uWorld 11 Flashcards
how can you tell the difference between reassortment and phenotypic mixing
in reassortment genomic changes present in the first generation progeny will be present in subsequent progeny
in phenotypic mixing there is no change in underlying viral genomes so subsequent progeny will revert to whatever is normal
what is phenotypic mixing
generally occurs when a host cell is connected with 2 viral staring and progeny irons contain UNCHANGED PARENTAL GENOME form one train and NUCLEOCAPSID (or ENVELOPE) PROTEINS from the OTHER strain
b/c no genetic change in the underlying viral genomes (no genetic exchange), subsequent progeny will revert to having only avian influenza type surface proteins and will again be noninfectious to human epithelium
what is genetic recombination
exchange of genes b/w 2 chromosomes (dsDNA) b crossing over within homologous regions
any genomic change in the first generation progeny will also be present in subewuent progeny
what is genetic reassortment
changes in genetic composition that occur when host cells are connected with 2 segmented viruses that exchange whole genome segments
cell connected by 2 viral strains, any genomic change in first generation progeny will also be present in subsequent progeny
what is genetic transformation
uptake of naked DNA by prokaryotic or eukaryotic cell
may also describe incorporation of viral DNA into a host cell chromosome; alters genetic composition of host cell but typically causes no genetic changes in progeny visions
hypercellular glomerulus on LM in 12 year old boy w/ fatigue and RBC casts, 1+ protein
whats he got?
post streptococcal glomerulonephritis (PSGN)
when hematuria, proteinuria, and urine RBC casts are present in patient with hyper cellular glomeruli on LM, PSGN is the most likely diagnosis
anti-streptolysin O, anti-DNase B, anti-cationic proteinase
low serum C3 concentration
cryoglobulins may also be present
“HUMPS” on elipthelial side of BM on EM (IgG and C3) w/ characteristic “STARRY SKY” appearance
what are telomeres made up of and what is telomerase
telomeres- repeat DNA sequences, usually GT-rich repeats (TTAGGG)
telomerase- RNA-dependant DNA polymerase made of up 2 molecules (human telomerase reverse transcriptase (TERT) and telomerase RNA (TR or TERC)
what are matrix metalloproteinases
proteases that degrade extracellular matrix proteins
modulate cell signaling by cleaving cell surface proteins, realizing apoptotic ligands, and inactivating chemokines/cytokins
generally increase cell proliferation and allow for tissue invasion and mets
when is phenazopyridine
urinary analgesic that provides symptomatic Relief of dysuria in urinary tract infections
not effective for BPH
what is tolterodine
antimuscarinic used to treat overactive bladder symptoms (urinary frequency, urgency, incontinence)
can cause urine retention
normally used in BPH only once another drug has addressed the bladder outlet obstruction
what should a patient be advised to expect during the first month following a vasectomy
VIABLE SPERM IN THE EJACULATE
vasectomy ha no effect on sperm distal to ligation thus patients can still have VIABLE SPERM in the distal vas for 3 MONTHS and at least 20 EJACULATIONS following vasectomy
sex can typically be resumed within a week following the procedure
FAILURE of OBLITERATION of the PROCESSUS VAGINALIS leads to what? (2 possible things)
persistent connection b/w the scrotum and the peritoneal cavity through the inguinal canal
if the opening is small and allows for FLUID LEAKAGE only, a communicating HYDROCELE develops
if the communication is large enough for PASSAGE of ABDOMINAL ORGANS, an INDIRECT INGUINAL HERNIA develop
give examples of ligands that once bound to their INTRACELLULAR RECEPTORS (either in cytoplasm or nucleus) can ACT DIRECTLY AS TRANSCRIPTION FACTORS by binding directly to target DNA sequences via ZINC FINGERS to regulate gene expression
steroid (ESTROGEN, ALDOSERONE, CORTISOL)
THYROID HORMONE
FAT-SOLUBLE VITAMINS
growth hormone binds what kind of receptor
tyrosine kinase
what is seen in symptomatic hypokalemia
muscle weakness
cramps
occasionally: rhabdomyolysis and cardiac arrhythmias (short T wave)
what is ALDOSTERONE ESCAPE
hypernatremia and pedal edema are rarely observed in primary hyperaldosteronism despite increased sodium absorption
high aldosterone levels lead to increased intravalscualr volume and therefore cause increased renal blood flow (w/ resulting pressure natriuresis) and augmented release of ANP; ultimately results in increased sodium excretion by renal tubules, which limits net sodium retention and prevents edema and hypernatremia
what is normal alveolar pO2 and pCO2
alveolar pO2: 104 mmHg- which lies b/w tracheal (150) and venous blood (40)
alveolar pCO2: 40 mmHg- which lies b.w tracheal (0) and venous blood concentration (45)
what would cause alveolar pO2 to be 145 (normal is 104) and pCO2 to be 5 (normal is 40)
POOR ALVEOLAR PERFUSION
under normal conditions venous blood only need to traverse about 1/3 of the total capillary length in order to completely equilibrate
if complete equilibrium occurs before the venous blood exits the pulmonary capillary- then it is perfusion-limited
in cases where perfusion is poor equilibrium may happen slowly or not happen at all- PE for example
what is seen in diffusion-limited gas exchange
what are some examples of when O2 exchange becomes diffusion-limited
alveolar gas does not equilibrate with the blood gas by the time that a given volume of blood reaches the end of the alveolar capillary
emphysema and pulmonary fibrosis, EXERCISE (high blood flow states)
what is seen in the stool form a strongyloides stercoralis infection
rhabditiform larvae in the stool
filariform larva penetrate the skin and migrate to the lungs → enter alveoli and travel to pharynx where they are swallowed and carried to small intestine → filariform larva mold into adults that lay eggs within intestinal mucosa → eggs hart into non-infectious rhabditiform larvae that are extorted into stool OR they mold directly into filariform larva and reinfect host (AUTOINFECTION)
auto infection can lead to a HYPERINFECTION0 can cause multiorgan dysfunction and septic shock
stimulation of what nerve can improve obstructive sleep apnea (w/ LOUD SNORING and GASPING RESPIRATIONS)
HYPOGLOSSAL- stimulation with an implantable stimulator causes the tongue to move forward slightly, increased the anteroposterior diameter of the airway
this has been shown to reduce the number of obstructive events during sleep
what characterizes obstructive sleep apnea
recurrent episodes of upper airway collapse during sleep
anatomical and neuromuscular mechanism have bene implicated
NEUROMUSCLAR WEAKNESS as a pathogenic mechanism of OSA is supported by the fact that apneas occur only during sleep, a time of muscle relaxation
the upper airway dilator muscles weaken during the transition form wake to sleep, leading to airway narrowing and ultimately collapse in OSA pts
what is responsible for development of gallstones in a pt with Crohn’s disease
INCREASED BILE ACID WASTING
bile acids can’t be reabsorbed if ileum is fucked thus RATIO of CHOLESTEROL/BILE AVIDS increased and CHOLESTEROL PRECIPITATES in bile of the gallbladder and forms gallstones
if a pt is on olanzapine what studies should be obtained at 3-month checkup
FASTING GLUCOSE and LIPID PANEL, blood pressure, waist circumference, weight
second-generation antipsychotics (olanzapine and clozapine) commonly used as first line due to less risk of extrapyramidal side effects
lots of METABOLIC SIDE EFFECTS though (weight gain, dyzplipiemia, hyperglycemia, increased risk of diabetes)
