اهم نقاط في محاضرات الجامعة
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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
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تجميعات دارتهن د. نوارة في نهاية المحاضرات
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Name the parasitic worms that cause biliary obstruction ?
سؤال حطاته د. نوارة
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هذينا اللي يجن في الامتحان اللي مشير عليهن بالاحمر شيت antiparasite
كلام د عبير
اقروهن توا ع السريع
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نأسف على بشاعة التصوير🤗
بس متوقع شورت نوت و قالت ضيفو ان الوارفر رخيص و يستخدمو فيه من زمان
🍓101
اسفين لبشاعة التصوير
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Forwarded from M A H A 🌼
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و هذا قال جايبه من قبل
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📍Drugs are given locally and systemic circulation terminate its action.
📍At physiological pH, the charged form LAs will be greater than the uncharged (pKa of most LAs 7.5-9)
📍Local anesthetics are less effective when they are injected into infected tissues
because the low extracellular pH favors the charged form (ionized).
📍All local anesthetics, except mepivacaine prilocaine and cocaine are vasodilators (MPC)v imppp
📌That’s why a vasoconstrictor (adrenaline) is added to LA to ⬆️ the duration and
⬇️ systemic absorption and systemic toxicity.

📍Redistribution is the major determinant of anesthesia duration IMP
📍LA with lower pKa has a rapid onset
📍higher solubility makes LA potent and with longer duration
📍Ester LAs have lesser duration because they are prone to hydrolysis (pseudocholinesterase).
📍Amide LAs metabolized in liver
📍Allergy is more common with ester than with amide و لو صارت مع نوع واحد معناها حتى الباقيات نفس الشي لان كلهن فيهن
(PABA)
📍Systemic absorption is determined by dosage, injection site, blood flow, tissue binding and chemistry of LA
📌Treatment for LAST include IMP
1- Antiseizure
2- Airway management.
3- Cardiopulmonary support.
4- Administration of 20% lipid emulsion infusion.

Lidocaine: Unfortunately,its use in spinal anesthesia is associated with TNS
🦷Articaine : for dental anesthesia,more effective and possibly safer than lidocaine

🍫Benzocaine:topical anesthesia, lead to (methemoglobinemia مع خوه من امه (الامايد) Prilocaine)

Bupivacaine:cardiotoxicity ❤️‍🩹
Low concentration is used to attain prolonged peripheral anesthesia and
analgesia for postoperative pain and labor pain.

may be used in spinal anesthesia
متاعين الفارما ماعجبهمش الوضع دارو واحد اخرى
Levobupivacaine: less cardiotoxicity,It is less potent🤦🏻‍♀️ but has longer duration of action.

Chloroprocaine: without the risk of TNS
rapidly hydrolyzed so less risk of systemic toxicity and less fetal exposure.
It is not preferred as epidural anesthetic because of its neurologic injury🤷🏻‍♀️

Mepivacaine:it causes vasoconstriction, When used for spinal anesthesia, it has less incidence of TNS.
Slowly metabolized by fetus🚫pregnancy

Prilocaine:highest clearance among amide anesthetics🧹
Its metabolites lead to methemoglobinemia قصة خوه يلي مبدري👆🏼
It is used for spinal anesthesia with less risk of TNS than lidocaine

Cocaine:restricted to topical anesthesia
It has intense vasoconstriction which help to reduce bleeding😍, its use
is avoided because it is abuse substance.🥲

EMLA:
lidocaine + prilocaine
هن ال2 فيهن حرف L
commonly used in children to permit the venipuncture for I/V catheter

افطنو لقصة يلي يديرن في MPC↩️VC
قال الدكتور تلقى 2 i معناها amide
كان 1 معناها ايستر
LA💉
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في IDA كله ⬇️ ماعدا
TOTAL IRON BINDING CAPACITY⬆️⬆️
ك PROPHYLACTIC نعطي
30-60mg/d elemental iron
ك ttt نعطي
200-400 mg/d elemental iron


هذينا فيهن 12-33% من elemental iron⬅️
oral:ferrous (gluc,sul,fum,)
ferric ammonium citrate


New Agents: Expensive
Polysaccharide-Iron Complex, Carbonyl Iron, Heme iron polypeptide(100%elemental iron)


Parenteral Iron therapy:
Iron Dextran

New agents Nanoparticles:
Ferric Carboxymaltose & Ferumoxytol (Only I/V)
impppppp


📍Advantages of Total Dose Infusion (TDI):
1)Avoids non-compliance of the patient.
2)Avoids unpleasant effects of IMI.
3)Allows delivery of the entire dose of iron necessary to correction deficiency
at one time
هذه قالت عليها مهمه⬆️

Acute Iron Toxicity:
Rx:➡️Deferoxamine.........الانتي دوت

chronic Iron Toxicity:
Rx:➡️phlebotomy
Deferoxamine ومعاه 2 اخرى يبدن بنفس الحروف


B12 deficiency anemia :
كله
نازل ماعدا MCV
Schilling test:
1. Testing for intrinsic factor antibodies
2.Testing for elevated homocysteine and methylmalonic acid levels.

Neurological manifestations


Rx: (Parenteral): Cyanocobalamin / Hydroxocobalamin
Oral VitB12: Cyanocobalamin
Hydroxocobalamin is preferred because:
1. More slowly absorbed.
2. More bound to plasma proteins.
3. Slowly excreted.
4. More sustained rise in serum cobalamin

given I/M or deep subcutaneous injections

Folic acid tablets should be prescribed with Vit B12 treatment, but folic acid cannot be
used before a confirmed diagnosis of anemia as may worse neurological symptoms

•Neomycin, colchicine, and Antiepileptic drugs (reduce the absorption of B12).
•Pernicious anemia: Vitamin B12 is given for life by IMI.



Folic acid deficiency anemia:
causes
:
Drugs: Phenytoin, Phenobarbitone & Oral contraceptives.Methotrexate, Trimethoprim Pyrimethamine (Treated by folinic acid)

Folate deficiency develops more rapidly than vitamin B12 deficiency?
The daily requirement is high and the body store of folate is low.
without neurological manifestation

Rx: Folic acid tablets
Therapeutic uses:
.Pregnant women.(To prevent neural tubal defect in newborns)
.Patients with liver disease &with hemolytic anemia.
.With Anticonvulsant drugs.
.Patients on dialysis (as Folic acid is removed frequently).


❖Erythropoietin (epoetin alfa & beta): are effective in treatment of anemia due to end-stage renal failure

❖Darbepoetin is long-acting erythropoietin
❖ Granulocyte colony-stimulating factor (G-CSF )(Filgrastim): is used in
cases of neutropenia
❖ Interleukin-11, Romiplostim are used in cases of thrombocytopenia

❖Agents used to treat sickle cell disease
:
Hydroxyurea is an oral ribonucleotide reductase inhibitor
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