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Quinolones A/E GCAT (nitrogen bases) G it upsets C onfusion (↓GABA) C artilage damage A llergy A naphylaxis T endon of achilles rupture

Sulphonamides A/E SHREK 😂❤ بإضافة A = shreak S teven-Johnson reaction H emolysis R enal impairment (crystaluria) E nzyme inhibitor K ernicterus A llergy-rash A granulocytosis طبعا GIT upsets موجودة فيهن كلهن

MeTroniDAzole A/E M etallic taste T eratogenic D isulfiram like reaction A taxia

Tetracyclines A/E (mnemonics) STARS S uper infections T eeth and bone discoloration - deformity A bdominal upsets R enal impairment S kin photo sensitivity

⁉️⁉️ Warfarin 🆚 Heparin

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)

نقاط مهمة mcq 📌 ⭐▫️beta bl only used in HF (carvedilol - bisoprolol - metoprolol) مهمة ▫️nitroprusside not used in chronic only acute ▫️nitrates + hydralazin used together in HF ▫️ACEI prevent myocardial hypertrophy & remodeling & lower BP w/o reflex tachy ▫️captopril contain SH + rapid onset + short duration ▫️ACEI used in early MI with aspirin + fibrinolytics + beta bl ⭐▫️ACEI CI with bilateral renal artery stenosis (مهمة) Explain b/c GFR is maintained by VC of the efferent arteriole by AgII ❔because they ↓ Ang-II → ↓ VC of the efferent arterioles → ↓ GFP and ↓ GFR →lead to aggravation of renal failure in both kidneys and hyperkalemia ▫️diuretics give for fluid control → ↓pulmonary congestion + ↓peripheral ankle edema ⭐▫️diuretics 1st choice in refractory pulmonary edema ⭐▫️drugs that lower mortality: (ACEl ARBs - beta bl - spironolactone) ▫️digoxin inhibits Na/K ATPase ▫️digoxin increase contractility ▫️digoxin can cause arrhythmia ▫️digoxin cause vagal stim. at (therapeutic dose) & sympathetic stim. at (toxic dose) ⭐▫️it inhibits SAN →↓HR (indicate optimal digitalization) + AVN block and increase ERP (مهمة) ⭐▫️digoxin drug of choice for HF + AF ▫️it has narrow safety margin and give yellow green coloured vision ⭐▫️digibind is first choice for TTT of digitalis toxicity ▫️dopamine given in AHF + cardiogenic shock ▫️Milrinone - Inamrinone are inodilators inhibit phosphodiesterase III ⭐▫️Sacubitril-Valsartan are inhibitor of neprilysin enzyme ⭐▫️Ivabradine TTT stable angina + CHF with ejection fraction less than 35% ▫️it selectively inhibit hyperpolar. of cyclic nucleotide channel (funny channels) on SAN

نقاط مهمة mcq📍 ▫️nitrates used for relaxationof sm. ms. are venulodilators and in high dose arteriodilators ▫️nitrates decrease O2 demand → increase O2 supply ▫️ميزة ال nitrates : redistribution of bl. to subendocardial ischemic areas و ديما يستخدم في الacute ⭐️⭐️⭐️▫️ preperations of nitroglycerin + ISDN: 1 sublingual tablets → 1st choice for acute angina attack 2 transdermal patch → for long term prophylaxis & CHF 3 IV infusion → AHF⭐️ + unstable angina ⭐️▫️DHP (nifidipine) → act in vessels ⭐️▫️Non-DHP (verapamil + diltiazem)→ act on heart and vessels (SAN-AVN) ▫️DHP can cause reflex tachycardia + ankle edema ▫️ NON-DHP can cause heart block +constipation (verapamil) ▫️verapamil drug of choice in HOCM ⭐️ + used in migraine ▫️beta bl. drug of choice in classic angina prophylaxis

