ุงู
ุณููููุงุช ุฏ. ู
ุญู
ุฏ ุงูุนู
ุงู
ู
โค6
ูุชุจุช ู
ุฌู
ูุนุฉ ุดูุฑุช ููุช ุงููู ุงุญุชู
ุงู ูุฌู ูู ุงููุงุฑู
ุง ูุฒููู ุชูุงุ
Anonymous Poll
57%
ุงูุง
43%
ูุฒูู ุจุนุฏ ุงูู
ุนู
ู
ูุฑุฑุช ุฃู ุฃูุถู ูุฒููู ุจุนุฏ ุงูู
ุนู
ู ูุฃู ุฏูุชูุฑุฉ ุฎุฏูุฌุฉ ุงุญุชู
ุงู ุชูุฒู ูููุณ ุนูู ุชูุงุตูู ุงูุฅู
ุชุญุงู ู ู
ู
ูู ุชููู ุนูู ุดู ูุฑูุฒูุง ูู ุงูุดูุฑุช~ ๐ค
โค20๐5
SN (cvs cns endo blood) .pdf
361.7 KB
โค20๐1
ุชุฌู
ูุนุฉ ุดูุฑุช ููุช ููููุฑุณุงุช ุงููุจุงุฑ (cvs - cns - endo - blood)
ูู ููุงุท ุณู ุนุชูุง ู ู ุชุณุฌููุงุช ุงูุฌุงู ุนุฉ ู ุงุถุงูุงุช ู ูู~ ๐๐ป
ูู ูู ุงุณุชูุณุงุฑ ุฃู ุชุนุฑููุง ุณุคุงู ู ูู ู ุถูุชุด ุฏุฒููู
@kukxu0
ูู ููุงุท ุณู ุนุชูุง ู ู ุชุณุฌููุงุช ุงูุฌุงู ุนุฉ ู ุงุถุงูุงุช ู ูู~ ๐๐ป
ูู ูู ุงุณุชูุณุงุฑ ุฃู ุชุนุฑููุง ุณุคุงู ู ูู ู ุถูุชุด ุฏุฒููู
@kukxu0
โค28๐1
Forwarded from Deleted Account
CamScanner 08-05-2022 19.07.pdf
7.2 MB
ุชุฑููุฒุงุช ุงู ุฌุงู
ุนู ูู ู
ููุฌ ูุจู ุงูุฌุฒุฆู
ุงูุญู
ุฏ ููู ู
ูุด ุดูุฑุช ููุช ูุจู ุงูุฌุฒุฆู ุจุณ ููุง ุณุงุนุงุช ููุช ูุฌูุฒ ููู ู ุฌูุช ุจูุฒูู ุชูุง ๐๐
ุงู ุดุงุก ุงููู ุญูุฒู ุจุงูู ุดูุฑุช ููุช ู ุงูุฅูุณุจูุงูู ุงููู ุจุนุฏ ุงูุฌุฒุฆู ุงูููู ุฃู ุจูุฑุฉ ๐ค
ุทูุจ ูู ูู ุญุฏ ูุงุชุจ ุงูุฅูุณุจูุงูู ูุจู ุงูุฌุฒุฆู ูุฏุฒูุง ุจูุด ูุฒููุง ู ูุณุชููุฏูุง ูููุง ููุฃุณู ุญุตูุชุด ูุฑุตุฉ ููู ูู ๐๐ป
@kukxu0
ุงู ุดุงุก ุงููู ุญูุฒู ุจุงูู ุดูุฑุช ููุช ู ุงูุฅูุณุจูุงูู ุงููู ุจุนุฏ ุงูุฌุฒุฆู ุงูููู ุฃู ุจูุฑุฉ ๐ค
ุทูุจ ูู ูู ุญุฏ ูุงุชุจ ุงูุฅูุณุจูุงูู ูุจู ุงูุฌุฒุฆู ูุฏุฒูุง ุจูุด ูุฒููุง ู ูุณุชููุฏูุง ูููุง ููุฃุณู ุญุตูุชุด ูุฑุตุฉ ููู ูู ๐๐ป
@kukxu0
โค31๐1
BRONCHIAL ASTHMA (SN)
โwrite MOA of SABA?
stimulate beta 2 receptors:
1. bronchodilation
2. inhibition of mast cell and cytokines
3. increase bronchial mucociliary clearance
โlist adverse effects of selective beta 2 agonists?
