امسيكيوات د. محمد العمامي

قررت أن أفضل نزلهن بعد المعمل لأن دكتورة خديجة احتمال تنزل فويس علي تفاصيل الإمتحان و ممكن تقول علي شن نركزوا في الشورت~ 🤍

تجميعة شورت نوت للكورسات الكبار (cvs - cns - endo - blood)
في نقاط سمعتها من تسجيلات الجامعة و اضافات مني~ 🙏🏻

لو في استفسار أو تعرفوا سؤال مهم مضفتش دزولي
@kukxu0

تركيزات ال جامعه في منهج قبل الجزئي

الحمد لله مفش شورت نوت قبل الجزئي بس ليا ساعات كنت نجهز فيه و جيت بنزله توا 🙂😂
ان شاء الله حنزل باقي شورت نوت و الإكسبلاين اللي بعد الجزئي اليوم أو بكرة 🤍

طلب لو في حد كاتب الإكسبلاين قبل الجزئي يدزها بيش نزلها و نستفيدوا كلنا للأسف حصلتش فرصة نلمهن 🙏🏻
@kukxu0

BRONCHIAL ASTHMA (SN)

❕write MOA of SABA?
stimulate beta 2 receptors:
1. bronchodilation
2. inhibition of mast cell and cytokines
3. increase bronchial mucociliary clearance

❕list adverse effects of selective beta 2 agonists?
1. tremors - anxiety
2. tachycardia
3. tolerance
4. hypokalemia and ms. cramps

❕what 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

❕mention disadvantages of ipratopium?
1. tolerance > blocks presynaptic M2 receptord > ACh release
2. delayed onset less effective than beta 2

❕write 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

❕list adverse effects of theophylline?
1. headache - insomnia - anxiety
2. tachy - arrhythmia
3. peptic ulcer
4. narrow safety margin (monitor serum lvl)

❕mention 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

❕write 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)

GIT (SN)

❕classify 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

❕list 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)

❕write 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

❕what 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)

❕write 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

❕write 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

❕list adverse effects of sucralfate?
1. nausea - vomiting - dry mouth
2. flatulence - constipation
3. AL toxicity: osteomalacia - encephalopathy

* triple therapy: omeprazole - clarithromycin - amoxicillin (14 days)

❕list 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

❕discuss advantage of PPI over H2 antagonists?*
1. higher efficacy better relief
2. more prolonged effect
3. more effect in H.pylori

❕mention 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

❕explain antacid drug interaction?*
1. change gastric urinary PH
2. delay gastric emptying
3. chelation: Al salts form insoluble complexes with other drugs

❕differentiate b/w 2 types of antacid?*
LOCAL ANTACID
•Al hydroxide > constipation
•Mg salts > diarrhea
•Ca carbonate:
1. constipation
2. rebound hyperacidity
3. milk alkali syndrome
4. increase CO2 flatulence

SYSTEMIC ANTACIDS
•NaHCO3 > 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

صح كثرت الأسئلة 😅 بس لاحظت أن حتى بعض الأمسيكيوات تبي حفظ كيف الشورت فحتساعدكم ان شاء الله على كل حال~
و تقدروا تختصروهن أو تشوفوا المهم بالنسبة لكم و ان شاء الله نلقوا نفس الأسئلة اللي قريناها~

من الخاص:
بنقولك في blood دكتورة قالت مرات تجيب شورت نوت مقارنه بين heparin و warfarin

وال CNS جزئية دكتورة نيروز قالت استخدامات فقط ي اما استخدامات Benzodiazepin أو استخدامات المورفين بسسسس قالت مش هنجيب شورت نوت غيرهن
قالت ال side effect مهمات مع ذكر السبب يعني ممكن تجي explain why

MOA of sitagliptin (SN)

شكرا لكل من دز و نبه عالنقاط المهمة في ميزان حسناتكم 🙏🏻🤍

ANTIVIRAL (SN)

❕write 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

❕write MOA and A/E of zidovudine?
▫️converted to triphosphate by thymidine kinase
▫️incorporate into chain of viral DNA > chain termination
1. myelosuppresion
2. headache insomnia anxiety
3. hyperpigmentation of nail - myopathy

-------------------------------------------
ANTIFUNGAL (SN)

❕write MOA of amphotericin B?*
1. binds to ergosterol and alters permeability by forming pores
2. allows leakage of ions > cell death

