test #47 5.6 Flashcards
POMC is a polypeptide cleaved to make..
ACTH
MSH
enkephalins
enkephalins, endorphins, dynorphins all bind to
endogenous opoids
bind to mu, delta, fatta receptors
somatomedin C
= IGF-1
released in response to growth hormone
middle meningeal artery is a brach of..
maxillary artery, which is a branch of the external carotid artery
epidural hematoma
occipital artery
branch of external carotid
supply posterior scalp & SCM
opthalmic artery
branch of internal carotid:
serves eye & orbit contents
also eyelid, forehead, nose, nasal mucosa
(internal carotid has no branch in neck)
artery responsible for nosebleeds
kiesselbach’s plexus,
sphenopalatine artery (branch of maxillary artery) anastamoses w/ opthalmic & facial
facial artery
branch of external carotid
couses over mandible anterior to insertion of masseter
supply oral region & nose & buccal
how does middle mengingeal artery enter skull
foramen spinosum
touch to anterior 2/3 of tongue
trigeminal V3
lingual n
touch to posterior 1/3 of tongue
glossopharyngeal CN IX
intrinsic muscles of tongue innervated by (2)
most: CN XII hypoglossal
palatoglossus -> CN X vagus
taste in pharynx & epiglottis
vagus CN X
ESR increased due to
acute phase reactants released by IL-6
fibrinogen, ferritin, CRP, serum amyloid A, serum amyloid P, complement
why does erythroyte sedimentation increase w/ inflammation
fibrinogen causes RBC to rouleaux –> sediment faster
cytokines impt for systemic inflammation (3)
IL-1, IL-6, TNF-alpha
bradykinin effects (4)
vasodilation
vascular permeability
smooth muscle contraction
pain
PAF effects
vasoconstriction
bronchoconstriction
platelet stimulation
also enhances leukocyte adhesion to endothelium, chemotaxis, phagocytosis, degranulation
epinephrine for anaphylactic shock
counteracts the..
1. vasodilation
by alpha-1 agonist vasoconstrction
- increased vascular permeability
by increases CO, B1 agonist - bronchoconstriction
by bronchodilating, B2 agonist
morphology of crytococcos neoformans
yeast only
round/oval encapsulated w/ narrow based buds
virulence: thick polysacch capsule
flutamide, cyproterone
blocks androgen receptor
testosterone/DHT
leuprolide, goserelin, nafarelin, histrelin
GnRH agonists
anorexia induced amenorrhea due to..
hypothalamic dysfunction
nonpulsatile GnRH
(NOT problem in pituitary/gonad)
most important mediator of sepsis
TNF-alpha
also IL-1, IL-6
liver cyst in person from endemic region (middle easy, south america, iceland, australia, new zealand, africa) or sheep/dog exposure
echinococcus granulosus
encapsulated calcified cyst
rupture: eosinophilia –> ANAPHYLAXIS
rx: bendazole
mitral stenosis can cause hoarseness bc..
compression of left recurrent laryngeal
via really enlarged left atrium
recurrent laryngeal innervates
all intrinsic muscles of larynx except cricothyroid
p-ANCA suggests..
microscopic polyangiitis
or churg-strauss (eosinophilia)
characterize churg strauss
adult onset asthma eosinophilia history of allergy mono or poly-neuropathy migratory/transient pulmonary infiltrate paranasal sinus abnormalities
mechanism of glucose-induced inhibition of lac operon
glucose decreases adenylyl cyclase, depleting cAMP
REDUCTION of cAMP, low CAP-DNA binding
(not related to repressor binding to operon)
operon
DNA sequence that has at least 2 regulatory sites: promoter & regulator (operon) in addition to gene coding for protein
lac operon
proteins required for metabolism of lactose
regulatory gene,
- repressor for lac operon
promoter gene,
- binding site for RNA pol
operator gene
- binding site for repressor
3 structural gene
- b-gal
- permease
low cAMP, (caused by glucose) shuts it off
culturing e. coli in lactose. what happens in lac operon
lactose (inducer) binds to repressor protein, which can no longer bind to operon.
increases transcription of lac operon.
anti-reticulin, anti-endomysial antibodies
along w/ anti-gliadin
in celiac sprue
urticaria (hives) histologically
DERMIS: mild, superficial infiltrate of mononuclear cells & eosinophils around dermal venules.
collagen bundles are parted by DERMAL EDEMA and lymphatic channels dilated w/ excess transudate
no epidermal changes
antigen induced degranulation of focal mast cells due to IgE antibody sentization
or, direct activatio nof mast cells
microvasculature hyperpermeability
urticaria vs. eczematous dermatitis
urticaria (wheel): DERMAL edema
eczematous dermatitis: spongiosis (epidermal edema) w/ acantholysis
staph aureus food posioning due to
exotoxin formed prior to ingestion
highly heat stable enterotoxin
rapid onset: less than 6 hrs
usu mayo containing (potato, macaroni salad)
(similar to b. cereus, but diff food)
b. cereus food poisioning
similar to staph aureus!