1. tremors - anxiety
2. tachycardia
3. tolerance
4. hypokalemia and ms. cramps
โwhat are indications of ipratopium?
1. asthma induced by psychogenic or beta stim.
2. asthmatic pt. intolerant to tachycardia or anxiety of beta 2 agonists or theophylline (cardiac - thyrotoxicosis - elderly)
3. acute severe asthma (adjuvant)
4. COPD
โmention disadvantages of ipratopium?
1. tolerance > blocks presynaptic M2 receptord > ACh release
2. delayed onset less effective than beta 2
โwrite MOA of methylxanthines?
1. inhibit phosphodiesterase > increase CAMP
a. direct BD
b. anti inf. decrease cytokines and mast cell mediators - inhibit late asthmatic response
2. block adenosine receptors
โlist adverse effects of theophylline?
1. headache - insomnia - anxiety
2. tachy - arrhythmia
3. peptic ulcer
4. narrow safety margin (monitor serum lvl)
โmention indications of theophylline?
1. bronchial asthma 2nd choice
a. short term relief of acute bronchospam
b. long term control (nocturnal asthma)
c. acute severe asthma
2. COPD
3. neonatal apnea
โwrite MOA of corticosteroids in bronchial asthma?
1. PLA2 > decrease LT PGs > decrease inf.
2. VC > decongestant
3. increase number of beta 2 > indirect BD (potentiate beta 2 agonist)
โwrite MOA of SABA?
stimulate beta 2 receptors:
1. bronchodilation
2. inhibition of mast cell and cytokines
3. increase bronchial mucociliary clearance
โlist adverse effects of selective beta 2 agonists?
1. tremors - anxiety
2. tachycardia
3. tolerance
4. hypokalemia and ms. cramps
โwhat are indications of ipratopium?
1. asthma induced by psychogenic or beta stim.
2. asthmatic pt. intolerant to tachycardia or anxiety of beta 2 agonists or theophylline (cardiac - thyrotoxicosis - elderly)
3. acute severe asthma (adjuvant)
4. COPD
โmention disadvantages of ipratopium?
1. tolerance > blocks presynaptic M2 receptord > ACh release
2. delayed onset less effective than beta 2
โwrite MOA of methylxanthines?
1. inhibit phosphodiesterase > increase CAMP
a. direct BD
b. anti inf. decrease cytokines and mast cell mediators - inhibit late asthmatic response
2. block adenosine receptors
โlist adverse effects of theophylline?
1. headache - insomnia - anxiety
2. tachy - arrhythmia
3. peptic ulcer
4. narrow safety margin (monitor serum lvl)
โmention indications of theophylline?
1. bronchial asthma 2nd choice
a. short term relief of acute bronchospam
b. long term control (nocturnal asthma)
c. acute severe asthma
2. COPD
3. neonatal apnea
โwrite MOA of corticosteroids in bronchial asthma?
1. PLA2 > decrease LT PGs > decrease inf.
2. VC > decongestant
3. increase number of beta 2 > indirect BD (potentiate beta 2 agonist)
โค6๐4
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GIT (SN)
โclassify peptic ulcer drugs?
1. drugs that inhibit gastric acid secretion
2. drugs that neutrilize gastric acid
3. mucosal protective drugs
4. anti H.pylori drugs
โlist drugs that inhibit gastric acid secretion?
1. H2 receptor antagonists (cimetidine - ranitidine - famotidine)
2. proton pump inhibitor (omeprazole)
3. anticholinergic drugs (pirenzipine - telenzipine)
4. prostaglandin analogues (misoprostol)
โwrite MOA of H2 antagonists?
