UWorld Test Review 3 Flashcards
name the 4 classes of anti-fungal drugs and their MOA
- polyenes (amphotericin B, nystatin): bind ergosterol in fungal cell membranes and create pores
- triazoles (ketoconazole, fluconazole, itraconazole, voriconazole): inhibit ergosterol synthesis
- echinocandins (caspofungin, micafungin): inhibit glucan synthesis (component of cell wall)
- pyrimidines (flucytosine): converted to 5-fluorouracil and interferes with fungal RNA/protein synthesis
which of the following cytokines is an important mediator of sepsis?
a. IL-3
b. IL-4
c. IL-10
d. LTB4
e. TGF-beta
f. TNF-alpha
f. TNF-alpha (tumor necrosis factor-alpha): stimulates systemic inflammation via leukocyte recruitment
others important for systemic inflammation are IL-1 and IL-6
Pt w/ PMH of Staph. aureus due to IV drug use now has aortic regurgitation. Which of the following changes is most responsible for maintaining cardiac output in the setting of this valvular abnormality?
a. concentric LV hypertrophy
b. decrease in LV preload
c. increase in aortic elasticity
d. increase in LV afterload
e. increase in LV stroke volume
f. sustained increase in HR
e. increase in LV stroke volume
regurgitation causes LV dilation (eccentric hypertrophy) —> increase in SV
oocytes are arrested in which state of meiosis immediately prior to fertilization?
metaphase of meiosis II
[frozen in prophase of meiosis I until ovulation]
where would type I vs II vs III vs IV collagen be found?
type I = bones, tendons, ligaments, cornea, blood vessels, scar tissue (mutation = osteogenesis imperfecta)
type II = cartilage, vitreous humor, nucleus pulposus (mutation = skeletal dysplasias)
type III = lungs, intestines, blood vessels, bone marrow, lymphatics, granulation tissue (mutation = Ehlers-Danlos)
type IV = basement membranes (mutation = Alport syndrome)
Pt arrives comatose to ED after car accident. CT of head within an hour shows no abnormalities. Pt dies several hours later, and autopsy is performed. Brain histopathology shows widespread axonal swelling, predominantly at the gray-white junction. Immunohistochemical staining of these axons shows an accumulation of alpha-synuclein and amyloid precursor. What is the most likely cause of these findings?
a. Diffuse cerebral hypoperfusion.
b. Glutamate mediated neuronal injury.
c. Interruption of white matter tracts
d. Secondary microvascular spasm.
c. Interruption of white matter tracts
diffuse axonal injury is type of TBI occurring form direct blunt force injury or abrupt changes in acceleration-deceleration —> shearing of white matter tracts —> normal axonal transport is inhibited, leading to accumulation of transported proteins (amyloid precursor, alpha-synuclein)
which 3 mutation sites have been associated with early-onset familial Alzheimer’s?
- amyloid precursor protein (APP) gene on chromosome 21
- presenilin 1 gene on chromosome 14
- presenilin 2 gene on chromosome 1
homozygous for apolipoprotein E-4 allele confers risk of:
a. familial hypercholesterolemia.
b. Hypertrophic cardiomyopathy.
c. diabetes mellitus type 2
d. Polycystic kidney disease.
e. Alzheimer’s disease.
e. Alzheimer’s disease.
7mo M presents with irritability and white patches in mouth. PMH notable for 3 episodes of otitis media and 2 episodes of bronchiolitis. Also has history of chronic loose stools. Child is small and ill-appearing. PE is notable for wheezing but cardiac exam is normal. Serum protein electrophoresis shows a very low gamma globulin level. Chest x-ray reveals an absent thymic shadow. What is the dx?
