Flashcards in test #41 4.30 Deck (127):
immunoglobulins made by Salk polio vaccine?
killed -- only IgG
injected intramuscularly, unable to stimulate mucosal secretory IgA
immunoglobulins made by Sabin polio vaccine?
live -- both IgG and IgA on (mucosal surfaces)
will colonize natural site of viral entry, producing a greater & more prolonged immune response there.
difference between Salk & Sabin's polio vaccine
Salk - killed. less effective in generating prolonged oropharyngeal & intestinal IgA
Sabin - live, will be able to colonize mucosal surface and secrete IgA
two primary sites of poliovirus replication
oropharynx & intestine
common sites of psoriasis
elbow, knees, gluteal cleft, lumbosacral area, glans penis, scalp
nail changes associated w/ psoriasis
yellow-brown discoloration w/ pitting, thickening, or crumbling
type of arthritis w/ psoriasis
often deforming, upper extremity, small joint
dactylitis (sausage fingers), pencil-in-cup defomity on x-ray
HLA subtype associated w/ psoriasis
HLAB27 too bc of psoriatic arthritis
who makes angiotensin converting enzyme?
pulmonary vascular endothelial cells
three direct effects of antgiotensin II
1. sodium retention (direct)
2. aldosterone production
negative predictive value.
"what's the probability that negative test results truly mean absence of disease"
of the people who tested negative, how many don't have the disease
relationship of NPV and prevalence
NPV decreases as prevalence increases
Gardos channel blockers for Sickle-cell anemia
Ca2+ dependent K+ channel blockers, reduces K+ & H2O efflux from erythrocytes
prevents dehydration & sickling in Sickle-cell anemia
which substances increase gastric acid production from parietal cells? block
increase: histamine, Ach, gastrin
predominant source of TGF-alpha
TNF-alpha, IFN-gamma, IL-6
what can severely impair cardiac output in patients w/ aortic stenosis
sudden drop in preload w/ loss of atrial contraction (i.e. atrial fibrillation)
bc left heart needs to generate lots of pressure to get blood out in aortic stenosis, now relies on atrial contraction for maximal preload (max LV filling)
in which pts is atrial contraction importrant
patients w/ poorly compliant left ventricles. needed to maintain adequate LV filling.
definition of preload
end-diastolic volume in ventricle
definition of afterload
where does CN I olfactory bundles enter skull?
what goes through optic canal
1. CN II
2. central retinal vein
3. opthalmic artery
what goes through superior orbital fissure?
1. CN III
2. CN IV
3. CN VII
4. CN V1
5. opthalmic vein
6. sympathetic fibers
middle meningeal artery & vein
internal acoustic meatus
spinal root of CN XI
jugular foramen (vernet) syndrome
loss of CN IX, X, XI
- loss of taste from posterior 1/3 tongue (CN IX)
- reduce parotid gland secretion (CN IX)
- loss of gag reflex (CN IX, X)
- dysphagia (CN IX, X)
- dysphonia/hoarseness (CN X)
- soft palate drop w/ deviation of uvula to normal side (CN X)
- SCN and trapezius paralysis (CN XI)
air in the gallbladder biliary tree suggests
where does gallstone lodge in gallstone ileus
trapped behind the ileocecal valve.
see it in ileum
obstruction of cystic or common bile duct by gallstone
mechanism of genomic imprinting
DNA methylation by DNA methytransferases
transfer methy from donors, like S-adenosyl-methionine (SAM) to CYSTEINE residues
describe airway resistance
upper respiratory tract: nasal passage, mouth, pharynx, larynx = 1/2
trachea & mainstem bronchus: HIGH
increases in MEDIUM-sized bronchi bc of highly turbulent flow (generation 2-5)
falls in smaller airways bc high cross-sectional area is combined high.
what constitutes "upper" respiratory tract
nasal passage, mouth, pharynx, larynx
what constitutes "lower" respiratory tract
trachea & 23 generation of airways
where is lower respiratory airway resistance highest
MEDIUM-sized bronchi (generation 2-5) bc of turbulent flow
moderately high in trachea too. falls after medium sized bronchi (bc summation of cross-sectional area = low)
ceftazidime (3rd gen)
cefepime (4th gen)
amikan, gentamycin, tobramycin
azetreonam works on
aerobic gram negatives
(bad against gram positive and anerobes)
what type of haemophilus produces ear infxn
h. flu vaccine won't prevent it
what kind of illness can nontypable h. flu cause?
part of upper respiratory normal flora
type of immunity conferred by conjugated vaccine
adding protein helps it be presented on MHC II.
