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45 Cards in this Set
- Front
- Back
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lesion to this hypothalamic nuclei will cause pt to turn fat
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Ventromedial
-eat → stim incr Leptin → stimulate Ventromedial nucleus of thalamus → signals "Satiety" (full) |
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lesion to this hypothalamic nuclei will cause pt to turn skinny
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Lateral
-eat → stim incr Leptin → inhibit Lateral area → turn off "hunger" signal -b/c Lateral area signal's hunger, and when eat, incr Leptin that inhibits this |
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lesion to this hypothalamic nuclei will throw off circadian rhythm
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Suprachiasmatic Nucleus
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this hypothalamic nucleus
regulates parasympathetic NS |
anterior & preoptic nuclei
Anterior = Cool off ("A/C" → Anterior Cooling) -cools by stim'ing PNS that → sweating, etc |
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this hypothalamic nucleus regulates sympathetic NS
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Posterior
-posterior regulates SNS and thus can incr body temp |
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hypothalamic nucleus to make ADH vs Oxytocin
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ADH → Supraoptic nucleus
Oxytocin → Paraventricular nucleus |
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hypothal nucleus to get retina input
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-suprachiasmatic nucleus (to reg circadian rhythm)
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lesion to this hypothal nucleus → Diabetes Insipidus
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Supraoptic Nucleus
-this makes ADH vs Paraventricular makes Oxytocin |
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motor control on which side of body would be affected by lesion of 1 side of Cerebellum vs 1 side of Cortical cerebrum
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Cerebellar lesion → Ipsilateral side
Cerebrum → Contralateral motor/sensory *why?* -Cerebellum → Contralateral Thalamus → cortex → cortical spinal tract → body is Contralateral to Cortex |
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ataxia/dystaxia of legs (even if trunk is supported) → broad-based, staggering gait, what is this?
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Anterior Lobe (Anterior Vermis) syndrome
-chronic EtOH abuse → Thiamine defic → degen of cerebellar cortex (starts @ anterior lobe) |
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-lack of voluntary mvmnts
-delays in initiating mvmnts & trouble stopping -dysmetria -intention tremor |
cerebrocerebellum (lateral hemisphere) lesion
dysmetria = impaired ability to control distance, speed, power of mvmnt |
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brain lesion causing:
-disequilibrium, abnrl eye mvmnts (cerebellar nystagmus esp when looking to side of lesion) |
Vestibulocerebellum (flocculonoduar lobe)
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adult brain tumor, pseudopalisading areas of necrosis & hemorrhage
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Glioblastoma (grade IV astrocytoma)
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kid brain tumor → polycythemia
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Hemangioblastoma
-can produce EPO → polycythemia *a/w von Hippel-Lindau disease |
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brain tumor a/w Neurofibromatosis II
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Schwannoma
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cell type in brain tumor a/w von Hipple-Lindau syndrome
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-foamy cells w/ high vascularity
Hemangioblastoma |
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brain tumor w/ foamy cells, high vascularity
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Hemangioblastoma
**a/w von Hippel-Lindau disease** |
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brain tumor → galactorrhea, amenorrhea, anovulation
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Pituitary Adenoma
-these are Sx of hyperPRL **in a M, hyperPRL would → impotence** |
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brain tumor w/ areas of dystrophic calcification
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Meningioma
-"areas of dystrophic calcification" = Psammoma bodies |
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brain tumor w/ fried-egg appearance
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Oligodendroglioma
-oligodentrocytes have the 'fried-egg' appearance |
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brain tumor w/ pervascular pseudorosettes
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Ependymoma "glioma"
-kids -GFAP(+) |
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brain tumor w/ bitemporal hemianopia
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Pituitary Adenoma, Craniopharyngioma
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worst brain tumor prognosis
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Glioblastoma
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CD surface marker:
displayed only by helper T cells |
CD4
-Th1, CD4: secrete IFNγ (activate macrophages, stim more Th1's, inhibit Th2), & IL-2 (stim CD8 cells (makes sense since Th1 work w/ CD8) -Th2, CD4: secrete IL-4, -5, -10, and help B cells make Ab CD8 = cytotoxic Th -kill virus infected cells (incl those w/o MHC expressed), neoplastic, donor grafts |
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CD surface marker:
-displayed by cytotoxic T cells (& suppressor T cells) |
CD8
CD8 = cytotoxic -kill virus infected cells (incl those w/o MHC expressed), neoplastic, donor grafts CD4 is Thelper cells -Th1, CD4: secrete IFNγ (activate macrophages, stim more Th1's, inhibit Th2), & IL-2 (stim CD8 cells (makes sense since Th1 work w/ CD8) -Th2, CD4: secrete IL-4, -5, -10, and help B cells make Ab |
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CD surface marker:
found on ALL T cells |
CD3 and CD2
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CD surface marker:
used to ID B cells |
CD19, CD20, CD21
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CD surface marker:
inhibits compliment C9 binding |
CD55, CD59
-defic in Paroxysmal Nocturnal Hemoglobinuria |
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CD surface marker:
endotoxin-R on macrophages |
CD14
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what cytokine:
promotes B cell growth/differentiation |
IL-4, IL-5
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what cytokine:
growth & activation of eosinophils |
IL-5
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what cytokine:
secreted by Th & activates macrophages |
IFNγ
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what cytokine:
enhances synthesis of IgE & IgG |
IL-4
"Hot T-Bone stEAk" = 1, 2, 3, 4, 5 as in: H, 1: IL-1 is pyrogen (w/ IL-6 & TNF-alpha) T, 2: IL-2 stim's T cells B, 3: IL-3 stim's B cells E, 4: IL-4 stim's IgE & IgG A, 5: IL-5 stim's IgA & eosinophils |
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what cytokine:
enhances synth of IgA & eosinophils |
IL-5
"Hot T-Bone stEAk" 1 = pyrogen w/ TNF-alpha & IL-6 2 = stim T cell 3 = stim B cell 4 = IgE & IgG 5 = IgA & eosinophils |
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kid w/ recurrent lung infections & granulomatous lesions...what process is deficient?
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Chronic Granulomatous Disease
-lack of NADPH oxidase → can't make H2O2, superoxide dismutase **(-) Nitoblue tetrazolium test |
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what structure gives rise to missing structure in kid w/ multiple viral & fungal infections, PE shows tetany
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DiGeorge syndrome
-failure of 3rd & 4th pharyngeal pouches → no Thymus & Parathyroid development → no thymic shadow on CXR |
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kid w/ repeated Staph abscesses; neutrophils don't respond to chemotactic stimuli
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Hyper-IgE syndrome "Job's syndrome"
-Th cells DON'T MAKE IFNγ → no neutrophil chemotaxis coarse Facies, cold staph Abscesses, retained primary Teeth, hyperimmunoglob E, Derm prob's (eczema) = FATED |
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recurrent bacterial infections after 6 mo
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Bruton's X-linked agammaglobulinemia
-defective Tyr Kinase gene → low levels of all Ig's |
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repeated viral, fungal, protozoal infections, heart problems
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DiGeorge syndrome
-failure of 3rd & 4th pharyngeal pouch develop |
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thrombocytopenic purpura, infections, derm problems, recurrent pyogenic infections
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Wiskott Aldrich
-X linked -progressive deletion of B & T cells |
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low IgA, cerebellar ataxia, poor smooth pursuit of target w/ eyes, small dilated blood vessels near skin surface
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Ataxia-Telangiectasia
"small dilated blood vessel near skin surface" = Telangiectasia -IgA defic -incr risk lymphoma & leukemia -incr AFP in kid > 8mo |
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risk if IL-12-R deficient, and why?
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defic IL-12-R → decr Th1 response → decr IFNγ → disseminated mycobacterial infections
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defective IL-2-R
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Severe Combined Immunodeficiency
-can also be caused by: Adenosine Deaminase defic, no MHC-II synth -recurrent viral, bacterial, fungal, and protozoal infections |
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recurrent bactieral and fungal infections, delayed separation of umbilicus
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Leukocyte Adhesion defic
-defect in LFA-1 integrin (CD18) -bad diapedesis & migration |
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giant cytoplasmic granules in PMNs
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Chediak-Higashi Disease
-defective LYST gene (for lysosomal transport) → defective phagocyte lysosome triad: partial albinism, recurrent respiratory tract & skin infections, neurologic disorders |
