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Pathology: Disaggregation of Granular and Fibrillar Elements of The Nucleus 5-HETE, N-Formylated Peptides (Formyl-Methyl)
Pathology: Disaggregation of Granular and Fibrillar Elements of The Nucleus 5-HETE, N-Formylated Peptides (Formyl-Methyl)
Pathology: Disaggregation of Granular and Fibrillar Elements of The Nucleus 5-HETE, N-Formylated Peptides (Formyl-Methyl)
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2) Significant variation in the shape and size of cells & nuclei
3) Large nuclei (high nucleus to cytoplasmic ratio) with deep staining & large
nucleoli
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❖ Chronic lead poisoning:
• Causes and risk factors for Chronic lead poisoning:
- Due to exposure & contct with dust, paint in homes built before 1978
- Risk factors include development of symptoms after new construction, living in
older homes.
• Diagnosis of Chronic lead poisoning:
- Screening should be done in children at high risk due to irreversible
neurological compromise.
- Measure blood lead level, urine δ amino-levulinic acid → both are elevated
• Mechanism & clinical picture of Chronic lead poisoning:
- Lead bind to sulfhydryl group on protein → replace calcium in cells → ↓↓
enzymes involve in heme synthesis.
- Neurological → cognitive impairment
- Gastrointestinal → constipation & pain
- Renal → interstitial nephritis
- Hematological → anemia
❖ Components of Lynsch syndrome: endometrial, ovarian colon
❖ Components of familial retinoblastoma: bilateral retinoblastoma + osteosarcoma
❖ Components of Li-Frumeni syndrome:
- consists of (sarcoma, Leukemia), (breast, brain) and adrenal cancer
- due to 2 hit hypothesis of TP53 tumor suppressor gene
❖ Mechanism of hereditary retinoblastoma:
- Rb gene (on chromosome 13) is tumor suppressor gene, one gene mutation is
inherited and the other allele must be mutated sporadically.
- 40% of retinoblastoma are hereditary (not always bilaterally)
- Osteosarcoma occur most commonly occur among the familial retinoblastoma
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❖ Commonest sources of brain metastasis : lung, RCC, melanoma
❖ Metaplasia :
o Squamous metaplasia in the bronchi → replacement of goblet cells by stratified
epithelium → loss of muco-ciliary mechanism ➔ ↑↑ respiratory infection
o Coloumanr → squamous metaplasia (as in bronchi) is more common than
Squamous → coloumnar metaplasia (Barrett’s esophagus
❖ Meniere disease:
o Caused by endolymph hydrops > ↑↑ pressure & volume due to ↓↓ resorption
o Classic triad :
1) low frequency tinnitus + sensation of fullness
2) Vertigo
3) sensory neural hearing loss → worsen over time
• DD with BPPV → no hearing symptoms only vertigo
❖ Keloid :
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• Pathogenesis: normally, in proliferative phase, contraction of actin filaments in
myofibroblasts occurs to approximate wound edges. TGF-β help differentiation of
fibroblast into myofibroblasts & this process should diminish after healing
• In keloid, unregulated ↑↑ in TGF-β → extension beyond borders of scar
• It occur after minor trauma & major trauma, may be painful, pruritic, raised
• L/M of keloid show haphazardly arranged of thick, pink collagen bundles
❖ Bone metastasis :
• Cancers of the pelvis (including prostate) spread to the LSS via vertebral
venous plexus which run up the entire spinal column by valveless system → to
regulate Intra cranial pressure.
❖ Wound healing :
• Matrix metalloproteinase (MMP) → most important in wound healing lead
to myofibroblast accumulation & scar tissue remodeling
• Myofibroblast → initiate wound contraction during healing by secondary
intention
• Excessive MMPs activity & firoblast → lead to excessive wound contraction &
deformity ➔ most commonly at palms & sole, serious burn, anterior thorax
❖ Genes responsible for Lynch syndrome : MSH2, MLH1, MSH6, PMS2.
Inactivation of tumor suppressor gene with deletion of the remaining normal allele
→ loss of heterozygosity → malignancy (inherit one mutation & loss of the other
during adulthood)
❖ McCune Albright syndrome :
• Mosaic somatic mutation of GNAS gene → stimulate α subunit of G-protein →
persistant stimulation of Gs coupled receptors ….≫≫≫≫≫ uilateral
• Fibroblast → ↑↑ IL-6 → ↑↑ osteoclast → fibrous dysplasia
• Melanocyte → Café au lait patches large, irregular usually unilateral
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• CRH & ACTH → Cushing syndrome
• TRH & TSH → thyrotoxicosis
• GHRH → acromegaly
• GnRH → precociuous puberty
❖ Cardiac ischemia :
o Ischemia of cardiac myocyte → STOP of Na/K ATPase, Sarcoplasmic reticulum
Ca+ ATPase → intra-cellular accumulation of Na, Ca+ & intra-mitochondrial
accumulation of Ca+ ➔➔➔ this leads to swelling of the myocyte & cessation of
muscle contraction.
❖ Giant cell arteritis:
• It is the most common systemic vasculitis in US
• Biopsy : intimal thickening, elastic lamina fragmentation, mutilnucleted giant
cells
• Optic complications: ischemic optic neuropathy → ophthalmic artery occlusion,
amaurosis fugax, CRA occlusion, cereberal infarction
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❖ PAS (periodic acid Schiff) staining:
• Mechanism of PAS (periodic acid Schiff) staining: oxidize carbo bonds →
brilliant magenta color upon reaction with fuschin-sulfurous acid
• Uses of PAS (periodic acid Schiff) staining: highlighting polysaccharides of
the fungal cell wall, muco-substances secreted by epithelia, BM (glycogen,
glycoprotein, glycolipid, mucin)
• Uses of Diastase with PAS staining: they are used together to determine
glycogen (diastase break glycogen → giving negative reaction), so in tissues with
glycogen → pink on PAS & negative in diastase
• Chracters of whipple disease staining: PAS positive (as they contain
glycoprotein present in cell wall of the bacteria), Diastase-resistance (to confirm
that the stain is not glycogen, but glycoprotein)
• How can demsontrate neutral lipid by histology: Nile red, sudan black (can be
used in frozen sections)
❖ Describe the liver biopsy findings in Sarcoidosis:
- Scattered granulomas affecting the portal triad is usually affected in 75% of cases
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