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uWorld Flashies > uWorld 11 > Flashcards

uWorld 11 Flashcards

1
Q

how can you tell the difference between reassortment and phenotypic mixing

A

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

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2
Q

what is phenotypic mixing

A

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

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3
Q

what is genetic recombination

A

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

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4
Q

what is genetic reassortment

A

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

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5
Q

what is genetic transformation

A

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

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6
Q

hypercellular glomerulus on LM in 12 year old boy w/ fatigue and RBC casts, 1+ protein
whats he got?

A

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

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7
Q

what are telomeres made up of and what is telomerase

A

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)

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8
Q

what are matrix metalloproteinases

A

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

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9
Q

when is phenazopyridine

A

urinary analgesic that provides symptomatic Relief of dysuria in urinary tract infections
not effective for BPH

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10
Q

what is tolterodine

A

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

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11
Q

what should a patient be advised to expect during the first month following a vasectomy

A

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

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12
Q

FAILURE of OBLITERATION of the PROCESSUS VAGINALIS leads to what? (2 possible things)

A

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

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13
Q

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

A

steroid (ESTROGEN, ALDOSERONE, CORTISOL)
THYROID HORMONE
FAT-SOLUBLE VITAMINS

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14
Q

growth hormone binds what kind of receptor

A

tyrosine kinase

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15
Q

what is seen in symptomatic hypokalemia

A

muscle weakness
cramps
occasionally: rhabdomyolysis and cardiac arrhythmias (short T wave)

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16
Q

what is ALDOSTERONE ESCAPE

A

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

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17
Q

what is normal alveolar pO2 and pCO2

A

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)

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18
Q

what would cause alveolar pO2 to be 145 (normal is 104) and pCO2 to be 5 (normal is 40)

A

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

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19
Q

what is seen in diffusion-limited gas exchange

what are some examples of when O2 exchange becomes diffusion-limited

A

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)

20
Q

what is seen in the stool form a strongyloides stercoralis infection

A

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

21
Q

stimulation of what nerve can improve obstructive sleep apnea (w/ LOUD SNORING and GASPING RESPIRATIONS)

A

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

22
Q

what characterizes obstructive sleep apnea

A

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

23
Q

what is responsible for development of gallstones in a pt with Crohn’s disease

A

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

24
Q

if a pt is on olanzapine what studies should be obtained at 3-month checkup

A

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)

25
Q

what nerves can be affected by an acoustic neuroma (tumor of the cerebellopontine angle)

A

CN VIII- sensorinueal hearing loss and tinnitus
CN V- loss of facial sensation (afferent limb of corneal reflect), paralysis of muscles of mastication
CN VII- facial muscle paralysis (upper and lower), loss of taste in anterior 2/3, decreased lacrimation/salicaiotn, hyperacusis (paralysis of stapedius)

26
Q

what tumor would one expect to find in the dorsal midbrain

A

GERM CELL TUMORS arising from the PINEAL GLAND
usually cause obstructive hydrocephalus with symptoms of increased ICP (headache, vomiting, altered mental status) and PARINAUD SYNDROME (upward gaze palsy)

27
Q

what is canagliflozin and what tests should be ordered before starting therapy with it

A

oral-antidiabetic agent SODIUM-GLUCOSE COTRANSPORTER 2 (SGLT2) INHIBITORS
leads to significant urinary loss of glucose
assess RENAL FUNCTION b4 initiating therapy and periodically thereafter
side effects:
UTI and GENITAL MYCOTIC INFECTIONs due to glycosuria
HYPOTENSION (elderly and ppl on diuretics)

28
Q

periodic liver function tests should be performed on patients taking what type of anti-diabetic drug

A

thiazolidnediones (pioglitazone, rosiglirazone)

also monitor for risks and signs of heart failure before and after starting

29
Q

thyroid function tests are routinely performed on ppl taking what two drugs

A

amiodarone

lithium

30
Q

advanced alzheimers is associated with diffuse brain atrophy of what areas

A

TEMPOROPARIETAL lobes and HIPPOCAMPUS

hippocampal atrophy is evident even in the early stages of the disease and can be detected by brain MRI

31
Q

what is the classic triad of congenital toxoplasmosis

A

hydrocephalus (causing macrocephaly), intracranial calcifications, CHORIORETINITIS

transmitted TRANSPALCENTRALLY and fetus affected ONLY if MOM is INFECTED w/ TOXO DURING FIRST 6 MONTHS of pregnancy

