facts from sim test 4.30 Flashcards
venous drainage to anal canal above/below the pectinate line
above: superior rectal vein -> inferior mesenteric -> portal circulation
below: middle & inferior rectal vein -> internal pudendal -> inferior mesenteric -> internal iliac -> IVC
most likely site for external hemorrhoids
posterior canal – poor perfusion
coarctation murmur
systolic, best auscultated in interscapular region
due to turbulent flow through narrow lumen
braf v600e mutation in? rx?
melanoma!. mutation in BRAF kinase.
rx: vemurafenib: BRAF kinase inhibitor
origin of gut tube lining from esophagus to above pectinate line
endoderm
VACTERL syndrome
mesodermal origins
vertebral defects anal atresia cardiovascular defects tracheoesophageal fistula renal defects limb defects (bone & muscle)
luminal epithelial derivatives: endoderm
lung, liver, gallbladder, pancreas, eustachian tube, thymus, parathyroid, thyroid follicular
toxic shock syndrome toxin (TSST-1) vs. toxic shock-like toxin
both toxin shock syndrome
TSST-1: staph aureus
Toxic shock-like toxin: S. pyogenes
both superantigens
arthus reaction
local subacute antibody mediated HSR Type III reaction.
intradermal injection of antigen induces antibodies, form antigen-antibody complexes in skin.
edema, necrosis, complement activation
Streptococcus mitis
alpha-hemolytic strep in mouth
modifications made in golgi (3)
- add N-olgosaccharides in asparagine
- adds O-oligosacch on serine/threonine
- mannose-6-phosphate to traffic to lysosomes
endosomes
sorting center for material from outside cell or from golgi – send to lysosome for destruction or back to membrane/golgi
I cell disease: defect & presentation
inherited.
defective in mannose-6-phosphotransferase –> lysosomal proteins secreted extracellular
presentation:
1. coarse facial features
2. clouded cornea
3. restricted joint movement.
high plasma levels of lysosomal enzymes.
often fatal
COPI vesicle trafficking protein
golgi -> golgi (retrograde)
gogi -> ER
COPII vesicle trafficking protein
golgi -> golgi anterograde
ER to golgi
clathrin
trans-golgi -> lysosomes; plasma membrane -> endosomes
–> receptor mediated endocytosis
peroxisome
membrane-enclosed organelle involved in catabolism of
- very long chain fatty acids,
- branched chain fatty acids, &
- amino acids
recurrent fungal and myobacterial infection?
IL-12 receptor deficiency
autosomal recessive
reduced Th1 response
reduced IFN-gamma
mnemonic for branchial arches
chew (1), then smile (2), then swallow stylishly (3), or simply swallow (4), & then speak (4)
1st branchial arch
M
cartilage: meckel cartilage: Mandible, Malleus & incus, spheno-Mandibular ligament
muscles: muscles of Mastication (temporalis, Masseter, lateral & Medial pterygoid), mylohyoid, anterior belly of digastric, tensor tympani, tensor veli palatini
CN: V2 and V3
treacher-collins
1st arch neural crest fails to migrate -> mandibular hypoplasia and facial abnormalities
2nd branchial arch
S
Reichert cartilage:
Stapes, Styloid process, lesser horn of hyoid, Stylohoid ligament
mucles of facial expression, stapedius, stylohyoid, plastysma, belloy of digastric
CN: VII
congenital pharyngocutaneous fistula
persistence of cleft & pouch –> fistula between tonsilar area and lateral neck
3rd branchial arch
cartilage: greater arch of the hyoid
muscle: stylopharyngeus
CN IX: glossopharyngeal
4th branchial arch
(w/ 6th for cartilage): thyroid, cricoid, arytenoid, cornuculate, cuneiform
muscle: most PHARYNGEAL constrictors; laryngeal: CRICOTHYROID, levator veli palatini
CN X: superior laryngeal branch (swallow)
6th branchial arch
(w/ 4th for cartilage): thyroid, cricoid, arytenoid, cornuculate, cuneiform
muscle: all intrinsic muscle of LARYNX, EXCEPT CRICOTHYROID.