doesn't stimulate a cell-mediated response (not on MHC I)
time frame for ischemic-related brain injury
hypoxia > 1 min = cessation of neuronal fxn
permanent damage to brain tissue in 4-5min
phenytoin, nifedipine, verapamil,
adverse effects of phenytoin
CNS: cerebeullum & vestibular, ataxia & nystagmus
gingival hyperplasia, coarsening facial features, hirsitism
interfere w/ folic acid absorption
teratogen: fetal hydantoin syndrome
mechanism of gingival hyperplasia w/ phenytoin
increases expression of PDGF, stimulating prolif of gingival cells & alveolar bone.
how are the 3 genes in lac operon coordinated to be made in equal amounts
prokaryotic mRNA can be polycistronic (on mRNA codes for several proteins)
3 genes regulated by SINGLE promoter, operator & regulatory elements
duodenal atresia occurs due to..
failure of duodenum to recanalizein early embryonic life
malrotation in gut
failure of midgut to rotate counterclockwise as it returns to abdominal cavity
when does vitelline duct normally obliterate
aminoglycoside resistance (i.e. via enterococci)
aminoglycoside-modifying agents that transfer diff chemical groups -- acetyl, adenyl, phosphate
outside of bacteria, so it can no longer bind to ribosomes.
aqcuired by plasmid / transposons
(2) penicillin-binding proteins
mutation in cell wall precursor turning D-ala-D-ala to D-ala-D-lactate
1. mutation in ribosome
2. increased efflux, influx
mutations in gyrase / topoisomerase gene
what is hepatic encephalopathy acutely triggered by
often GI bleed, increasing ammonia & nitrogen in gut for absorption
relationship between alpha-ketoglutarate, glutamate, and glutamine
alpha-ketoglutarate + NH3 --> glutamate
(via glutamate dehydrogenase, both ways)
glutamate + NH3 --> glutamine
(via glutamine synthase)
glutamine ---> glutamate + NH3
describe glutamate-glutamine cycle
glutamate made 2 ways
1. glutamine -> glutamate + NH3
2. alpha-ketoglutarate + NH3 --> glutamate
(via glutamate dehydrogenase)
in synaptic cleft, glutamate is taken up by astrocytes
1. glutamate + NH3 --> glutamine
(via glutamine synthase)
glutamine is shuttled back into neurons
how does hyperammonia affect glutamate-glutamine cycle
1. in astrocyte, excess NH3 creates toxic accumulation of glutamine
2. in neuron, excess NH3 promotes excess consumption of alpha-ketoglutarate --> glutamate
this leaves less alpha-ketoglutarate for TCA in neurons!
which 2 substances are depleted in the brain during hyperammonia? accumulated?
(too much glutamine formation in astrocytes
(used to make more glutamate)
accumulate: glutamine in astrocytes! swell
formed by bacteria in gut & normally cleaved by liver. elevated in hepatic encephalopathy.
strong ionotropic agent
increase cardiac cAMP, increased contractility
rx: during angioplasty in patients w/ acute coronary syndrome
deciding between uricosuric (probenicid) agents vs. allopurinol/febuxostat?
if has uric stones, don't want to add more uric acid in urine. give febuxostat / allopurinol.
sudden liver failure after surgery?
consider hepatic necrosis caused by halothane!
halothane side effects
type 1: aminotransferase elevation, mild syptoms
type 2: fulminant hepatitis. extensive hepatocellular damage.
RAPID ATROPHY - widespread centrilobular hepatocellular necrosis & inflammation of portal tracts & parenchyma
decreased albumin levels is a sign of..
chronic liver injury. NOT aute.
half-life of 20 days.
presentation of fulminant hepatitis caused by halothane
(albumin takes 20 days to rise)
anti-topoisomerase I specific for..
scleroderma (anti Scl-70)
characterestics of esophageal motility
fibrosis of distal esophagus
1. esophageal hypomotlity
2. loss of tone in LES
manifests as GERD
drug induced lupus
procainamide, hydralazine, isoniazid, d-penicillamine
presentation of sjogren
keratoconjunctivitis sicca (dry eye)
xerostomia (dry mouth
may be parotid enlargement
increased risk of non-hodgkin lymphoma
anomaly in antiphospholipid syndrome
thombophilia w/ paradoxical increased PTT
hydronephrosis vs. autosomal dominant polycystic kidney disease
hydronephrosis: smooth surface
ADPKD: cyst bumps visualized on surface
cysts in ADPKD and ARPKD
ADPKD: large cysts, from anywhere.
-lumpy bumpy cysts seen on gross exam of surface
ARPKD: small cysts in collecting duct.
- generally smooth surface
shrunken kidney on ultrasound can suggest?
medullary cystic disease -- inherited
tubulointerstitial fibrosis, progressive renal insufficiency. medullary cysts usu NOT visualized.