severe combined immunodeficiency (SCID): presents with severe viral/bacterial infections, mucocutaneous candidiasis, persistent diarrhea, failure to thrive
labs show absent CD3+ T cells and hypogammaglobulinemia + thymic hypoplasia due to severe T cell deficiency
[NOT DiGeorge because this would present with craniofacial abnormalities, cardiac abnormalities, and hypocalcemia due to parathyroid hypoplasia]
what are the distinctive features of the following primary immunodeficiencies:
a. Chediak-Higashi
b. chronic granulomatous
c. DiGeorge
d. SCID
e. Wiskott-Aldrich
a. Chediak-Higashi: albinism, pyogenic infections, progressive neuro dysfunction
b. chronic granulomatous: bacterial + fungal infections, granulomas
c. DiGeorge: heart disease, dysmorphic facies, hypocalcemia (parathyroid hypoplasia)
d. SCID: bacterial + viral infections (infancy), chronic diarrhea, mucocutaneous candidiasis
e. Wiskott-Aldrich: recurrent infections that worsen with age, easy bleeding, eczema
which of the following pathways mediates EPO signaling?
a. adenylate cyclase/ cAMP
b. arachidonic acid/phospholipase A2
c. Janus kinase 2/ STAT
d. phosphatidylinositol/ inositol triphosphate
e. Ras/mitogen-activated protein kinase
c. Janus kinase 2 (JAK2/STAT)
[STAT = signal transducer and activator of transcription]
which of the following pathways mediates glucagon signaling?
a. adenylate cyclase/ cAMP
b. arachidonic acid/phospholipase A2
c. Janus kinase 2/ STAT
d. phosphatidylinositol/ inositol triphosphate
e. Ras/mitogen-activated protein kinase
a. adenylate cyclase/ cAMP
this pathway also mediates effects of ADH (V2 receptor) and corticotropin
which of the following pathways mediates ADH signaling at V1 vs V2 receptors?
a. adenylate cyclase/ cAMP
b. arachidonic acid/phospholipase A2
c. Janus kinase 2/ STAT
d. phosphatidylinositol/ inositol triphosphate
e. Ras/mitogen-activated protein kinase
a. adenylate cyclase/ cAMP = ADH at V2 receptor
d. phosphatidylinositol/ inositol triphosphate = ADH at V1 receptor
which of the following pathways mediates GnRH and oxytocin signaling?
a. adenylate cyclase/ cAMP
b. arachidonic acid/phospholipase A2
c. Janus kinase 2/ STAT
d. phosphatidylinositol/ inositol triphosphate
e. Ras/mitogen-activated protein kinase
d. phosphatidylinositol/ inositol triphosphate
as well as ADH at V1 receptors
which of the following pathways mediates growth factor signaling?
a. adenylate cyclase/ cAMP
b. arachidonic acid/phospholipase A2
c. Janus kinase 2/ STAT
d. phosphatidylinositol/ inositol triphosphate
e. Ras/mitogen-activated protein kinase
e. Ras/mitogen-activated protein kinase
therefore, uncontrolled activation = malignancy
4yo M presents with 3 days of fever, irritability, and oral lesions. PE shows painful ulcers on tongue and gingiva, as well as swollen gums and cervical lymphadenopathy. What is the most likely dx? What would histology show?
HSV-1 gingivostomatitis - peak age for primary infection is 6mo-5yrs, causes painful vesicles covering lips and gingiva (may include palate, tongue, oropharynx)
histology shows multinucleated giant cells on Tzanck smear
mothers with which blood type are most at risk for causing fetal hemolysis? why?
maternal antibodies (anti-A/B) are of IgM type, but mothers with blood type O also produce IgG which can cross placenta
78yo F presents with acute vision loss in L eye that developed over an hour. It is not painful, but the patient has had L-sided headaches for the past 3 weeks and aching in the shoulders that has slowly worsened over the last month. PE shows decreased pupillary light reflex in the L eye with impaired acuity. What is the dx and the tx?
dx: giant cell (temporal) arteritis - presents with fever/fatigue/weight loss + headache + jaw claudication + visual disturbances (ischemic optic neuropathy) + polymyalgia rheumatica
labs show elevated erythrocyte sedimentation rate and C-reactive protein
temporal artery biopsy shows intimal thickening, elastic lamina fragmentation, and multinucleated giant cells
tx: glucocorticoids
what is the cause of visual disturbances in giant cell (temporal) arteritis? what is the treatment?
presents with fever/fatigue/weight loss + headache + jaw claudication + visual disturbances (ischemic optic neuropathy) + polymyalgia rheumatica
labs show elevated erythrocyte sedimentation rate and C-reactive protein
temporal artery biopsy shows intimal thickening, elastic lamina fragmentation, and multinucleated giant cells
tx: glucocorticoids
what do labs and histology show in giant cell (temporal) arteritis?