نقاط مهمة mcq❕ ▫️nitroprusside for emergencies ▫️thiazide for HTN with diabetes or osteoporosis (low dose) ▫️hydralazine inhibit calcium release from sarcoplasmic riticulum ▫️minoxidil + diazoxide are k channel openers ▫️CCBs increase renal bl. flow and decrease aldosterone and used in pt with asthma ▫️methyl dopa drug of choice in pregnancy ▫️labetolol in pre eclampsia ▫️beta bl. not used in diabetic pt. ▫️ARBs act on AT1 receptors only + prevent cough

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📌Metabolic Bone Ds 1- Paget ds 🔸⬆️ Osteoclast activity 🔸Male ⬆️50 yr 🔸activating mutations in RANK impppp 🔸imppp INactivating mutations in OPG↪️ juvenile paget ds 🔸Measles or RNA Vs may play a role 3 phases :imp 📍osteolytic stage↪️⬆️osteoclast activity نلقى الخليه فيها 100 nuclei 📍mixed st↪️prominant osteoblast / osteoprogenitor cs 📍osteosclerotic st ↪️ hallmark is mosiac pattern (puzzele like) of lamellar bone 2-Osteoporosis *due to osteopenia (reduce bone mass) 📍primary : most common form 🔸occurs in postmenopausal / elderly persons 📍secondary : ass with defined cause 3-Rickets & Osteomalacia ↪️⬇️ Vi D 4- HYPERparathyrodism ——————————————————————————— 📌Osteomyelitis always secondary to infecton سؤال شورت نوت جاي من قبل كيف توصل البكتيريا للعظم؟؟ 1- infection begins in metaphyseal end (congestion / oedema / exudate of neutrophils) 2- infection spread into endosteum causing periosteitis 3- reach subperiosteal space forming subperiosteal abscesses , penetrate the cortex creating draining skin sinus tract(cloaca) 4-erosion and infarction necrosis of cortex (sequestrum) formation of new bone surrounds sequestra (involucrum) 📍in vertebral pyogenic osteomyelitis infection begins from Disc (discitis) 📌Complications : septicemia/fracture/sq cell carcinoma/amyloidosis/acute bacterial arthritis A-Bone Forming Tumors: 1-Benign ➡️Osteoid Osteoma: 🔸⬇️2cm / femur or tibia / sever pain relieved by asprin 2- Benign Aggressive ➡️Osteoblastoma: 🔸⬆️2cm / vertebrae (laminae and pedicles) /pain unresponsive to asprin 📍Both are more common in 10-20yr. 📍malignant transformation is rare. 3-Malignant➡️ Osteosarcoma: Malignant mesenchymal tumor 🔸most common primary malignant T 🔸⬇️20yr / man 🔸elderly ass with paget ds 🔸arise in metaphyseal region (50% near the knee) 🔸RB mutatations 70% of sporadic osteosarcoma 🔸TP53 mutated in individuals with Li fraumeni syndrome 🔸painful enlarging mass 🔸20% of Pt➡️ lung metastasis 🔸Codman triangle is characteristic of osteosarcoma on radiographic image 🔸M/S: bizarre tumor giant cell B-Cartilage Forming Tumors: 📍characterized by formation of hyaline or myxoid cartilage 1-Osteochondroma: 🔸most common Benign bone tumor 🔸Involve metaphysis of long bone 🔸10-30yr age group / male⬆️ 🔸85% solitary & sporadic 🔸as a part of multiple hereditary exostosis syndrome (mutation in EXT1 or EXT2 gene) 2-Chondrosarcoma: malignant tumor C- Miscellaneous Tumors: 1-Giant cell tumors (osteoclastoma): 🔸benign but locally aggressive 🔸epiphyses of long bones(common around knee) 🔸20-40yr 🔸neoplastic cells are primitive osteoblast that express high level ( RANKL) 2-Ewings sarcooma: 🔸malignant characterized by primitive round cells without obvious differentiation second most common in children 🔸⬇️20yr / boy 🔸highly aggressive 🔸painful mass in diaphyses (especially femur) 🔸homer wright rosettes indicate neuroectodermal differentiation ——————————————- 📍secondary tumors :metastatic cancer to bone more common than primary 📍prostatic tumors are blastic. 📌Rh arthritis : 🔸70% Pt blood contain Anti -CCP Ab 🔸joint fusion (ankylosis) 🔸HLA DR4 🔸80% of individuals have autoantibodies to Fc portion of IgG (rh factor) 🔸all small joint except distal interphalangeal 📌Gout: 🔸 transient attack initiated by monosodium urate crystals 🔸Tophi are the pathognomonic Hallmark of gout 📌 osteoarthritis: 🔸over age 50yr (most imp factor) 🔸 chondrocytes die➡️ loose bodies 📍 osteophytes: mushroom shaped bony outgrown (Small bony projections at joint margin ) 📍 Ganglion & synovial cysts: 🔸 around joint of wrist , pea sized 🔸Myxoid degeneration of C.T #pathology Bone