1. competitive inhibitor suppress basal and meal stimulated acid secretion in a linear dose dependant manner
2. reduce secretion stimulated by histamine as well as by gastrin and cholinomimetic agents
โwhat are A/E of H2 blockers?
1. headache diarrhea constipation
2. tolerance (rebound hyperacidity)
3. sedation - hallucination (cimetidine)
4. antiandrogenic (cimetidine): gymecomastia - impotence - mestrual problems - galactorrhea
5. enzyme inhibition (cimetidine)
6. hypotension - brady (if give IV)
โwrite MOA of proton pump inhibitors?
1. are lipophilic weak bases (PH 4-5)
2. after int. absorption diffuse into acidified compartments (parietal cell)
3. becomes protonated (active form)
4. forms a covalent disulfide bond with H/K ATPase
5. irreversibly inactivates enzymes
โwrite MOA of sucralfate?
1. in acidic environment PH<4 it polymerizes by cross linking molecule to form sticky viscous gel that adhere ulcer
2. act as physical barrier
3. stim. PG and HCO3
4. bind to epithelial - fibroblast growth factor
โlist adverse effects of sucralfate?
1. nausea - vomiting - dry mouth
2. flatulence - constipation
3. AL toxicity: osteomalacia - encephalopathy
* triple therapy: omeprazole - clarithromycin - amoxicillin (14 days)
โlist advantages of famotidine and ranitidine over cimetidine?*
FAMOTIDINE:
1. most potent
2. 50% decomposed by acid
3. 50% bioavailability
4. excreted mainly by kidney
5. no enzyme inhibiting
RANITIDINE
1. more potent -less enzyme inhibiting
2. anti H.pylori
3. 50% bioavailability
4. 50% metabolized in liver
โdiscuss advantage of PPI over H2 antagonists?*
1. higher efficacy better relief
2. more prolonged effect
3. more effect in H.pylori
โmention uses of anti secretory drugs?*
1. PU 2. anti H.pylori 3. GERD
4. zollinger ellison syndrome
5. stress ulcer
6. acute gastritis
7. bleeding esophageal varices
โexplain antacid drug interaction?*
1. change gastric urinary PH
2. delay gastric emptying
3. chelation: Al salts form insoluble complexes with other drugs
โdifferentiate b/w 2 types of antacid?*
LOCAL ANTACID
โขAl hydroxide > constipation
โขMg salts > diarrhea
โขCa carbonate:
1. constipation
2. rebound hyperacidity
3. milk alkali syndrome
4. increase CO2 flatulence
SYSTEMIC ANTACIDS
โขNaHCO3 > rapid onset potent
1. systemic alkalosis
2. rebound hyperacidity
3. Na dangerous in HF HTN renal ds.
4. increase CO2 flatulence
5. alkaline urine - renal stones
โclassify peptic ulcer drugs?
1. drugs that inhibit gastric acid secretion
2. drugs that neutrilize gastric acid
3. mucosal protective drugs
4. anti H.pylori drugs
โlist drugs that inhibit gastric acid secretion?
1. H2 receptor antagonists (cimetidine - ranitidine - famotidine)
2. proton pump inhibitor (omeprazole)
3. anticholinergic drugs (pirenzipine - telenzipine)
4. prostaglandin analogues (misoprostol)
โwrite MOA of H2 antagonists?
1. competitive inhibitor suppress basal and meal stimulated acid secretion in a linear dose dependant manner
2. reduce secretion stimulated by histamine as well as by gastrin and cholinomimetic agents
โwhat are A/E of H2 blockers?
1. headache diarrhea constipation
2. tolerance (rebound hyperacidity)
3. sedation - hallucination (cimetidine)
4. antiandrogenic (cimetidine): gymecomastia - impotence - mestrual problems - galactorrhea
5. enzyme inhibition (cimetidine)
6. hypotension - brady (if give IV)
โwrite MOA of proton pump inhibitors?