CN X: recurrent laryngeal branch (speak)
which branchial arches make up the posterior 1/3 of tongue
arches 3 & 4
mnemonic for branchial pouches
ears, tonsils bottom to top
1. ear (endoderm-lined structures: middle ear cavity, eustachian tube, mastoid air cells)
- tonsil: epithelial lining of palatine
- dorsal wings: inferior parathyoid
ventral: wings: thymus
4: dorsal wings: superior parathyroids
4th & 5th pouch – parafollicular cells of medullary thyroid
cleft lip follows failed fusion of..
maxillary & medial nasal processes (primary palate)
cleft palate follows failed fusion of..
two lateral palatine processes
or lateral palatine process w/ nasal septum / medial palatine fossa
kinase vs. phosphorylase
kinase: adds phosphate using ATP
phosphorylase: adds inorganic phosphate w/o consuming ATP
how do epi & glucagon increase glycogenolysis
both increase adenylate cyclase -> cAMP -> PKA -> glycogen phosphorylase kinase -> glycogen phosphorylase -> glucose from glycogen
what stimulates glycogen phosphorylase kinase (3)
- PKA (from glucagon/epi stim)
- Ca2+/calmodulin complex
- Ca2+ directly
anti-Ro, anti-La
or
anti-SSA, anti-SSB
Sjorgen syndrome
anti-Jo, anti SRP, anti-Mi-2
polymyositis, dermatomyositic
anti-Scl-70
or
anti-DNA topo I
Scleroderma (diffuse)
anti-smooth muscle
autoimmune hepatitis
1st generation sulfonylurea (2)
tolbutamide
chlorpropamide
2nd generation sulfonylurea (3)
glyburide
glimepride
glipizide
what stimulates Th17 formation
TGF-beta & IL-6
what stimulates Treg formation
TGF-beta
TGF-beta (3)
- anti-inflammatory
- TH17 formation (w/ IL-6)
- Treg formation
regulation of nf-kB
normally inhibited by IkB, released when ikB is phoshparylated.
nfKb then goes to nucleus –> transcription factor
carbon dioxide transport in RBC
- HCO3- (90%)
- carbaminohemoglobin: co2 bound to hb at n-terminus of globin (not heme) –> favors O2 unloading by stabilizing taut form (5%)
- dissolved CO2 (5%)
carboxyhemoglobin, methemoglobin, carbaminohemoglobin
carboxyhemoglobin: CO in place of O2
methemoglobin: Fe3+, does not bind O2 as readily (high affinity for cyanide)
carbaminohemoglobin: CO2 bound to Hb at N-terminus of globin (NOT HEME). CO2 binding favors taught form (oxygen unloading)
haldane effect
lungs: oxygenation of Gb promotes dissociation of H+ from Hb (shifts equilibrium towards CO2 formation –> release)
Bohr effect:
peripheral tissue, H+ from tissue shifts curve to right, unloading O2
majority of CO2 carried as
HCO3-
SLE presentation
usu: rash, joint pain, fever
RASH OR PAIN
rash: malar or discoid
arthritis
soft tissue/serositis
hematologic disorder (cytopenia
oral-nasopharyngeal ulcer
renal disease, raynaud
photosensitivity, positive VDRL
antinuclear antibodies
immunosuppressants
neurologic disorder (seizure, psychosis)
renal disease in lupus
nephrotic: membranous nephropathy
nephritic: diffuse proliferative glomerulunephropathy
cause of death in lupus (3)
- cardiovascular disease
- immunosuppresion
- renal disease
gingival hyperplasia side effect (4)
phenytoin, verapamil, cyclosporine, nifedipine
metoclopramide
D2 receptor antagonist
INCREASE resting tone, contractility, LES tone, motility
does not influence colon transport time.