(shrunken, as opposed to polycystic kidney --> large)
mucosa in lactase deficiency
potential complication of pancreatitis.
leakage of pancreatic secretions -- induce inflammatory response --> granulation tissue & fibrosis forms to trap fluid
cyst vs. pseudocyst
cyst: lined w/ epithelial cells
pseudocyst: granulation tissue
most common location for pancreatic pseudocyst:
lesser peritoneal sac, bordered by stomach, duodenum, transverse colon
the only radiolucent stone
uric acid stones
colorless octahedron crystals
calcium oxalate or calcium phosphate
rectangular prism "coffin-lid" crystal
struvite (AMP or triple phosphate
proteus mirabilis / vulgaris, klebsiella, staphlococcus
yellow, red-brown, diamond or rhombus
flat, yellow, hexagonal crystals
which 2 stones ppt in basic environment
calcium phosphate (or neutral)
inheritance of alpha-1 antitrypsin
co-dominant, affects lung and liver
genotype in alpha-1-antitrypsin deficiency
homozygous for Z allele - decrease secretion of A1AT secondary to abnormal protein folding.
STUCK IN ER
liver consequences in alpha-1-antitrypsin deficiency
accumulation of anti 1-antitrypsin.
liver issues before lung issues usually
1. cirrhosis (2nd most common cause of death) and
2. hepatocellular carcinoma
histology of liver w/ alpha 1-antitrypsin deficiency
intracellular granules of unsecreted A1AT.
stain reddish pink w/ PAS
resist digestion by diastase
symptoms of scurvy
impaired collagen formation
bleeding into JOINT SPACE
secondary peridontal infection
hyperkeratotic papular rash
impaired wound healing
weakened immune response
vitamin K deficiency vs. vitamin C deficiency
both have bleeding diathesis, but vitamin K usu doesn't present w/ PAINFUL GUMS
acrodermatitis enteropathica, growth retardation, infertility
increase cAMP, increase Ca2+ release during contraction. increases HR & contractility (independent of adrenergic receptors)
histological diagnosis of celiac
small intestine: MOST: duodenum and proximal jejuneum
flattening of mucosa w/ loss of villi and chronic inflammatory infiltration of lamina propria
antibodies seen in celiac (3)
common finding in GI malabsorption?
steatorrhea: foul, smelling, bulky, floating, greasy stoof
dfiferential of steatorrhea (3)
1. pancreatic insufficiency
- chronic pancreatitis, cystic fibrosis
2. intestinal mucosal defect
- celiac, tropical spru, whipple, chron.
3. bacterial proliferation
small bowel diverticulosis, diabetic neuropathy. bacteria eat nutrients
differentiate cause of steatorrhea?
1. sudan III stool stain: identidy fat
2. quantitative analysis of amt of fat
then bariums studies to see what caused it.
what do you need for diagnosis of malabsorption
major pathophysiology w/ prolonged NSAID use
chronic interstitial nephritis
clinically: see modest elevation in serum creatinine, evidence of tubular dysfxn, fanconi syndrome (aminoaciduria, glycosuria, hypophosphatemia, hypouricemia)
key: multiple symmetrically distributed tender spots over patients' muscles, joints, tendons (spine of scapula, lateral epicondyle, medial fat pad of knee)
demo: 20-50y/o. mostly women
widespread musculoskeletal pain w. stiffness, paresthesia, poor sleep, emotional disturbance.
muscle pain & stiffness severe in morning. exacerbated w/ exercise.
morning stiffness of neck, shoulder, pelvic girdle.
weight loss, fever, increased ESR
presentation of ankylosing spondylitis
low back stiffness, resolves w/ exercise.
usu affects males
PE: decrease anterior flexion of spine.
formula for clearance
urine concentration x urine flow rate
normal filtration rate
common side effects of first-generation anti-histamine
and lipophilic --> sedation / cognitive dysfxn
second generation antihistamine
NO anti-muscarininc, anti-5HT, anti-alpha-adrenergic.
not lipohilic --> no sedation / cognitive dysfxn
hydroxyzine, promethazine, chlorpheniramine, diphenhydramine
1st gen anti-histamine
2nd gen anti-histamine
minimal sedation & anti-muscarinic
wax & waning lymphadenopathy
most common indolent non-hodgkin lymphoma in adults
indolent course, marked by remission & recurrence
wax & wane
t(14,18) bcl-2 overexpression
diffuse large cell lymphoma often involves..
waldeyer ring (oropharyngeal lymphoid tissue)
most common aggressive non-hodgkin's lymphoma in adult
cutaneous T-cell lymphoma
proliferating CD4+ T cell infiltrate dermis & epidermis --> PAUTRIER MICROABSCESSES.
manifest w/ plaques that may be confused w/ psoriasis or eczema
generalized erythema, scaling, thickening of skin
clinical presentation of hairy cell leukemia
splenomegaly & pancytopenia in older men
BRAF mutation w/ glutamic acid for valine at position 600 (V600E)
antibody rx for mutant BRAF in melanoma?
inhibitor of mutant BRAF in melanoma
most common AGGRESSIVE non-hodgkin lymphoma
diffuse large B cell lymphoma
rapidly enlarging mass