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Core I


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pseudohypoparathyroidism (type Ia)
gene mut in G alpha; loss of GTPase activity or accelerated Guanine Nucleotide Exchange; since in body, the G protein is deactivated
mut. in Ga causing loss of GTPase activity or accelerated Guanine nucleotide exchange, testes are cooler so protein dn denature
cholera toxin
modifies a subunit on Gs that's critical for GTPase activity so STUCK ON
pertussis toxin
Gi protein, STUCK OFF
B1--PKA phosphorylates VSCC
+ve inotropic +ve chronotropic relax sm. m., secretion, steroidogenesis, hungry state
B1 (heart) B2 (bronchiole)
B1 E=NE B2 E>>>NE
Evidence Cycle
1. asking foreground Q 2. Accessing best evidence 3. Appraising evidence critically 4. Applying evidence to pt sit 5. Assessing performance of plan
Asking Foreground Q
1. Pt Popn 2. Intervention 3. Comparison or Control 4. Outcome 5. Methods
Critically Appraise Article
Is the study valid? (must face diagnostic uncertainty, blind v. gold standard) What are the Results? How can be applied to my situation?
Congenital Adrenal Hyperplasia (CAH)
Genetic defect in cortisol production -> elevated ACTH -> adrenal cortical hyperplasia -> intrauterine production of androgens -> masculinization of XX fetuses (female pseudohermaphrodite)
Benign Prostatic Hypertrophy (BPH)
Western⬝ male -> nodular hyperplasia -> urinary frequency, urgency, retention, UT infections, increased gland/stroma ratio
Squamous metaplasia of bronchial epithelium
Barrettʼs metaplasia of esophagus
⬢ Squamous -> columnar epithelia of intestinal type ⬢ Chronic reflux esophagitis ⬢ Increased risk of cancer
Reversible subcellular response to injury
Cell may recover if stimulus withdrawn – “Hydropic change” due to cell swelling – “Fatty change” due to altered fat metabolism – ER, mitochondrial swelling – Membrane blebs – Clumped chromatin
– Cell cannot recover if stimulus withdrawn – More swelling with breaks and ribosome detachment – Myelin figures (concentrically swirled membranes) – Fragmented chromatin • Pyknosis - condensation • Karyorrhexis - fragmentation • Karyolysis - dissolution
cell gets bigger karyolysis corrupt plasma membrane inflamm. c. engulf necrotic cell corpose tz destroyed always abN
cell gets smaller nucleosome fragments plasma memb intact no inflamm, corpse may be engulfed by adj c. tz intact N or abN
Coagulative Necrosis
ischemia, toxic exposure w/o redundant Blood Supply pale&wedge shaped dual blood supply-wedge shaped hemorrhagic
Caseous Necrosis
TB, leprosy, myobacterial
Fat necrosis
pancreatic injury release lipases with saponified Ca salts and FA
Fibrinoid Necrosis
med. arteries following vasculitis
metastatic v. dystrophic calcification
hypercalcemia (metastatic), necrosis w/o abN serum Ca++ (dystrophic)
-oncogene block cell death -overexpressed in follicular lymphoma
activator, executioner, inflammatory
oncogene (promote growth) overexpressed in follicular lymphoma
prevent death in nutrient deprivation/accelerate cell death in stress
RIP1 PARP1 (normally promote DNA stability)
a1-antitrypsin mutation
defect in protein folding reduce solubility and degradation resulting in accumulation in intracellular aggregates
Mallory Bodies; Hyaline Glomerulosclerosis, hyaline in lung
aggregated intermed. filament protein, fibrin and plasmaexcess glomerular bm
switches TNF induced cell death from Apoptosis to Necrosis
Niemann Pick Anthracotic Pigment
lackof enzyme ingestion of undigestible material
Insulin(IR, P13K, PDK1, AKT)--|FOXO1-->longevity, antiaging
PTEN--longevity/antiaging SIRT1-longevity/antiaging
NAD-dependent deacetylates histones (Acetylated histones-Active genes) Sir2 starved mice, longevity, Resveratrol-activates Sir2
Huntington-Gilford Progeria
deletion mutation in lamin A, an intermediate filament of nuclear envelope
Werner Syndrome
-mut DNA helicase WRN of the RecQ family -WRN-dna recomb repair/telomere maintenance -premature aging
Telomerase deficiency
hayflick limit (#celldivisions) BM failure and pulmonary fibrosis
reg. insulin/FOXO, longevity reg. FGF23-->Phosphate reabsorption, leading to phosphate toxicity
--self-priming strand displacement --Small, linear ssDNA • Non-enveloped • Parvoviruses DNA information is insufficient,require helper virus or rapidly dividing cells. – Dependovirus (Adeno-associated virus (AAV)) Req. co-infection with a helper virus (adenovirus or herpesvirus) • No disease in humans • Common viral vector used in gene therapy – Parvovirus B19: Requires dividing cells for replication • Erythema infectiosum (childhood illness, fever, rash) • Aplastic anemia (sickle cell disease, hemolytic anemia) • Fetal loss
Non-enveloped, icosahedral symmetry, dsDNA circular genome (5-8 kb). • Viral genome can persist in episomal [(papilloma (pa) or integrated (polyoma (po)]. • Replication/assembly in nucleus, virions released via cell lysis • Narrow host range – Papilloma replication only in differentiating cells • Multiple splicing events • Multiple promoters
Strand displacement
do not require RNA primer --adenovirus --parvovirus --pox virus
require RNA primer -papovirus -papilloma -polyomavirus

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