross resistant duo to modifications or blocking proteins which synthesis by bacteria in the binding site or by synthesis of CAT ( Chloramphenicol acetyl transferase ) and bind to the drug which change its structure and cannot bind to the binding site of the ribosomes 50s
-spectrum: bactriostatic ( Braod spectrum)
1-Gram +
2-Gram -
3-Anaerobic bacteria
4-Atypical organisms: calm my leg , BCR
-uses : its only used as 3rd choice
1-atypical organisms
2-typhoid fever
3-meningitis
-Advera effect :
-VIP-1-BM suppression :sever irreversible ( Aplastic anaemia : complete BM failure)
-VIP-2-grey baby syndrome : duo to immaturity of glucronic transferase and the first 2-4 weeks of life and , also functional immaturity of renal tubules impaired execration
-VIP-3-Dermatitis
4-Neurotoxicity : Paychosis , prephrial neuropathy
-C.I :

Question 22

Explain The DNA-RNA Inhibitors ( Quinolons and floraquinolons ) Drugs , chemistry , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 22

-Drugs :
1gen-Nalidixic acid tab ( prototype ) -ve
2gen-Ciprofloxacin tab/amp 8h , -ve
3gen-Levofloxacin Tab/amp -ve,+ve,Atypical 12h
4gen-Moxifloxacin tab -ve,+ve,atypical,anaerobic
—Chemistry : consist of Floride , and MW its more then 500 , lipid sulable
-Pharmcokintics:
1-Absorpation : Complete, make complex with metals but not like Tetracycline
2-Distribution:
2.1 BBB : Pass and can treat CNSI
2.2 Placenta / breast milk :pass and teratogenic
2.3 body fluids :good accumulation of phagocytes
3-metabolism: liver
4-Execration : renal and unchanged so are capable of treating UTI except Moxifloxacin
-mechanism of action : its inhibit the bacterial Topisomarse which is required for relaxation of The DNA to form a RNA masenger to form a new DNA , we have 4 type of topisomarse 1,2,3,4 these drugs inhibit 2nd ( gyrse ) and 4th especially in :
1-Gram - : gyrase
2-Gram + : topisomarse 4th
-spectrum: bactericidal ( broad spectrum)
1-Nalidixic acid : mainly G-
2-Ciprofloxacin : Mainly G- , few G+
3-Levofloxacin : G-,G+ , Atypical
4-Moxifloxacin : G-,G+,atypical,Anearobic
-resistant: Cross resistant but not raoid duo to point mutation in the gyrase and topisomarese
-uses :
1-UTI
2-Resp infection
3-osteomyelitis
4-meningitis
4–Atypical
-Advera effect :
-VIP-1-Muscloskletal adverse effect : cause arthropathy in the growing cartilage
2-CNS : increase seizures, duo to inhibation of GABA Receptor
3-prolangtion of QT interval : leading to fetal ventricular tachy arrhythmias
-C.I :
2-Pregnancy
2-children under 18

Question 23

Explain The Bacterial metabolites Inhibitors ( Sulfonamides , Trimethroprim ) Drugs , chemistry , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 23