🔹️Papillary type (90%) not associated with Early P53 mutation ♦️Renal BENIGN TUMORS ✔Adenoma ✔Angiomyolipoma ✔Oncocytoma 🔹️The most common type of renal cancer in patients who develop dialysis-associated cystic disease Papillary types #pathology Renal

♦️Chronic glomerulonephritis is one of the most common causes of chronic kidney disease in humans. ♦️ACUTE KIDNEY INJURY (AKI)most common cause of acute renal failure ♦️Diabetic glomerulosclerosis; It is a major cause of chronic renal disease 📌Azotemia is : elevation of blood urea nitrogen 📌Uermia : is Azotemia + Clinical manifestations 📑 Uermia:- 1. (acidosis) 2. ( anemia and bleeding diathesis ) 3. ( secondary hyperparathyrodism ) 4. Uremic gastroenteritis 5. Uremic fibrinous pericarditis 6. Peripheral neuropathy 🪢 Nephrotic Syndrome v.imp ✔Heavy proteinuria >3.5 g/day ✔.Hypoproteinemia ✔Severe edema ✔Hyperlipidemia ✔Lipiduria 🪢 Nephritic Syndrome v.imp ✔Grossly visible hematuria (with Casts) ✔Mild to moderate proteinuria ✔Azotemia (with Oliguria) ✔Edema ✔HTN 💡Primary Glomerular Diseases ✔Minimal change glomerular disease ✔Membranous glomerulonephritis ✔Membranoproliferativeglomerulonephritis ✔IgA nephropathy ✔Acute diffuse proliferative glomerulonephritis 🔸️Minimal Change Disease 1,sudden onset 2,Children ( 2 -6 years) 3, after (respiratory infection immunization.) 4,proteinuria highly selective, 5 Respond rapidly to corticosteroid therapy 🔸️Membranous glomerulonephritis 1,adults. 2 diffuse thickening 3,deposits along the subepithelialside 4,The basement membrane material protrudes between deposits as ‘spikes’ . 🏷these spikes thicken to produce domelike 5, non selective 🔸️Membranoproliferative GN ✔adults. ✔proliferation of mesangial cells & leukocytes. ✔The GBM is thickened ✔The GBM ↪↪"tram track" ▫️Type I MPGN) 🗯circulating immune complexes 🗯Subendothelial granular deposits of C3 & IgG ▫️Type II MPGN 🗯C3 nephritic factor (C3NeF) 🗯Intra-membranous deposit C3; deposit as irregular granular-linear worse prognosis 📌Diabetic glomerulosclerosis;. Nodular GS ( Kimmelsteil-Wilson disease); 🔹️Acute Proliferative (Poststreptococcal, Post infectious) ✔group A β-hemolytic streptococci ✔ in children 6 to 10 ✔hypercellularity ✔subepithelial (humps) ✔inflammatory manifestation ✔ urine appearing smoky brown( cola color 🥤 ) 🔹️Rapidly progressive GN (RPGN) ✔crescents ✔ distinct ruptures in the GBM ✔three groups ✔ GOOD PASTURE SYNDROME (anti-GBM disease)↪Cross reaction of the antibody with pulmonary capillary basement membranes results in lung hemorrhage, ✔ endothelial proliferation, and mesangia 📣Crescents are formed by proliferation of parietal cells 🔸️ may obliterate Bowman's space & compress the glomeruli tuft. 🔹️IgA nephropathy is the commonest cause of recurrent gross hematuria or microscopic hematuria & is the most common glomerular disease worldwide 🔹️IgA nephropathy 1. Children 2. 1-2 Days after Upper RTI or GI infection 3. mesengial proliferation 4. Mesengial Deposits 5. IgA granular deposits 🔹️Alport syndrome : defect in the collagen IV X-chromosome, males splitting and lamination of the lamina densa, often producing a distinctive basket-weave appearance .🥅 🎗Lupus nephritis ▫️Class I : lupus with no renal lesion 20% ▫️ Class II : mesangail “ proliferative “ nephritis 10% ▫️Class III : focal proliferative nephritis 10% ▫️Class IV : diffuse proliferative nephritis 50% ▫️Class V : membranous nephritis 📌Class III, IV, V may show: 🔸️Focal necrosis of capillary wall & PNL infiltrate 🔸️Fibrinoiddeposits 🔸️Capillary thrombi 🔸️Wire-loop thickening of capillary wallمهمه ! 🔸️Crescent formation 🪢 Renal stone Calcium oxalate (phosphate) 75% 🪢 Struvite --> (Mg, NH3. Ca, PO4) 🏷 sponge-like appearance ✔Childhood polycystic kidney disease ✔CYSTIC DISEASES OF RENAL MEDULLA 🏷 Swiss-Cheese appearance CYSTIC DISEASES OF RENAL MEDULLA 📑BladderUrothelial (transitional) tumors : 1) papilloma 2) Papillary urothelial neoplasms of low malignant potential(PUNLMP) 3) Low grade and high grade papillary urothelial cancers 4) Carcinoma in situ. 📌types of transitional cell carcinoma ; 🔹️Flat type (10%) associated with early P53 mutations #pathology Renal

