test #28 4.19 Flashcards
examples of delayed-type hypersensitivity reactions
(1) contact dermatitis
(2) granulomatous inflammation
(3) tuberculin skin test
(4) candida extract skin reaction
delayed-type HSR mediated by..
T-lymphocytes (not Ab or complement).
reaction takes 1-2 days, bc antigen taken up by dendritic cells, present to CD4+ cells on MHC II.
Th1 cells secrete IFN-gamma, recruit & stimulate macrophages –> monocytic infiltrate.
[also occurs when ‘walling off’ TV
increased WBC post-corticosteroids
falsely elevated. due to demargination (release from vascular walls) of cells
2 disorders of mast cells
urticaria pigmentosum. systemic mastocytosis
what two factors drive angiogenesis
VEGF and FGF
- vascular ENDOTHELIAL growth factor
- fibroblast growth factor
VEGF: angiogenesis in variety of tissues: normal, chronically inflammed, healing, neoplastic. increases endothelial cell motility and proliferation –> new capillaries.
FGF-2: made by many cells. significantly involved in (1) promotion of endothelial cell proliferation, migration, and differentiation. also: impt in (2) embryogenesis (stimulating angioblast production)
[FGF: angiogenesis, embryonic develoment, hematopoiesis, wound repair]
somatomedin C
IGF-1
synthesized by growth-hormone influenced hepatocytes. stimulate cell growth and multiplication.
barrier to angiogenesis
laminin in basement membranes
non-viral-dependent nucleotides analogues
cidofovir (activated by cellular kinase) & tenofovir
rx for thymidine kinase-deficient (acyclovir-resistant) varicella?
fosacarnet: (PYROPHOSPHATE analog viral DNA polymerase inhibitor)
cidofovir: broad spectrum NUCLEOTIDE. analogue of cytidine monophosphate (activated by CELLULAR kinase)
factitious disorder vs. malingering
both CONSCIOUSLY creates symptoms.
factitious: for 1’ gain (sick role/medical attn)
malingering: for 2’ gain (avoid work, compensation)
munchausen syndrome
chronic factitious disorder
conversion disorder
unconscious; somatic.
post-stressor.
sudden neurological symptoms (loss of sensory/motor) with NO physical evidence.
somatic disorder vs. factitious & malingering
somatic disorder syndromes (i.e. conversion, hypochondriaisis, somatization) are UNCONSCIOUS
factitious & malingering: CONSCIOUS
somatization disorder (vs. conversion disorder)
somatoform disorder, several symptoms
usu begins <30 y/o. impact social/occupation.
4 pain
2 GI
1 sexual
1 neuro
with no physical exam / imaging evidence
(differs from conversion, which has specific NEURO and POST-STRESSOR)
hypochondriasis
somatoform disorder
preoccupation/fear of having serious illness despite medical evaluation & assurance.
often, mistinterpretation of normal bodily symptoms (gas = colon cancer). associated w/ Dr. shopping
body dysmorphic disorder
think body is pathologically flawed, when in fact, it is not.
chromosome 3p deletion
VHL
von-Hippel Lindau
autosomal DOMINANT.
cerebellar hemangioblastomas, clear cell renal carcinoma, and pheochromocytoma.
RCC develops in 40% of patients.
tumor supressor
cerebellar hemangioblastoma, clear cell renal carcinoma, pheochromocytoma
VHL (tumor supressor chr. 3)
location of RB
chr. 13
osteosarcoma and retinoblastoma
location of NF-1
chr. 17
WT-1 location
chr. 11
location of chemoreceptor trigger zone (area postrema)
dorsal surface of medulla, caudal end of fourth ventricle.
adhesion molecules
integrin, cadherin, selectin, Ig superfamily members
laminins bind to
collagen, fibronectin, laminin in ECM
fibronectin
large glycoproteins produced by fibroblasts & some epithelial cells. binds to integrin, matrix collagen, glycosaminoglycans. mediations cell adhesion
heparan sulfate
proteoglycan component of ECM.
associated w/ reticular fibers and basal laminae. helps w/ endothelial cell attachment to BM.
does not bind to cell surface integrins.
hyaluronic acid
glucuronic-acid containing glycosaminoglycan in ECM.
contributes to water retention in ECM -> lubricant properties. viscous, gel-like consistency.
elastic fibers
core of elastin protein surrounded by fibrillin
keratan sulfate
galactose-containing glycosaminoglycan. role in maintaining type I collagen fibril organization in cornea.
aromatase deficiency
present early:
- mom virilization (androgens)
female:
- ambiguous/male genitalia
- primary amenorrhea & tall (no estrogen to fuse epiphyseal plate
male
- tall w/ osteoperosis
aromatase rxns (2)
androstenedione -> estrone
testosterone -> estrogen
aromatase deficiency vs. 21-b hydroxylase deficiency in girls
aromatase deficiency
- has mom virilization
- no hypotension w/ salt wasting & hyperkalemia
auscultation site determined by..
position closest to where sound waves reverberate. NOT at position of valve
glomerular splitting of basement membrane (2)
MPGN II and Alport syndrome
Alport syndrome
triad:
1. glomerulonephritis
2. sensorineural deafness
3. eye problems
mutation in alpha-side chain of collagen type IV.
thinning and splitting of basement membrane
X-linked dominant.
nasal mucosal ulcerations “saddle nose” w/ glomerulonephritis
granulomatosis w/ polyangiitis (wegner’s)
HSP 4 signs
IgA / C3 deposits everywhere 1. palpable purpura 2. abdominal pain 3. arthralgia usu self-limiting, but can get.. 4. glomerulonephritis & end-stage renal failure
usu post-infectious
drugs w/ negative chronotropic effects
(1) b-blockers
(2) non-DHP calcium blockers
(3) digoxin (independent vagal effects)
(4) amiodarone
(5) sotalol (class III w/ b-blocking effects)
(6) cholinergic agonists
what cell type exerts master control over iron metabolism?
HEPCIDIN, made by liver parenchymal cells
fate of Fe2+ in GI system
absorbed via DMT-1 channel in duodenum, bind to intracellular FERRITIN..
(1) stay in enterocyte, and pass in stool when sloughed off
(2) exist basolaterally via FERROPORTIN -> bind to transferrin in blood -> taken up by cells via transferrin receptor
PATH determined by hepcidin!
hepcidin
acute phase reactant. binds to ferroportin in enterocytes & macrophages & degrades it.
BLOCKS release of Fe2+. prevents iron overload.
anemia of chronic disease
increased levels of hepcidin (from liver) down regulate ferroportin. trap Fe2+ in macrophages and enterocytes.
filtered load =
GFR x Px
excretion rate =
V x Ux
RPF estimated w/
PAH clearance – fully cleared
GFR estimated w/
creatinine clearance (similar to inulin)
normal filtration fraction
20% (GFR/RPF)
when does glucose begin to appear in urine? when are glucose transporters maximally saturated?
- begin at 200mg/dL
- saturated at 375mg/dl
normal GFR
100ml/min
180L/day
when GFR is normal (100ml/min), large decreases in GFR, causes ___ in serum creatinine
small increases in serum creatinine
when GFR is very low (<60ml/min), small changes in GFR causes ___ in serum creatinine
LARGE increases in serum creatinine
serum creatinine can be normal after loss of how much GFR
even after 50% loss!