use: diabetic / postsurgery gastroparesis, antiemetic
toxicity: antiparkinson. interact w/ digoxin and diabetic meds.
irradiated blood? washed?
irradiate: destroys DNA (WBC) prevents graft vs. host
washed: remove all plasma, less often done
autosomal dominant polycystic kidney disease vs. hydronephrosis
hydronephrosis: smooth surface
ADPKD: rough and bumpy surface
tanner stages
1: childhood (prepubertal)
2: pubic hair (pubarche) and breast bud (thelarche)
3: pubic hair darkens & curly, penis size/length increase, breast enlarge (adrenarche)
4: penis width increasese, darken scrotal skin, development of glans, raised areolae
5: adult: areola are no longer raised
HTN, bradycardia, and respiratory depression
cushing reaction
- increased cranial pressure constricts arterioles –> cerebral ischemia –> reflex sympathetic increase in perfusion pressure – HTN
- HTN increases stretch –> reflex baroreceptor induced bradycardia
baroreceptor innervation (aortic arch & carotid)
carotid sinus: glossopharyngeal (both high & low)
aortic arch: just high
both go to solitary nucleus
describe hypotension detection at carotid sinus
hypotension -> less stretch -> decreased glossopharyngeal firing in solitary nucleus of medulla
- relieves tonic inhibition on sympathetic
- decreases firing of parasympathetic
–> vasoconstriction, increase HR, contracility, BP
describe hypertension detection at carotid sinus:
hypertension -> increased stretch -> increased afferent glossopharyngeal firing in solitary nucleus
- tonic inhibition of sympathetic
- stimulation of parasympathetic
decrease HR (increased AV node refractory)
(aortic arch & vagus will also respond)
what stimulates carotid & aortic chemoreceptor (peripheral)
- PO2 < 60mmHg
- increased PCO2
- low blood pH
what stimulates central chemoreceptors?
- pH
- PCO2
(not directly to O2
CREST
calcinosis, raynaud phenomenon, esophageal dysmotility, scerlodactylyl, telangiectasia
anti-centromere
side effects of niacin (3)
- hyperuricemia
- hyperglycemia
- facial flushing
sorbitol dehydrogenase in tissues. lens? schwann cells, retina, & kidney?
usu glucose -> sorbitol (w/ aldolase reductase &NADPH)
sorbitol -> fructose
w/ sorbitol dehydrogenase & NAD+
most tissues have sufficient sorbitol dehydrogenase
lens: less active, can be overwhelmed
schwann cells, retina, kidney: much less active, but exists!
arteries coming off of celiac trunk
- common hepatic
- splenic
- left gastric (near lesser curvature). anastomose w/ right gastric (from common hepatic) & gives off esophageal branch
common hepatic splits into (3)
- gastroduodenal -> anterior superior & posterior superior pancreaticoduodenal artery & right gastricepiploic (around greater curvature)
- hepatic artery proper
- right gastric artery -> less curvature, anastomose w/ left gastric
inferior epigastric artery comes off of
external iliac artery
ulcer on posterior wall of duodenum can cause bleeding from..
gastroduodenal artery (from common hepatic, from celiac trunk
ruptured ulcer on lesser curvature of stomach results in bleeding from
left gastric (from celiac)
what does the ventral pancreatic bud contribute? dorsal bud?
main pancreatic duct & pancreatic head (uncinate process specf)
everything else: body, tail, isthmus, accessory pancreatic duct –> dorsal bud
special embryology of spleen
supplied by foregut (celiac artery) but arises from mesentary of stomach –> MESODERM
(pancreas, liver, gallbladder, etc –> endoderm
histology of abetalipoproteinemia
decrease synthesis of apolipoprotein B-48, can’t make chylomicrons. decreased secretion of cholesterol, VLDL into blood stream –> fat accumulation in enterocytes
failure to thrive, acanthocytosis, ataxia, night blindness
Wernicke’s area specifically located
posterior section of superior temporal gyrus
diabetic neuropathic pain is often..
BURNING