⛔atrophy ⬇️ decrease in size of the cell(atrophic cell not' dead but if stimulation continues ↪die by apoptosis. increase autophagic vaculoes -residual bodies-lipofuscin pigment. (Brown atrophy) 🔹️mechanism of atrophy: decrease protein synthesis increase protein degradation (by ubiquitin-proteasome pathway) 🔹️causes of atrophy➡ 1/reduced workload(in case of cast) 2/inadequate nutrition 3/ageing 4/loss of innervation 5/decreed B.supply- 6/ loss endocrine stimulation. 🔹️types of atrophy: 🖇physiological atrophy➡ atrophy of ductus arteriosus -atrophy of thymus in adult- atrophy of gonads in old age. 🖇pathological atrophy 💥generalized atrophy ↪atrophy due to starvation-senile atrophy. 💥localized atrophy⬇️ 🔸️ischaemic atrophy 👉small atrophic kidney in atherosclerosis of renal .A. 🔸️disuse atrophy👉 wasting of ms of limb immobilised in cast. 🔸️neuropathic atrophy👉 poliomyelitis. 🔸️endocrine atrophy👉hypopituitarism lead to atrophy of thyroid ;adrenal & gonads. 🔸️pressure atrophy➡. erosion of spine by tumour in nerve root 🚫hypoplasia incomplete growth of organ 🚫agenesis complete failure of development of organe in embryogenesis. 🏷 hypertrophy----> increase in size of cell ✔✔hypertrophy without hyperplasia affect mainly perminant cell(heart-skeletal ms-nerve cell) 🔹️ physiological hypertrophy: ❗enlargment of uterus during pregnancy due to estrogen stimulation- ❗ breast enlargment during pregnancy ❗-skeletal .ms hypertrophy d/t increase workload. 🔹️pathological hypertrophy ❗hypertrophy of uterine smooth ms (effect of estrogen secreted by ovarian tumor) ❗lt.v.hypertrophy- ❗Rt.v.hypertrophy. 🏷 hyperplasia: increase in number of cells. Du to 1-hormonal stimulation 2-tissue loss(labile cells & stable cells). 🖇physiological 🔹️hormonal. proliferation of epith.of breast at puberty& during pregnancy d/t estrogen stimulation. 🔹️compensatory: occure when portion of tissue removed or diseased. e.g➡compensatory hyperplasia of remaining liver after hepatectomy. 🖇pathological 🔸️.adenomatous hyperplasia of endometrium after normal M.C d/t increased esreogen /progesterone ratio. 🔸️hyperplasia of thyroid follicle in 1ry hyperthyroidism. 🔸️hyperplasia associated with viral infection(HPV) 🔸️benign prostatic hyperplasia. 🔸️ important in wound healing. 🚫Estrogen: Hyperplasia and hypertrophy _▪︎ Normal : pregnancy (uterus and breast) 🏷Metaplasia:reversible changes ;ons cell type replaced by another cell type. 💭metaplasia fertile soil for malignant transformation التغير ح نسميه حسب نوع الcell الي طلعلي '! ⛔ types of metaplasia: 1-epithelial(reversible) 🔸️Seq.metaplasia. (replacement of columnar epith by st.seq.epith). . 🔸️columnar metaplasia barrett esophagus..(normal st.seq.epith.of lower esophagus replaced by gastric or intestinal type columnar epith 2-mesenchymal (irreversible) 🔸️fibroblast to chondroblast to produce cartilage. 🔸️fibroblast into osteoblast to produce bone.(myositis ossificans) كل ال adaptation ح تكون reversible إلا النوع هذا. 🚩 barrett esophagus: metaplasia >>> ✔adaptation ✔dysplasia >>precancer >> cancer. #pathology Adaptation