-Drugs :
1-Trimethoprim/sulfamethoxazole tab ( Bactriocidal )
2-Sulfadiazine argentum oint 1%-50ml
—Chemistry : they consist of sulfer group and amino acid group ( So2NH2) this what is responsible for the effect but the R chain is only for pharmcokintics
-NB!
1-individual drug : bacteriostatic
2-Combined drug : bactriocidial
-Pharmcokintics:
1-Absorpation :good
2-Distribution:
2.1 BBB : pass and can treat CNSI
2.2 Placenta / breast milk :pass and its tertaoginic
2.3 body fluids :good reach
3-metabolism: liver
4-Execration : renal in acetylation metabolite with good concentration and can treat UTI , but we should alklain the urin first or it will lead to crystallurea
-mechanism of action :they are bacterial metabolites inhibitors of folic acid which us essential for DNA synthesis , in the norm , the bectrai synthesis the folic acid by this pathway :
-Paraaminobenzonic acid with help of Dihydroprotrate synthase transfer into dihydrofolic acid then with help of Dihydrofolate reducatse transfer into tetrahydrofolic acid then to purines then to DNA
- so the sulfa interfers with the first dihydroprotrate synthase but bacteria with time can modify it , but the Trimethoprim interferes with dinydrofolate reductase
- So now we useing the combination called Co-trimoxazol = Trimethoprim +Sulfamathoxazol to interfere the both phases
-spectrum: wide spectrum ( narrow )
1-few G+
2-Few G-
3-Atypical organisms
-uses :
1-UTI
2-Streptococcal
3-Puemocystis carinii ( PCP )
4-Toxoplasma
-Advera effect :
1-Allergy skin rash : Steven Johnson syndrome
2-Crystallurea
3-Kernectrus : displacement of billerubin in the albumen and can pass CNS in childrenunder 2 years the BBB not will developed and can cause permanent brain damage
4-BM suppression
-C.I :
1-Children under 2 years
2-Pregnancy-Drugs :
1-Trimethoprim/sulfamethoxazole tab ( Bactriocidal )

Question 24

Explain The Bacterial metabolites Inhibitors ( metronidazole ) Drugs , chemistry , Pharmcokintics, Mechanism of Action , resistance, Spectrum, Uses , adverse effects

Answer 24

Drugs : Metronidazole tab/Amp
—Chemistry :consist of Nitro group and Mw its 137 ( prodrug )
-Pharmcokintics:
1-Absorpation :Complete
2-Distribution:
2.1 BBB : Pass and can treat CNSI
2.2 Placenta / breast milk :pass and not teratogenic
2.3 body fluids :reach
3-metabolism: liver
4-Execration : renal unchanged but cant treat UTI bcs its spectrum only anaerobic bacteria and the UTI its gram - , but can discolour the urin dark brown and its not harmful
-mechanism of action :
NB! :
1-OIL : oxidation is lose of electrons
2-RIG : redaction is gain of electrons
—- the metronidazole uptake by all type of bacteria but its only effect the anaerobic bacteria bcs its mechanism works on PFOR
Pyruvate:ferrodoxine oxido reductase
Which is responsible for generation kf the ATP in the anaerobic bacteria by oxidation and reduction so as we know metronidazole consist of Nitro group so the PFOR reduction the oxygen in the Nitro group and becomes free radical compounds and unstable which is cytotoxic free radical and bind to DNA and damage the DNA
-Resistant: its very slow or by efflux ( pumping out )
-spectrum: bactericidal
1-All Anaerobic bacteria
2-Protozoa :Entomoab hustolytica
3-Tricomons viginitis
-uses :
1-Anaerobic bacteria
2-Clustridum defesil
-Advera effect :
1-GIT upset
-VIP-2-Metallic taste
3-CNS toxicity : headech , increase seizures in epileptic patients
-VIP-4-Steven jhonsn syndrome
-VIP-5- Sever BM suppression

Question 25

explain Oxazolidinones , mechansim , spectrum , C.I

Answer 25

-Drug : Linezolid (T 0,6; A 0,2% - 100 ml)
-mechansim :. inhibits protein synthesis (binding to the P site of the 50S ribosomal subunit and preventing formation ribosomal
complex)
-Spectrum : is effective against Gr(+) bacteria including MRSA,
Vancomycin resistant enterococci (VRE), Gr(+) anaerobes
* Linezolid is bactericidal against streptococci, pneumococci and B. fragilis and bacteriostatic against enterococci and
staphylococci.
-C.I :is a weak reversible MAO inhibitor. Linezolid is contraindicated in patients taking any drug which inhibits MAO A or B, in patients with uncontrolled hypertension

Question 26

explain the Isoniazid for treatment of TB , mechansim ,spectrum , advers effect

Answer 26

-drug : Isoniazid Tab 0.3 Amp
-mechansim : Mechanism of action
* It is a prodrug activated by a mycobacterial catalase–peroxidase.
* It targets the enzymes which are essential for synthesis of mycolic acid.
* Inhibiting mycolic acid leads to a disruption in the bacterial cell wall.
-Antibacterial spectrum: M. tuberculosis
-Side effect :
1.Hepatitis
2.Neurotoxicity (Due to a relative pyridoxine deficiency. This can be avoided by supplementation of 25-50 mg per day of pyridoxine).
* Peripheral neuropathy
* Convulsions in patients prone to seizures.