1. are lipophilic weak bases (PH 4-5)
2. after int. absorption diffuse into acidified compartments (parietal cell)
3. becomes protonated (active form)
4. forms a covalent disulfide bond with H/K ATPase
5. irreversibly inactivates enzymes
โwrite MOA of sucralfate?
1. in acidic environment PH<4 it polymerizes by cross linking molecule to form sticky viscous gel that adhere ulcer
2. act as physical barrier
3. stim. PG and HCO3
4. bind to epithelial - fibroblast growth factor
โlist adverse effects of sucralfate?
1. nausea - vomiting - dry mouth
2. flatulence - constipation
3. AL toxicity: osteomalacia - encephalopathy
* triple therapy: omeprazole - clarithromycin - amoxicillin (14 days)
โlist advantages of famotidine and ranitidine over cimetidine?*
FAMOTIDINE:
1. most potent
2. 50% decomposed by acid
3. 50% bioavailability
4. excreted mainly by kidney
5. no enzyme inhibiting
RANITIDINE
1. more potent -less enzyme inhibiting
2. anti H.pylori
3. 50% bioavailability
4. 50% metabolized in liver
โdiscuss advantage of PPI over H2 antagonists?*
1. higher efficacy better relief
2. more prolonged effect
3. more effect in H.pylori
โmention uses of anti secretory drugs?*
1. PU 2. anti H.pylori 3. GERD
4. zollinger ellison syndrome
5. stress ulcer
6. acute gastritis
7. bleeding esophageal varices
โexplain antacid drug interaction?*
1. change gastric urinary PH
2. delay gastric emptying
3. chelation: Al salts form insoluble complexes with other drugs
โdifferentiate b/w 2 types of antacid?*
LOCAL ANTACID
โขAl hydroxide > constipation
โขMg salts > diarrhea
โขCa carbonate:
1. constipation
2. rebound hyperacidity
3. milk alkali syndrome
4. increase CO2 flatulence
SYSTEMIC ANTACIDS
โขNaHCO3 > rapid onset potent
1. systemic alkalosis
2. rebound hyperacidity
3. Na dangerous in HF HTN renal ds.
4. increase CO2 flatulence
5. alkaline urine - renal stones
โค7๐5
๐๐ฃ๐ ๐ช๐๐๐ฃ ๐๐ ๐ฅ๐๐ค ~๐ pinned ยซุชุฌู
ูุนุฉ ุดูุฑุช ููุช ููููุฑุณุงุช ุงููุจุงุฑ (cvs - cns - endo - blood) ูู ููุงุท ุณู
ุนุชูุง ู
ู ุชุณุฌููุงุช ุงูุฌุงู
ุนุฉ ู ุงุถุงูุงุช ู
ูู~ ๐๐ป ูู ูู ุงุณุชูุณุงุฑ ุฃู ุชุนุฑููุง ุณุคุงู ู
ูู
ู
ุถูุชุด ุฏุฒููู @kukxu0ยป