labs show elevated erythrocyte sedimentation rate and C-reactive protein
temporal artery biopsy shows intimal thickening, elastic lamina fragmentation, and multinucleated giant cells
which of the following would best treat visual disturbances caused by giant cell arteritis?
a. acetazolamide
b. clopidogrel
c. methylprednisolone
d. sumatriptan
c. methylprednisolone (tx w/ glucocorticoids)
a. acetazolamide = carbonic anhydrase inhibitor/ diuretic, tx idiopathic intracranial HTN and angle-closure glaucoma
b. clopidogrel = anti-platelet
d. sumatriptan = migraine treatment
how do levels of the following change as fetal lungs mature?
a. lamellar bodies
b. sphingomyelin
c. phosphatidylglycerol
d. lecithin
lecithin (aka phosphatidylcholine) / sphingomyelin (L/S) ratio increases (>2) - lecithin increases while sphingomyelin remains low
lamellar bodies increase - organelles within type 2 pneumocytes that store/secrete surfactant
phosphatidylglycerol increases - component of surfactant
as fetal lungs mature, the ratio of _____ to ______ increases
lecithin (aka phosphatidylcholine) / sphingomyelin (L/S)
ratio increases (>2) because lecithin increases while sphingomyelin remains low
what is used to treat the following?
a. gonorrhea with neg. chlamydia NAAT
b. chlamydia with neg. gonorrhea NAAT
c. gonorrhea with pos. or uncertain chlamydia status
a. gonorrhea with neg. chlamydia NAAT = ceftriaxone
b. chlamydia with neg. gonorrhea NAAT = azithromycin or doxycycline monotherapy
c. gonorrhea with pos. or uncertain chlamydia status = ceftriaxone + doxycycline
Fracture of the greater trochanter will impair the function of which of the following muscles? what is the action of the muscle?
a. adductor Magnus.
b. Gluteus medius
c. Iliopsoas.
d. Rectus femoris.
e. Sartorius.
b. Gluteus medius - originates from ilium, inserts on greater trochanter; action = hip abduction
a. adductor Magnus - inserts on medial condyle of distal femur
c. Iliopsoas - inserts onto lesser trochanter (primary flexor)
d. Rectus femoris - attaches to lower leg via patellar tendon
e. Sartorius - inserts on pes anserinus
the pes anserinus is the common tendon for which 3 muscles?
- Sartorius.
- Gracilis.
- Semitendinosous.
pes anserinus is on superior medial surface of tibia
Crystalline-induced kidney injury most commonly occurs from which two types of drugs?
- acyclovir
- sulfonamide
what is the meaning of the following urinary cast findings?
a. Hyaline
b. Waxy.
c. Granular/muddy brown.
a. Hyaline (Tamm-Horsfall protein) = nonspecific, concentrated urine, prerenal azotemia
b. Waxy (degenerated hyaline cast) = chronic kidney disease.
c. Granular/muddy brown (sloughed tubular cells) = acute tubular necrosis
what kind of drugs are anastrozole, letrozole, and exemestane?
aromatase inhibitors - block conversion of testosterone to estradiol
used to treat ER-positive tumors
which of the following would cause an increase in both renin and aldosterone?
a. adrenal cortical tumor
b. adrenal medullary tumor
c. juxtaglomerular cell tumor
d. pituitary tumor
e. primary HTN
c. juxtaglomerular cell tumor - secretes renin
high renin + high aldosterone = secondary hyperaldosteronism (renovascular HTN, malignant HTN, renin-secreting tumor, diuretic use)
low renin + high aldosterone = primary hyperaldosteronism (aldosterone-producing tumor, bilateral adrenal hyperplasia)
low renin + low aldosterone = non-aldosterone causes (congenital adrenal hyperplasia, Cushing syndrome, exogenous mineralocorticoids)
what is the histological finding of the following opportunistic causes of diarrhea in HIV patients?
a. cytomegalovirus
b. cryptosporidium
c. microsporidium
d. mycobacterium avium complex
a. cytomegalovirus: multiple ulcers + mucosal erosions, large cells w/ basophilic inclusions
b. cryptosporidium: non-ulcerative inflammation, basophilic clusters on surface of mucosal cells
c. microsporidium: distortion of villus without inflammation, small spores with diagonal/equatorial belt-like structure
d. mycobacterium avium complex: granulomas, acid-fast staining bacilli
______ must be ligated during an oophorectomy to prevent heavy ovarian bleeding
suspensory ligament of the ovary (aka infundibulopelvic ligament) - contains the ovarian artery
Where are the SA node and AV node found in the heart?