Question 27

explain 1st line an 2nd line of treatrment of TB

Answer 27

1st line
* Ethambutol
* Pyrazinamide
* Isoniazid (T 0,3; A 10% - 5 ml)
* Rifampin (Caps 0,15; A 0,6 for i.v.)
* Rifabutin
2nd line
* Aminoglycosides
* Paraaminosalicylic acid
* Capreomycin

Question 28

Explain life cycle of Viruses , types of viral infected cell ,

Answer 28

—virus life cycle :
1-Start with attachment : the virus endocyite to the cell
2-Uncouting : by the M2 proton channel
3-Replaction phase : in the nucleus the virus gets 2 pathways
3.1: viral genome to form a new virus
3.2 mRNA : which is for inhibition of host cell raibosm and start synthesis the virus proteins
4-Translation : in the ribosm and synthesis polyproteins of the virus
5-Processing : by enzyne called proatase : and its cutting the polyproteins into proteins
6-Assembly
7-release : normally virus released without enzymes but in influnza its need enzyme called Nueruaminadase

——faith of viral cell infection:
1-Apoptosis
2-Servival
3-Cancer

Question 29

Explain Virus replication in RNA virus , DNA virus , Retrovirus

Answer 29

1-RNA virus : in the nucleus host cell with help of RNA polymarese synthesis mRNA and viral genom
2-DNA viruses : in the neuclus of host cell with help of Integrase enzyme the virus integrate with Host cell DNA and becoma letant virus , then every-time the immune system becomes week the virus activated and with help of enzyme DNA polymerse synthesis mRNA and viral genome
3-Retroviruses :before entering the nucleus with help of enzyme called Reverse transcriptase its transform from RNA into DNA then enters the nucleus and integrate with host cell DNA with enzyme called integrase , then every time the immune system get week the virus activates and synthesis mRNA and viral genome by enzyme called DNA polymers

Question 30

Explain Treatment of HIV ( retrovirus) fusion inhibitors,RT inhibitors ,integratese inhibitors,Protease inhibitors

Answer 30

1-Fusion inhibitors
-Drugs :
-Enfuvirtide : binds to Gp41 subunit of HIV-1 viral envalople that attaches to receptors on CD4 of host cell membranes and prevent the attachment
——-
2-RT inhibitors :
-Drug :
-zidovudine : its nucloside analogue so its competitive inhibtitor of Reverse transcriptase enzyme duo to similar structural components
-Side effect : Animea and myopathy
————
3-Integrase inhibitors :
-Drug : Raltegravir tab
-they inhibit the insertion of proviral DNA into host cell genomes by inhibiting the integrase enzyme
————-
4-Protase inhibitors:
-Drug : Saquinavir Caps
-its peptied like analog that binds to protase enzyme in active site and inhibits the activity of the protase enzyme which is the processing of polyproteins resulting if formation of immature non fractional virus particles
-side effect : metabolism side effect such as hypoglycaemia, hypolipidemia

Question 31

Explain treatment of HBV , Drugs , mechanism, side effect

Answer 31

-Drugs :
1-Lamivudine tab : its inhibit HBV DNA polymarase by converting inter-cellularly to triphospah form then it competes with cytosine triphosphate for incorporation into developing viral DNA strains resulting of termination of Viral DNA replication
2-Interferon-a A/3milin IU
-mechanism: the exact mechanism are unknown but its through these 3 mechanisms:
1-interfere with viral replication
2-stimulate of apoptosis
3-regulation of immune response
—Side effect :
1-Immune distrbance
2-Fatuge
3-neurotoxicity
4-Anemia and BM depression