๐๐ฃ๐ ๐ช๐๐๐ฃ ๐๐ ๐ฅ๐๐ค ~๐ pinned ยซุงูุญู
ุฏ ููู ู
ูุด ุดูุฑุช ููุช ูุจู ุงูุฌุฒุฆู ุจุณ ููุง ุณุงุนุงุช ููุช ูุฌูุฒ ููู ู ุฌูุช ุจูุฒูู ุชูุง ๐๐ ุงู ุดุงุก ุงููู ุญูุฒู ุจุงูู ุดูุฑุช ููุช ู ุงูุฅูุณุจูุงูู ุงููู ุจุนุฏ ุงูุฌุฒุฆู ุงูููู
ุฃู ุจูุฑุฉ ๐ค ุทูุจ ูู ูู ุญุฏ ูุงุชุจ ุงูุฅูุณุจูุงูู ูุจู ุงูุฌุฒุฆู ูุฏุฒูุง ุจูุด ูุฒููุง ู ูุณุชููุฏูุง ูููุง ููุฃุณู ุญุตูุชุด ูุฑุตุฉ ููู
ูู ๐๐ป @kukxu0ยป
ุตุญ ูุซุฑุช ุงูุฃุณุฆูุฉ ๐
ุจุณ ูุงุญุธุช ุฃู ุญุชู ุจุนุถ ุงูุฃู
ุณููููุงุช ุชุจู ุญูุธ ููู ุงูุดูุฑุช ูุญุชุณุงุนุฏูู
ุงู ุดุงุก ุงููู ุนูู ูู ุญุงู~
ู ุชูุฏุฑูุง ุชุฎุชุตุฑููู ุฃู ุชุดูููุง ุงูู ูู ุจุงููุณุจุฉ ููู ู ุงู ุดุงุก ุงููู ููููุง ููุณ ุงูุฃุณุฆูุฉ ุงููู ูุฑููุงูุง~
ู ุชูุฏุฑูุง ุชุฎุชุตุฑููู ุฃู ุชุดูููุง ุงูู ูู ุจุงููุณุจุฉ ููู ู ุงู ุดุงุก ุงููู ููููุง ููุณ ุงูุฃุณุฆูุฉ ุงููู ูุฑููุงูุง~
โค22๐1
ู
ู ุงูุฎุงุต:
ุจููููู ูู blood ุฏูุชูุฑุฉ ูุงูุช ู ุฑุงุช ุชุฌูุจ ุดูุฑุช ููุช ู ูุงุฑูู ุจูู heparin ู warfarin
ูุงู CNS ุฌุฒุฆูุฉ ุฏูุชูุฑุฉ ููุฑูุฒ ูุงูุช ุงุณุชุฎุฏุงู ุงุช ููุท ู ุงู ุง ุงุณุชุฎุฏุงู ุงุช Benzodiazepin ุฃู ุงุณุชุฎุฏุงู ุงุช ุงูู ูุฑููู ุจุณุณุณุณ ูุงูุช ู ุด ููุฌูุจ ุดูุฑุช ููุช ุบูุฑูู
ูุงูุช ุงู side effect ู ูู ุงุช ู ุน ุฐูุฑ ุงูุณุจุจ ูุนูู ู ู ูู ุชุฌู explain why
MOA of sitagliptin (SN)
ุดูุฑุง ููู ู ู ุฏุฒ ู ูุจู ุนุงูููุงุท ุงูู ูู ุฉ ูู ู ูุฒุงู ุญุณูุงุชูู ๐๐ป๐ค
ุจููููู ูู blood ุฏูุชูุฑุฉ ูุงูุช ู ุฑุงุช ุชุฌูุจ ุดูุฑุช ููุช ู ูุงุฑูู ุจูู heparin ู warfarin
ูุงู CNS ุฌุฒุฆูุฉ ุฏูุชูุฑุฉ ููุฑูุฒ ูุงูุช ุงุณุชุฎุฏุงู ุงุช ููุท ู ุงู ุง ุงุณุชุฎุฏุงู ุงุช Benzodiazepin ุฃู ุงุณุชุฎุฏุงู ุงุช ุงูู ูุฑููู ุจุณุณุณุณ ูุงูุช ู ุด ููุฌูุจ ุดูุฑุช ููุช ุบูุฑูู
ูุงูุช ุงู side effect ู ูู ุงุช ู ุน ุฐูุฑ ุงูุณุจุจ ูุนูู ู ู ูู ุชุฌู explain why
MOA of sitagliptin (SN)
ุดูุฑุง ููู ู ู ุฏุฒ ู ูุจู ุนุงูููุงุท ุงูู ูู ุฉ ูู ู ูุฒุงู ุญุณูุงุชูู ๐๐ป๐ค
โค26๐1๐1
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ANTIVIRAL (SN)
โwrite MOA of acyclovir?*
(require 3 phosphorylation steps)
1. inhibits viral DNA synthesis
2. competitive inhibitor with deoxy GTP for viral DNA polymerase
3. bind to template (irreversible) > chain termination
โwrite MOA and A/E of zidovudine?