📌 fatty change (steatosis)➡️ most comm site (liver) 🖇 alcohol and diabetes associated with obesity are the most common causes of fatty change 🖇 fatty ch is reversible except in CCI4 poisoning 📍 Russell bodies :in multiple myloma (Ig accumulation in plasma Cs) 📍 Mallory bodies or alcoholic hyalin :inclusions composed of aggregated intermediate cytokeratin filaments 📍 Neurofibrillary tangle : in alzheimer ds is an aggregated protein inclusion contain microtubule associated proteins 📌 in poorly controlled DM glycogen accumulates in renal tubular epithelium , cardiac myocytes , β cells 📌 Carbon is the most comm exogenous pigment 📍 Anthracosis 📍 coal workers pneumoconiosis 📌Lipofuscin "wear & tear pigment" insoluble brownish yellow ➡️brown Atrophy . seen in ( heart , liver , brain ) as a function of age or atrophy ⚠️it is not injurious to the cell but imp as a marker of past free radical injury 📌 Melanin act as screen against harmful UV radiation 📌 Hemosiderin : golden yellow brown. can be identified by prussian blue dye . 📍 Hemosiderosis: acc of hemosiderin without organ damage 📍 hemochromatosis : extensive acc with tissue damage 🔸hereditary hemochromatosis caused by mutation in Hfe gene 📌 Dystrophic calcification 📍 normal Ca deposit in dead tissue 📍 mostly in area of necrosis 📌 Metastasis calcification 📍 Deposit Ca in living tissue because hypercalemia 📍Causes : 1_ hyperparathyrodism 2_ hyperthyroidism 3_ Vit D toxicity 4_ Addison disease 5_ sarcoidosis 6_ bone marrow tumor 7_ immobilization 8_ milk alliance syndrome #pathology Accumulation

Mech of apoptosis: 1_initiation phase 🔸Intrinsic(mitochondrial) pathway: caspase( 9) 🔸extrinsic (death receptor): caspase (8,10) 2_Execution phase: caspases (3,6,7) 🔹 Apoptosis inhibited by (BCL-2 /BCL-x) 🔹 Apoptosis activated by (Bax, Bak , Bid) 📌Several mechanisms are known or suspected in cellular aging:- • DNA damage • decreased cellular replication • aging of tumor suppressor gene • accumulation of metabolic damage • abnormal growth factors signaling #pathology cell injury