Question 32

Treatment of Herpes virus ,Drugs , mechanism,uses

Answer 32

-Drugs :
1-Acyclovir tab/oint
2-Ganciclovir tab/A
-mechanism: they are purine analogues, they are pro drugs that are activated inside the viral infected cell Aciclovir is converted by viral
thymidine kinase to aciclovir monophosphate
✔Aciclovir monophosphate is then converted to aciclovir triphosphate by host kinases
✔Aciclovir triphosphate inhibit HSV-specified DNA-polymerases and prevent viral DNA synthesis
-Uses :
1-Acyclovir : Herpes V 1-2
2-Ganciclovir : cytomegalovirus

Question 33

Treatment of influenza virus , uncouting inhibitors, release inhibitors

Answer 33

1-Uncoating inhibitors:
-Drugs: Rimantadine tab
-its bind to the M2 proton channel of the virus which lead to inhibition of virus uncoating and its active exassivly aginst influza A only
-uses : Influenza A
————-
2-Release inhibitors
-Drug : oseltamivir Caps 0,075
-mechanism: its inhibit the nuroaminadse enzyme with is responsible for budding of the virus
-side effect : neurpsychtric effect ,livedo reticularis
-uses : influenzaA,B

Question 34

Type of fungal infection, list of fungais caused diseases

Answer 34

-type of infection:
1-Superficial: candida , onychimycosis , dermatophytes
2-Systemic or deep : such as fungal pneumonia , fungal siptecemia , fungal meningitis , its not common and only happens with patients who immune comprised such as Chemotherapy,immunosuppressants
——-List of fungal and its diseases:
1-Yeast : candida , cryptococcal
2-mold fungi. : aspergilles
3-Dimorphic , histoplasm capselutum ,blasyimycosis

Question 35

Explain anti fungal drugs , on scheme , Outer membrane , Ergostrerol pathway and its drugs , DNA drugs

Answer 35

1-Outer membrane : its synthsis by enzyme called B-glucan synthase
-Drug effect on this phase is : Echinocandins ( fungin )
2-Ergosterol pathway :
2.1 start with Squlene transform into squlene epoxide by enzyme called squlene epoxidase : drug effecting this enzyme is Allymines
2.2 then from squlene epoxide transform into Lanosterol by enzyme called 14-a-Demithylase : drug effecting this enzyme ( Azoles )
2.3 From lanosterol transform into ergosterol and here the effect on the ergosterol directly by drugs called ( Polynes )
3-Drug effecting the DNA its Griseofulvin

Question 36

classification of antifungal according to Action , Chimical steructur

Answer 36

1- Action :
Fungicidal - cause death of fungi
Fungistatic - delay and stop the growth of fungi
2- By chimical structre :
2.1 Antifungal antibiotcs : Polyenes ,Echinocandins
2.1 Synthatics : Azoles ,Allylamines

Question 37

Explain Echinocandine ,( outer membrane inhibitors) , drugs , mechanism,spectrum , Pharmcokintics,side effect ,uses

Answer 37

-Drugs :
1-Caspofungin
2-micafungin Pwoder ( systemic use )
-mechanism: they are outer membrane synthesis inhibitors by inhibition of B-(1-3)-D-glucan synthase which is lead to disruption of the glucan formation and destroy cell intergtry
-Spectrums :
1-Candida ; fungcidal
2-Aspergills : Fungostatic
-Pharmcokintics:
-Abs : poor
2-Dist : high concentration in tissue and organ
3-metabolism: in liver without cyp450 ( no drug drug interaction )
-Side effect : Fever , Dyspepsia
-uses :
1-invasive Candida
2-Invasive Asprgillosis ( which resistant to standard therapy )

Question 38

explain Allymines , Drugs , Mechanism , Spectrum , Pharmacokintics , Uses

Answer 38

-Drugs terbinafine tab / oint
-mechansim : Inhibition of squalene epoxidase
whch is lead to decrease synthesis of ergosterol in the early stages and accumulation of toxic squalene result of abnormality of the cytoplasmic membrane
-Spectrum : Dermatophytes, Candida
-Pharmacokintics :
-abs : 70%
-Dist : high concentraion in skin and nalis
-Metabolsim : in liver
-uses :
1.onychomycosis caused by dermatophytes
2.skin candidiasis