โซ๏ธconverted to triphosphate by thymidine kinase
โซ๏ธincorporate into chain of viral DNA > chain termination
1. myelosuppresion
2. headache insomnia anxiety
3. hyperpigmentation of nail - myopathy
-------------------------------------------
ANTIFUNGAL (SN)
โwrite MOA of amphotericin B?*
1. binds to ergosterol and alters permeability by forming pores
2. allows leakage of ions > cell death
โlist A/E of amphotericin B?**
1. fever chills
2. renal impairment (due to decrease GFR)
3. hypotension (shock with hypokalemia)
4. anemia (due to reduced erythropoietin production)
*pharmacokinetics of fluconazole* mcq ู ูู
*imidazoles & triazoles* ู ูู ุงููุฑููุงุช ุจููุงุชูู
โlist A/E of griseofulvin?
1. headache vomiting diarrhea
2. photosensitivity peripheral neuritis
3. hepatotoxicity
4. coumarin anticoagulant activity altered
โwrite MOA of acyclovir?*
(require 3 phosphorylation steps)
1. inhibits viral DNA synthesis
2. competitive inhibitor with deoxy GTP for viral DNA polymerase
3. bind to template (irreversible) > chain termination
โwrite MOA and A/E of zidovudine?
โซ๏ธconverted to triphosphate by thymidine kinase
โซ๏ธincorporate into chain of viral DNA > chain termination
1. myelosuppresion
2. headache insomnia anxiety
3. hyperpigmentation of nail - myopathy
-------------------------------------------
ANTIFUNGAL (SN)
โwrite MOA of amphotericin B?*
1. binds to ergosterol and alters permeability by forming pores
2. allows leakage of ions > cell death
โlist A/E of amphotericin B?**
1. fever chills
2. renal impairment (due to decrease GFR)
3. hypotension (shock with hypokalemia)
4. anemia (due to reduced erythropoietin production)
*pharmacokinetics of fluconazole* mcq ู ูู
*imidazoles & triazoles* ู ูู ุงููุฑููุงุช ุจููุงุชูู
โlist A/E of griseofulvin?
1. headache vomiting diarrhea
2. photosensitivity peripheral neuritis
3. hepatotoxicity
4. coumarin anticoagulant activity altered
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ANTICANCER (SN)
โwrite MOA of alkylating agents (cyclophosphamide)?*
1. work by covalent binding of alkyl group to guanine
2. cross link DNA in intra strand & inter strand manner > interrupt DNA replication
โwrite MOA of cytotoxic antibiotics (doxorubicin)?*
1. intercalate with DNA base pairs causing breakage of DNA
2. inhibit enzyme topoisomerase II > damage - apoptosis
โwrite MOA of trastuzumab?*
1. binds to HER2 > inhibit signaling + activation
2. activate ADCC
โlist A/E of anticancer drugs?**
1. bome marrow suppression
2. damages lining of the mouth and intestines > bacteria enter blood
3. nausea vomiting
4. temporary hair loss
5. rashes - sterility
6. peripheral neuropathy - ototoxicity
7. tumor lysis syndrome > arrhythmia - seizures - acute kidney failure - death
โwrite MOA of alkylating agents (cyclophosphamide)?*
1. work by covalent binding of alkyl group to guanine
2. cross link DNA in intra strand & inter strand manner > interrupt DNA replication
โwrite MOA of cytotoxic antibiotics (doxorubicin)?*
1. intercalate with DNA base pairs causing breakage of DNA
2. inhibit enzyme topoisomerase II > damage - apoptosis
โwrite MOA of trastuzumab?*
1. binds to HER2 > inhibit signaling + activation
2. activate ADCC
โlist A/E of anticancer drugs?**
1. bome marrow suppression
2. damages lining of the mouth and intestines > bacteria enter blood
3. nausea vomiting
4. temporary hair loss
5. rashes - sterility
6. peripheral neuropathy - ototoxicity
7. tumor lysis syndrome > arrhythmia - seizures - acute kidney failure - death
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