exotoxin formed prior to ingestion
heat stable
but, diff food: here, reheated rice
exotoxin staph aureus diseases (3)
- toxic shock
- scalded skin
- gastroenteritis
pulsatile notching vessels under ribs
coarctation of aorta
could also have headache & epistaxis from HTN in blood to head – post-ductal in adults
3 major risk factor for squamous cell carcinoma of esophagus
alcohol
smoking
n-nitroso-containing foods (smoked fish, etc)
(asia: chewing betel nut & n-nitroso compounds)
3 major risk factors for adenocarcinoma
barrett’s esophagus
GERD
obesity
tobacco use
anytime you see a squamous cell carcinoma
expect keratin pearls
mu opiod receptor responsible for
respiratory & cardiac depression
reduce GI motility
also: dependence, euphoria, sedation
kappa opiod receptor responsible for..
miosis
also: dysphoria, sedation
delta opiod receptor responsible for..
antidepressant effects
naloxone
opiod receptor antagonist, especially mu
good for overdose / intoxication rx
terbinafine antifungals act on..
block squalene expoidase
prevent conversion of langosterol to ergosterol
rx for dermatophytosis (i.e. tinea corporis)
terbinafines
MRI of MS
periventricular plaques of demyelination (axons in tact)
MLF damage
impaired adduction of eye during lateral gaze
BUT
intact adduction w/ ocular convergence
i.e. not a problem w/ nerve or muscle
what’s inside an acute MS plaque?
- demyelination w/ preservation of axon
- accumulation of lipid-laden macrophages
- astrocytosis (response to injury)
- infiltration by lymphocytes / mononucear cells
overtime: damage of axons, neurons, oligodendrocytes
hypertensive heart results in what type of dysfxn
DIASTOLIC
concentric hypertrophy; net decrease in LV chamber size
filling and diastolic fxn is normal though
what causes hepatic injury w/ hepatitis B infxn
NOT direct cytopathic effect if virus
instead, MHC I expression of HbsAg & HbcAg activates CD8+ T cells to attack
damage tapers when HBV is incorportated into host genome & antiviral antibodies appear
risk of hepatocellular carcinoma remains elevated
autoimmune hepatitis
due to antigen mimicry w/ generation of self-antigen recognizing CD4+ T lymphocytes that damage hepatocytes
location of broca
inferior frontal gyrus
MCA covers what impt territories
all lateral hemispheres
- frontal eye fields
- broca (inferior frontal gyrus)
- wernicke (posterior superior temporal gyrus)
- primary motor cortex esp face/hands
- some perforating branches to internal capsule & basal ganglia
left hemipshere is dominant (side of language) in what people
most left & right handed people
ACA infarct can present w/
hemiplegia of lower extremities
urinary incontinence
primitive reflexes
- contralateral loss of pain & temp
- ipsilateral deficits of CN V,
- ipsilateral facial CN VII
- ispilateral vestibulococh CN VIII
- horner’s
- cerebellar symptoms
AICA occlusion causeslateral inferior pontine syndrome
contralateral loss of pain & temp w/ ipsilateral defecits in CN V, VIII, IX, X, & XI w/ Horner
notably: dysphagia & hoarseness
PICA, lateral medullary
abdominal pain, distension
w/
fever, diarrhea, shock
in ulcerative colitis patient..
think: toxic megacolon
toxic megacolon is more common in..
ulcerative colitis
pathogenesis of toxic megacolon
complete cessation of neuromuscular activity in intestinal wall.
rapid colonic distension -> prone to rupture
segmental necrosis
perforation risk!
diagnosis of toxic megacolon
sufficient w/ plain abdominal x-ray: colonic dilatation, maybe fluid levels
- chora
- aggression/apathy/depression
- dementia
hungtington
w/ hungtingtons, when does expansion of CAG repeats occur?
in spermatogenesis!
when receive abnormal gene from father, tend to have ANTICIPATION
no expansion from mama
emotional lability
insatiable hunger & thirst
in child
prader-willi
mutation in chr. 15 of papa
(same gene as angelman)
happy puppet
jerky movement (like marionette)
pathological happy disposition
angelman
mutation in chr. 15 of mama
(same gene as prader-willi)
multiple myeloma
neoplastic B-lymphocytes mature into plasma cells that synthesize abnormally large amounts of monogclonal Ig or Ig fragments (light chains)
- impaired hematopoesis (bc bone marrow filled w/ plasma cells)
- lytic bone lesions
- hypercalcemia
- AL amyloidosis
- renal dysfxn
lab abnormalities in multiple myeloma
rouleaxu erytheocytes in blood
bence jones protein in urine
M peak on serum protein electrophoresis – monoclonal proliferation
prognosis for esophageal cancer
generally poor, present w/ incurable locally advanced or metastatic disease
histology of reflux esophagitis (3)
elongation of papillae
basal cell hypertrophy
intraepithlieal EOSINOPHILS
usu leads to barett esophagus
benign tumor of esophagus
super rare, but could be leiomyoma
why do colonic diverticula form? describe mechanism & fate
mechanism: pulsion
structure: false
mucosa & submucosa herneat through weak spots in colonic muscular layer; due to increased intraluminal pressure (i.e. constipation)
false diverticula (2)
colonic & zenker in upper esophagus
presentation of colonic diverticula
lower GI bleed
traction diverticula
inflammation & scarring.