SA node - right atrium near the opening of the superior vena cava
AV node - right atrium near the septal cusp of tricuspid valve
[a-fib often originates in the area around the pulmonary veins in the left atrium)
pt is started on ramipril for HTN and their serum creatinine increases - why?
“-pril” = ACE inhibitor
ACEi cause efferent arteriole dilation, which lowers intraglomerular pressure and prevents kidneys from maintaining GFR in setting of decreased renal perfusion
many pts see increase in serum creatinine within 2-5 days of starting ACEi
which of the following explains the hemoglobinuria seen in acute hemolytic transfusion reaction?
a. CD8+ mediated cytotoxicity
b. complement mediated cell lysis
c. endotoxin-induced TNFalpha surge
d. IgE-mediated reaction to serum proteins
b. complement mediated cell lysis
anti-ABO Abs (mainly IgM) bind antigens and activate complement –> C3a + C5a cause vasodilation/ shock symptoms while C5b-C9 form MAC
which of the following is first to be released during an allergic reaction?
a. histamine
b. leukotriene D4
c. major basic protein
d. platelet-activating factor
e. prostaglandin D2
a. histamine - from preformed granules
b. leukotriene D4 - synthesized via 5-lipoxygenase
c. major basic protein - released from eosinophils in late stage of Type I hypersensitivity, causes local tissue damage
d. platelet-activating factor - secondary inflammatory mediator, must be synthesized from phospholipid prior to release
e. prostaglandin D2 - synthesized via cyclooxygenase
the type of hepatitis virus that has a high mortality rate in pregnant women also:
a. is an unenveloped RNA virus
b. is transmitted parenterally
c. is associated with chronic hepatitis
d. infects only HBsAg+ individuals
e. has oncogenic properties
Hep E: unenveloped RNA virus (a), fecal-oral route in Asia/Africa/Mexico, incubation 6 weeks
b. is transmitted parenterally = Hep B, C, D
c. is associated with chronic hepatitis = Hep C
d. infects only HBsAg+ individuals = Hep D
e. has oncogenic properties = Hep B, C
weakness with hip flexion and knee extension = injury to which muscle?
rectus femoris
what transporter facilitates intracellular Ca2+ efflux from cardiomyocytes during myocyte relaxation?
- Na+/Ca2+ exchange pump (NCX)
- Ca2+-ATPase pump (SERCA)
22yo F presents w/ 5d history of nausea, constipation, and abdominal pain. She also reports trouble concentrating and tingling in her limbs. She has had similar episodes in the past. She does not take medication, but has been restricting her diet to lose weight. Pt receives an IV infusion of heme and the symptoms rapidly improve. What is the dx? What enzyme is being downregulated by the treatment?
dx: acute intermittent porphyria (AIP) - AD deficiency of porphobilinogen (PBG) deaminase
presents w/ abdominal pain, neuro manifestations, port-wine urine, PBG + ALA in urine [NO photosensitivity]
tx: glucose or hemin –> inhibit hepatic aminolevulinate synthase (ALAS) (rate-limiting enzyme in heme synthesis)
what brings on an attack of acute intermittent porphyria (include some examples), and how does it present?
acute intermittent porphyria (AIP) = AD deficiency of porphobilinogen (PBG) deaminase
attack also requires induction of aminolevulinate synthase (ALAS) (rate-limiting step) via medications (phenobarbital, phenytoin), alcohol, smoking, progesterone (puberty), or low-calorie diet
presents w/ abdominal pain, neuro manifestations, port-wine urine, PBG + ALA in urine [NO photosensitivity]