Question 39

explain Azoles , Drugs , Mechnasim

Answer 39

-Drugs :
1-imidazol dervativs : miconazole ( systamic)
, ketoconazole (local )
2-triazol dervativs : Fluconazole , itraconazole (systmic )
-Mechaims : they are Selective inhibition CypP450-dependent
α-dimethylase which lead to Inhibit conversion of lanosterol to ergosterol and result of Disruption of growth and death of fungal cells
———————————————————————————

Question 40

-explain Ketoconazole ,spectrum , pharmacokintics , side effect , uses,
-explain itraconazole ,spectrum , pharmacokintics , side effect , uses,
-explain fluconazole ,spectrum , pharmacokintics ,uses,

Answer 40

1- Ketoconazol
-Spectrum of action : broad spectrum
1.dermatophytes (Trichophyton, Microsporum, Epidermophyton )
2.Candida .
3.dimorphic fungi
-Pharmacokinetics
-abs : Variable absorption
-metabolism : Biotransformation in the liver with cytP450
-Dist : Poor penetration through the BBB
-side effect : High toxicity (hepatotoxicity, ↓ adrenal cortex, ↓ testosterone, gynecomastia, oligospermia, sexual dysfunction). After itraconazole development - only topically!
-Uses :
1.candidiasis
2.dermatomycosis
3-Prostate cancer
——————————————————————————-
2-Itraconazol
-spectrum : Broad spectrum
yeast and mold fungi
-Pharmacokinetics
-abs : bioavailability is variable
metabolsim : biotransformation in the liver, inhibit cytP450 (drug interaction)
-Dist : high concentrations in the skin
-side effect : Less side effects (hepatotoxicity, etc.) than in ketoconazole.
-uses :
1.onychomycosis (main application)
2.candidiasis,
3.apergillosis, .
4.blastomycosis
—————————————————————————————–
3-Fluconazol
-Spectrum of action
Yeast (Candida spp., Cryptococcus spp.)
NB! Does not work against mold fungi (Aspergillus spp.)
-Pharmacokinetics
-Abs : food does not affect bioavailability
-Dist : penetrates the BBB , high [C] in CSF, skin and urine
-Metabolsim : biotransformation in the liver, inhibit of cytP450 (interaction)
-uses:
1. superficial and invasive candidiasis
2.cryptococcosis

Question 41

explain the Polyenes , Drugs , mechansim , spectrum , pharmacokintics , side effect , lipds forms of amphotericin , uses ,( of each drug )

Answer 41

-Drugs :
1.Amphotericin B ( systamic , Emrgncy only A/powder )
2.Nystatin ( local ) tab 250k IU
-Mechansim : selective binding to ergosterol of fungi cell membrane and pore formation in the membrane which lead to cell contnt leakge and cell death (fungicidal action)
—Amphotericin B :
-Spectrum : Broad spectra
all invasive mycoses
-Pharmacokinetics:
-Metabolism: in the liver, excretion by the kidneys (cumulation).
-Dist : Does not penetrate BBB (is not used for CNS infections)
-Side effect :
1.Nausea, vomiting
2. Decreace Bp up to shock
3.anemia duo to decrease Erythropoiten
4.Nephrotoxicity
-Lipid forms of Amphotericin B :
1.Amphotericin B liposomal
2.Amphotericin B cholesteryl sulfate complex
-Uses : in emergncy
aspergillosis
candidiasis
cryptococcosis
blastoplasmosis
histoplasmosis

—Nystatin :
-spectrum :Candida
-Pharmacokinetics : Poorly absorbed from the digestive tract
- Side effects : Dyspepsia (nausea, vomiting, diarrhea, abdominal pain)
-uses : Candidiasis (oral mucosa, oropharynx, intestines, vulvovaginitis)