📌 causes of cell injury: • Hypoxia • Immune reaction • Micro organisms • Chemicals & drug • Aging • nutritional imbalance • physical agent • genetic agent 📌 Types of cell injury: • ischemic & Hypoxic cell injury •free radical mediated cell injury • chemical mediated cell injury • Cellular Aging 📌Increasing in cytosolic Ca :- • activation of cellular enzymes➡️ membrane damage, nuclear damage, ⬇️ ATP • ⬆️ mitochondrial permeability transition➡️ decrease in ATP 🧬 Injury to plasma membrane is the central factor in pathogenesis of irreversible cell injury 🧬Ca influx play an important role in membrane damge 📌 Effects of free radicals:- • lipid peroxidation of membranes • Nonperoxidative mitochondrial damage • DNA damage • protein oxidation 🧬 free radicals oxidation ➡️lipid, protein, DNA Termination of free radicals • spontaneous decay e.g(Superoxide) • enzymatic degradation :- 🔸SOD decomposes Superoxide into (H2O2 and O2) 🔸 glutathione peroxidase converts (OH into H2O2) 🔸 catalase decomposes H2O2 into(O2 & H2O) 🔸 Antioxidant block initiation or activation of free radicals 📌necrosis(cell death): 🔸️death of "group" of cell in living organism 🔸️*induction of necrosis due to pathological injury .(irreversible) 🔸️causes of necrosis 1-digestion of cell by enzyme. 2-denaturation of protein. 🔬Morphology of necrosis Under microscopic :- 1-changes in nucleus: 📌 pyknosis: condensation & shrinkage of DNA 📌 Karyorrhexis: fragmentation of pyknotic nuclear mass 📌 karyolysis: fading of basophila of chromatin. 2-changes in cytoplasm:- ⬆eosinophilia d/t loss of RNA cytoplasm become vaculated & appear moth-eaten 💭Gross morphology(types of necrosis) 🔸-coagulative necrosis(most comm ) --->preservation of basic outline of coagulated cell for some days. e.g:all hypoxic death cell except brain (myocardial infarction -infarction in solid organ). Wedge shaped infarct , yellow pale 🔸-liquefactive necrosis----> progressive catalysis of cell structure ;with loss of basic outline of cell. e.g:- focal bacterial infection -brain infraction 🔸-caseous necrosis--->appeare white cheesy caseation & granuloma. e.g:tuberculous infection 🔸-Fat necrosis----->2 type •enzymatic :in acute pancrititis . •traumatic: e.g trauma to subcutanous tissue of breast form breast lump(mistaken for malignancy) 🔸-fibrinoid necrosis ---->immunologic injuries to arteries & arterioles. e.g (polyarteritis nedosa) 🔸-gangrenous necrosis----> massive necrosis and putrefaction 🖇📍1-Dry gangrene (coagulative necrosis predominant) 🔸️in limbs 🔹️2ry to chronic Deprivation 🔹️ Artery occlusion 🔸️black -foul smell (( formation of hydrogen sulphide-)) 🔸️mummification & dryness . 🔸️line of demarcation & separation 🖇📍2-Wet gangrene 🔸️from sudden A &V occlusion 🔸️ strangulated hernia; intussusception; volvulus)- 🔸️no fluid evaboration- 🔸️presence of bacteria with rapid invasion of necrotic tissue 🔸️produce moist gangrene +toxaemia.(poor prognosis) e.g:- bed sores, diabetic foot, 🔹diabetic gangrene start as dry then due to bacterial butrefaction & edema turn in wet gangrene 🖇📍3-Gas gangrene: 🔸️ M.O causing cell necrosis & gangrene - formation of gas giving bad smell & crackling noises after palpitation - mortality high due to toxin & toxemia. 🖇📍4-infective gangrene 🔹️bacteria causing both necrosis & putrefaction •noma pudenda •cancrum oris •meleneys post operative synergistic gangrene. 📌Reversible cell injury structure and function can be regained after removal patholohic stimuli, can be recognized under microscope:- 🔸Plasma membrane changes 🔸 Mitochondrial changes (swelling) 🔸 Nuclear changes Such have clumping of n chromatin 🔸 swelling ER , detachment of ribosomes, dissociation of polysomes #pathology cell injury