❕list 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 مهم

*imidazoles & triazoles* مهم الفروقات بيناتهن

❕list A/E of griseofulvin?
1. headache vomiting diarrhea
2. photosensitivity peripheral neuritis
3. hepatotoxicity
4. coumarin anticoagulant activity altered

ANTICANCER (SN)

❕write 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

❕write MOA of cytotoxic antibiotics (doxorubicin)?*
1. intercalate with DNA base pairs causing breakage of DNA
2. inhibit enzyme topoisomerase II > damage - apoptosis

❕write MOA of trastuzumab?*
1. binds to HER2 > inhibit signaling + activation
2. activate ADCC

❕list 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

EXPLAIN PART

CNS

❗explain why BZDs cause antergrade amnesia?
▫️b/c events are not transformed from short term memory to long term memory

❗explain why long acting BZDs are not used in sleep disorders?
▫️to prevent day time sedation

❗explain why barbiturates cause more hangover?
▫️b/c marked reduction in REM - stage 3, 4 NREM

❗explain why barbiturates CI in acute intermittent porphyria?
▫️b/c increase heme synthesis

❗explain why methadone and buprenorphine are used in detoxification of addicts?
▫️b/c it has lower dependance and abuse potential - long duration of action

❗explain why pethedine is preferred during labor?
▫️b/c it has less respiratory depression in neonates and does not delay labor

❗explain why pethedine should not be used in chronic pain?
▫️b/c less potent rapid and shorter duration

❗explain why fentanyl is preferred in anaesthesia?
▫️b/c strong analgesic and sedation in preanesthesia
induce and maintain anesthesia

❗explain why remifentanyl induces less ventilatory depression than morphine?
▫️b/c ultra short acting metabolized by blood and tissue esterase

❗explain why naltrexone is used in management of chronic opioid toxicity while naloxone is used in acute?
▫️b/c naltrexone: decrease craving for opioids after weeks
naloxone: works within 2 min only

❗explain why morphine CI with BPH?
▫️b/c cause urine retention

❗explain why morphine CI in bilary colic?
▫️b/c cause contraction of the gall and constriction of sphinctor

❗explain why NO used in combination with oxygen?
▫️b/c it moves quickly and retard oxygen uptake during recovery causing diffusional hypoxia

❗explain why local anesthetic less effective when they are injected into infected tissues?
▫️b/c low PH favors charged form with less neutral base available for diffusion across membrane

❗explain why epinephrine is added to LA?
▫️b/c it's VC > increase duration and reduce systemic absorption and toxicity

❗epenpherine should not be administrated in areas as fingers and toes?
▫️b/c it may cause ischemia - necrosis

❗explain why allergy to one type of ester means allergy to all?
▫️because PABA is the allergic metabolite produced by all esters

❗explain why monotherapy is preferred in anti epileptic drugs?
▫️b/c they are either enzyme inducers or enzyme inhibitors

❗explain why use of phenytoin is limited?
▫️due to: 1. irregular bioavailability
2. saturation kinetics unpredictable serum lvl.
3. drug interaction if combined

❗explain why barbiturates and BZDs are not 1st choice agents in ttt of epilepsy?
▫️due to sedation and tolerance

❗explain how optimization of L-dopa therapy could be achieved by it's combination with peripheral dopa carboxylase inhibitors?
▫️b/c does not cross BBB > increase lvl. of dopamine and decrease peripheral side effects

❗Levodopa cause fluctuation in response (on - off phenomena)?
1. decrease sensitivity of D receptors
2. fluctuation in L-dopa plasma (short half life)
* corrected by giving drug holidays (3-21 days)

❗explain why pyridoxine should be avoided in parkinsonism pt. using L-dopa?
▫️b/c vit. B6 enhance activity of dopa decarboxylase and increase peripheral metabolism of L-dopa

❗explain why low protein diet is advised in parkinson?
▫️b/c protein to interfere with how levodopa is absorbed on the body

❗explain why non ergot DA agonist (pramipexil) are preferable to ergots in ttt of parkinson?
▫️b/c ergot alkaloids cause VC - urine retraction and stim. central D receptor

❗explain why lithium not used with loop diuretics?
▫️b/c it competes with Na for tubular reabsorption
Na depletion > increase lithium reabsorption > increase serum lithium > toxicity

❗TCAs and antidepressants should be used cautiosly in bipolar disorder?
▫️b/c antidepressants may cause a switch to manic behaviour