Question 42

Explain DNA effecting Antifungal drug , mechanism,spectrum, side effect , uses

Answer 42

-Drug : Griseofulvin tab
-mechanism: its inhibit fungal cell mitosis and nuclear acid synthesis, and also bind and interferes with Spindle and cytoplasmic microturbules by binding to a and B tubulin
-Spectrum: its fungustatic
1-Dermatophytes , skin infection
-Side effect : N,V,D
-Uses :
1-its used in local skin , nail’s infection
2-As adjuvant drug with amphotericin B

Question 43

Explain life cycle of Plasmodium

Answer 43

1-Start with mosquito biting the body
2-Sporozites in the blood stream then to the liver
3-in the liver there is parasities division called dromantic focai ( only in relapse type such as ovale,vivax )
4-then its leaves the liver to blood circulation and called mirozites and attack the RBCs and keep division inside the RBCs
5- the. It have 2 pathway either it’s become Gematocytes for transmission or attack the RBCs again.

Question 44

Explain 4-Aminoquinin family,Drugs,mechanism,side effect , uses, C.I

Answer 44

-Drugs :
1-Chloroquine tab
2-Mefloquine tab
Both rapid acting
-mechanism: plasmodium digest the host HB in the same time from digestion of HB heme is toxic for parasite so plasmodium polymarse is transform the Heme into non toxic form , so the 4-aminoquinin inhibt the plasmodium plymarse which is result of cell death from toxicity
-Side effect : mefloqunin less side effect
1-GIT , N,V,D
2-CVS: prolong QT duo to same family of Antiarrthmic drug quinidin
3-bluerd vision : duo to pertacepation of chloride and iode
—Uses :
1-Prophlyxis of malaria
2-Treatments of malaria
3-Ambausis
—CI :
Paitnt with paorsis or prophlia bcs acute attack may occurred

Question 45

Explain Primaquine , Drug , mechanism,side effect , uses ,

Answer 45

-Drug : Primaquine tab
-mechanism: its form quinoline-quinin metabolites which are electron-transferring redox compound thats act as cellular oxidant the drug us tissue Schizonatic and also limit malaria transmission by binding on Gematocytes
-Side effect :
1-GIT
2-headeacg
3-sever toxicyt of G6PD deficiency
-uses :
To pervent relapse by acting on hypnozties and its radical cure

Question 46

Explain Antufolate , Drugs , mechanism,side effects, uses ,

Answer 46

-Drugs : proguanil tab
-mechanism: its sulf counting drug and act as anti metabolites drug of Paraaminobenzonic acid by inhibating dihydroptorate
-Side effect :
1-GIT
2-hypersistivte
3-in high dose its compatative protein binding
-uses : usally combind with pyrimathmine for causal prophylaxis

Question 47

Explain types of Helmintics infections

Answer 47

1-Nematodes
2-Cestods
3-Trematodes

Question 48

-Explain treatment of nematodes , Drug , mechanism, side effect ,uses
-Explain treatment of cestod , Drug , mechanism, side effect , uses
-Explain treatment of trematodes , Drugs , mechanism, spectrum of each

Answer 48

-Drug :
1-Mebendazole
2-Pyrantel
-mechanism: acts as slecctivly by inhibiting macrotubules synthesis and glucose uptake in nematodes
-side effect : gut irration
-Uses : nematodes
-C.I : pregnancy duo to teratogenicity
————————————————————————-
-Drug : Niclosamide tab
-mechanism: act by uncoupling oxidative phosphorylation or by activating ATPase
-Side effect :
-GIT irritation :
-Uses : cestodes
——————————————————————————-
-Drug : Albendazol tab : by inhibiting microtubules assembly
-Spectrum and uses :
Braod spectrum ( all 3 types )
-Side effect : reversable leukpina
———
2-Drug : Praziquantel tab : its increasing membrane permeability to calcium , casuing marked contraction intinally followed by paralysis of the muscle of the helmentics and then vaculazation and parasite death
-spectrum uses : Braod spectrum includes 3 types