true: contains 3 layers
example: midesophageal diverticula, which occur w/ mediastinal lymphadenitis and periesophageal scarring
location & predisposition for colonic diverticula
usu sigmoid colon
constipation : risk factor
lack of peroxisomes prevents
special form of beta oxidation for
very long chain fatty acids
or alpha oxidation for branched chain fatty acids (phytanic acid)
accumulate fatty acids in tissue
Zellweger syndrome
absence of peroxisomes
infant unable to make myelin in CNS
present: hypotonia, seizures, hepatomegaly, metal retardation, early death
Refsum disease
defective alpha oxidation in peroxisomes
leads to neuro disturbances bc accumulate phytanic acid
rx; avoid chlorophyll in diet
what types of fatty acids does the mitochondria NOT oxidize
very long chain fatty acids
or
fatty acids w/ branch points at odd number carbons
(peroxisome does)
rx for NARDs
supplemental oxygen at high concentration
nasal continuous positive airway pressure
mechanical ventilation w/ intratracheal surfactant
concern w/ oxygen therapy in neonate
retinal damage
local hyperoxia –> upregulate VEGF –> retinal detachment/blindness
retinopathy or prematurity
or
retrolental fibroplasia
causes of acute MR
spontaneous rupture of chordae tendinae, infective endocarditis w/ destruction of valve leaflets, chordal rupture, ischemia /rupture of papillary muscles
compliance =
V/P
left atrial compliance in acute MR? chronic?
acute: normal compliance, so will lead to pulmonary edema
chronic: increased compliance, less prone to pulmonary edema, but more protein to Afib & thromboemboli
thiamine deficiency on TCA cycle
most severely impairs alpha-ketoglutarate dehydrogenase –> succinylCoA
dehydrogenases require thiamine, lipoate, CoA, FAD, NAD+
thiamine, lipoate, CoA, FAD, NAD+ are important for..
alpha ketoglutarate dehydrogenase
pyruvate dehydrogenase
acyl-CoA dehydrogenase
thiamine needed for
transketolase (specific)
alpha ketoglutarate dehydrogenase
pyruvate dehydrogenase
acyl-CoA dehydrogenase
rate limting step in TCA
isocitrate dehydrogenase
isocitrate -> alpha-ketoglutarate
first NADH produced
what step of TCA makes GTP
succinyl CoA -> succinate
succinylCoA synthetase
substrate level phosphorylation
what step of TCA makes FADH
succinate dehydrogenase
succinate -> fumarate
order things are made in TCA
starting w/ isocitrate -> alphaketo
NADH (isocitrate -> alpha-keto) NADH (alphaketo -> succinylcoa) GTP (succinylcoA -> succinate) FADH (succinate -> fumarate) skip (fumarate -> malate) NADH (malate -> oxaloacetate)
alcohol dehydrogenase & acetaldehyde dehydrogenase both
increase NADH/NAD+ ratio
though all of TCA is inhibited w/ alcohol, thiamine dependent ones are especially inhibited
mifepristone RU-486
anti-progestin
abortifacient
decidual necrosis and expulsion of products of conception
misoprostol
prostaglandin analogue, also abortifacent
also increases gastric mucosal barrier
methotrexate on pregnancy
inhibits trophoblast division
used for ectopic pregnancy
common complication after subarachnoid hemorrhage
secondary arterial vasospasm
can lead to cerebral ischemia
present: new onset confusion / focal neuro defect 4-12 days after initial insult
can also have rebleed: see on CT
rx to prevent vasospasm after a subarachnoid hemorrhage
nimodipine, selective Ca2+ channel blocker
linear velocity V =
Q/A
or total flow = velocity x cross sectional area; where flow = constant
addition of what in a pt w/ hemophilia will induce clotting
thrombin! will then activate fibrinogen -> fibrin
fatal toxicity w/ digoxin
arrthythmia due to hyperkalemia
associated NF-1 findings
meningioma, astrocytoma, glioma, pheochromocytoma
inheritance of NF-1
single gene autosomal dominant
how is INH neurotoxic?
chemically similar to vitamin B6, can compete with it in synthesis of ntx (GABA) resulting in defective end products
also increases urinary excretion of pyridoxine
neurotoxic bc causes VITAMIN DEFICIENCY
drug is not directly toxic!
counteract isoniazid toxicity
supplement w/ B6
neurotoxicity due to vitamin deficiency!