32
Q

what lipid lowering drug when used in mono therapy can lead to increased TRIGLYCERIDE levels

A

BILE ACID RESINS (cholestyramine)
main side effects are GI upset and impaired absorption of nutrients and drugs
increase hepatic production of TGs and increase release of TG-heavy VLDL particles into the circulation, leading to HYPERTRIGLYCERIDEMIA

33
Q

angiogenesis is primarily driven by what two substances

A

vascular endothelial growth factor (VEGF)

fibroblast growth factor (FGF)

34
Q

what two antivirals are nucleotide analogs

A

tenoFOVIR
cidoFOVIR- broad spectrum antiviral analogue of cytidine monophosphate
can be converted to the active triphosphate moiety solely by cellular kinases, thus its efface does not depend on the presence of a virally encoded kinase

35
Q

how do osteocytes remain connected to one another

A

GAP JUNCTIONS are used to send signals and exchange nutrients and waste products with the osteocytes within neighboring lamellae

36
Q

what is an osteocyte and what is its function

A

osteoblasts that are trapped in the ossified matrix
serve to maintain the structure of the mineralized matrix and control the short-term release and deposition of calcium (calcium homeostasis
plasma calcium concentration directly dictates metabolic activity of osteocytes while PTH and calcitonin indirectly influence their metabolic activity
can also sense mechanical stress and send signals to osteoblasts helping to regulate bony remodeling

37
Q

what are ependymal cells

A

ciliated glial cells that line the ventricles and central canal of the CNS to make up the choroid plexus
produce CSF

38
Q

what is seen weeks to months after an ischemic brain infarct

A

necrotic area appears as a CYSTIC CAVITY surrounded by a wall composed of dense fibers formed by ASTROCYTIC PROCESSES (GLIAL SCAR)

39
Q

what causes hypoglycemia in alcoholics or someone who has has too much alcohol

A

increased NADH/NAD+ rain which inhibits all other pathways hat require NAD+ like GLUCONEOGENESIS

lactate can not be converted to pyruvate and instead the reaction is driven from pyruvate toward lactate
excess NADH inhibits conversion of malate to oxaloacetate
pyruvate and oxaloacetate are intermediates in gluconeogenesis; w/o them no gluconeogenesis happens

40
Q

what maintained euglycemia in the initial phase of binge drinking

A

glycogenolyisis (which is not inhibited by alcohol)

eventually hepatic glycogen is depleted and glucose levels drop

41
Q

what are the different stages of sarcoidosis

A

Stage I: bilateral hilar lymphadenopathy
Stage II: bilateral hilar lymphadenopathy w/ pulmonary infiltrates (upper lobes most common)
Stage III: lung infiltrates only (no more hilar lymphadenopathy)
Stage IV: lung fibrosis

42
Q

what is dermatomyositis

A

autoimmune disorder that presents with proximal muscle weakness and skin involvement including VIOLACEOUS discoloration of the UPPER EYE LIDS (HELIOTROPE RASH), and a raised, violaceous, scaling eruption on the knocks (GOTTRON’S SIGN)
CPK levels are typically elevated

43
Q

severe chest pain NOT RELIEVED by REST or NITROGLYCERINE, diaphoreses, dyspnea, nausea, lightheadedness, and/or palpitations along w/ ST elevations suggest what

A

transmural MI from RUPTURED ATHEROSCLEROTIC PLAQUE with FULLY OBSTRUCTIVE THROMBUS

44
Q

what is TEMPOROMANDIBULAR DISORDER (TMD)

A

characterized by constellation of symptoms:
unilateral facial pain that worsens with jaw moment
headache
ear discomfort
symptoms can originate from:
temporomandibular joint (TMJ) derangement, pathologic contraction of muscles of mastication, and/or hypersensitivity of the nerves that supply the jaw

45
Q

what is seen in enteropeptidase (jejunal brush border enzyme) deficiency

A

both PROTEIN and FAT malabsorption as trypsin is required to activate enzymes required for both lipid and protein digestion
disease causes: DIARRHEA, FAILURE TO THRIVE, and EDEMA (due to hypoproteinemia)

46
Q

bile salts are formed form cognation of bile acids with what

A

GLYCINE and TUARINE

47
Q

where is pepsinogen secreted from and what activates it to pepsin

A

CHEIF cells of the stomach release pepsinogen

HCl exposure in stomach activates pepsin, initiating protein degradation

uWorld Flashies (62 decks)

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