أول شيء الدكتورة قالت ان الجزئية هدي متقدمة واجد بالنسبة لثالثة فناخدوا عليه نقاط معينة نركزوا عليها~

هدي بداية تسجيل المحاضرة قالت شن المهم و شرحت باثوفسيولوجي بيش نفهموا ال drugs

اللي قالت عليهن يجن شورت نوت

1 list vaughan william classification

2 adverse effects of class I a

3 adverse effects of Amiodarone

4 precautions should be done to pt taking Amiodarone

نقاط مهمة mcq 🔴

▫️every anti arrhythmic drugs have pro arrhytmogenic actions

▫️procainamide has moderate dissociation rate - moderate conduction block + ganglion blockade

▫️drugs inhibit action of quinidine: (digoxin - beta bl. - verapamil) ↓AVN

▫️class I a used on broad sprectum
▫️class I b on ventricular arrhythmias
▫️class I c on SV arrhythmias
▫️class III (Amiadarone) broad spectrum (terminate PSVT)
▫️class IV (verapamil) SV arrhythmias (2nd choice if PSVT with asthma)

▫️lidocaine blocks inactivated Na channels in ischemic tissue

⭐▫️lidocaine best used after MI or cardiac surgery

▫️(case) pt developed arrhythmia after cardiac surgery which drug of choice?
lidocaine

▫️class 1b (lidocaine) not used orally and can cause convulsions

▫️class Ic marked (AVN) conduction block

▫️class 1c (propafenone) CI in bronchospasm

⭐▫️Amiodarone (مهمة كلها) K channel bl

⭐▫️(case) use beta bl. in exercise - thyrotoxicosis - pheochromocytoma

▫️Adenosine used in emergency - PSVT (drug of choice)
CI in asthma (case)

▫️(case) verapamil drug of choice in prophylaxis PSVT

▫️(case) beta bl. drug of choice in SV arrhythmia after MI

▫️(case) lidocaine drug of choice in ventricular arrhythmia from MI or from digitalis toxicity

▫️cinchonism is adverse affects of quinidine (tinnitus - loss of hearing - blurred vision)

ان شاء الله كملت جزئية السي في اس و كل النقاط المهمة تساعدكم في التاتوريال و الفاينل و ربي يوفقنا~ 🙏🏻

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