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USMLE Wrong Answer Facts > UWorld QBank - 2nd round - part 3 > Flashcards

UWorld QBank - 2nd round - part 3 Flashcards

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USMLE® Step 1 flashcards
1
Q

How are the attachments of the cruciate ligaments positioned in a sagittal anterior view of the right knee for example?

A

ACL - goes from lateral condyle of femur towards the medial condyle of the tibia

PCL - goes from media condyle of femur towards lateral condyle of tibia

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2
Q

What is reverse T3 and how would levels be affected in primary hypothyroidism that is being treated with T3?

A

inactive form of thyroid hormone generated from peripheral conversion of T4 (similar to T3, but NOT produced in thyroid)

T3 treatment would increase T3 levels but not T4, therefore rT3 levels would remain low

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3
Q

What are the characteristic serum hormone levels in Klinefelter’s syndrome?

A
  • Consistent elevation of plasma gonadotropins , mainly FSH
  • Elevation of estradiol
  • Reduction of testosterone
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4
Q

What is transmural inflammation of the arterial wall with fibrinoid necrosis characteristic of? What are the key symptoms and associations of this disorder?

A

Polyarteritis Nodosa - may occur in all organs except lung
Sx = Fever, Abdominal pain, Peripheral neuropathy, weakness and weight loss
-Associated with Hepatitis B in 10-30% of cases (liver infection)

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5
Q

What is the main complication that can occur with severe aortic stenosis ? (Hint: patient may present with dyspnea)

A
  • patients develop decreased CO, many w/ concentric LV hypertrophy (decreased LV compliance)
  • Become dependant on LA contractions and kick to keep normal LV filling
  • If A-fib occurs -> LV preload becomes significantly decreased -> Major hypotension -> blood build up in LA and pulmonary veins -> pulmonary edema
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6
Q

What are the differences between a chancre, gumma, and chondyloma lata?

A
  1. Chancre - painless ulceration w/ raised indurated borders in primary syphilis (1-3 weeks post contact, resolves some weeks after)
  2. Chondyloma lata - large, gray wart-like growths in genital or perianal region in secondary syphilis (hand and feet rash)
  3. Gummas - painless indurated granulomatous lesions -> progress to white-gray rubbery lesions that may ulcerate in TERTIARY syphilis (years post infection, look for Neuro signs, tabes dorsalis or aortic aneurysm)
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7
Q

What neurovascular bundle sits above the thyroid gland and lateral to the thyroid cartilage? What will damage here cause?

A

Superior laryngeal artery and vein and Superior laryngeal nerve (at risk of damage during thyroidectomy)

-Damage would cause denervation of the cricothyroid muscle (all other laryngeal muscles innervated by recurrent laryneal nerve)

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8
Q

What is the most common recurrent complication following reactivation of VZV in the thoracic dermatome? Cranial dermatome?

A

Post-herpetic neuralgia - stabbing, intermittent pain lasting for months potentially (chances of having pain increase with age)

VZV infection of trigeminal ganglion -> Herpez zoster ophthalmicus -> visual impairment

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9
Q

What leads to elevations of CD4+ cells in bronchoalveolar lavage fluid? CD8+?

A

CD4+ - sarcoidosis

CD8+ - Hypersensitivity pneumonitis

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10
Q

What are the major adverse effects of succinylcholine?

A
  1. Malignant hyperthermia in susceptible patients
  2. Severe hyperkalemia (in patients with burns, myopathies, crush injury and denervation)
  3. Bradycardia (PANS stimulation) or Tachycardia (SANS ganglion effects)
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11
Q

What diseases are associated with MEN1?

A
  • Pituitary Adenoma (prolactin, CTH)
  • Parathyroid tumor (hypercalcemia)
  • Pancreatic Tumor (which is gastrin secreting 70% of time -> zollinger ellinson syndrome; also can have insulinoma, and VIPoma)
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12
Q

What pathology findings are consistent with liver cirrhosis? Chronic viral hepatitis?

A 
Cirrhosis = nodular regeneration
CVH = Periportal fibrosis
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13
Q

From which cells does renal cell carcinoma originate from?

A

Proximal renal tubules

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14
Q

What conditions precipitate uric acid stone formation?

A

Low pH (uric acid is soluble at physiologic pH), and the lowest pH is at the collecting ducts

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15
Q

What is pretibial myxedema?

A

Lower leg skin thickening and induration (classically like an orange peel), which is a late manifestation of Grave’s disease (this is the autoimmune response to TSH receptor, like exophthalmia)

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16
Q

What occurs during the maintenance and recovery phase following acute tubular necrosis?

A

Maintenace (1-3days) - oliguria -> fluid overload, increased BUN/Cr, HyperK+, high anion gap metabolic acidosis (H+ retention), Muddy brown casts, high FeNa+

Recovery - Vigorous diuresis (w/ poor functioning tubular cells) -> Hypokalemia, Mg, PO4 and Ca (Hypokalemia being most serious complication)

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17
Q

Which drugs are selective arteriolar vasodilators and what are their main side effects?

A

Hydralazine and Minoxidil (lower blood pressure, good for patients refractory to other meds)

SE: Reflex Tachycardia and Edema (Selective arteriolar vasodilation -> significant vasodilation and reduction in arterial pressure -> Reflex SANS activation via baroreceptors -> Increased HR, contractility and increased RENIN activity -> Na+ and Fluid retention - give these drugs with sympatholytics and diuretics)

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18
Q

Which drugs provide decreased mortality risk benefit for CHF?

A

Spirinolactone and Carvedilol (along w/ other beta-blockers, but this is best for CHF) - Carvedilol is nonspecific and has effects on beta1, 2 and alpha 1 (introduce slowly to avoid exacerbation of CHF, do not use in unstable CHF)

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19
Q

What is Milrinone?

A

Phosphodiesterase inhibitor, increases cardiac contractility and decreases preload and afterload. Can only be given via IV, so used in short term therapy (some studies have shown increased mortality with CHF)

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20
Q

How may enterococci develop resistant to aminoglycosides (e.g. Gentamicin)?

A

Aminoglycoside-modifying enzymes on cytoplasmic membrane surface that transfer different chemical groups (acetyl, adenyl, phosphate) to the antibiotic -> decreasing ability of drug to bind ribosomes

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21
Q

How do VREs gain resistance against vancomycin?

A

Acquired resistance mediated by plasmids/transposons -> proteins synthesized that act as ligases that alter D-ala-D-ala cell-wall precursors (e.g. to D-ala-D-lactate), which are targets of vancomycin

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22
Q

What is a precursor to NAD+?

A

Tryptophan

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23
Q

What is arginine a precursor for?

A

NO, Urea, ornithine, agmatine, and necessary to form creatine

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24
Q

How do eosinophils participate in parasitic defense?

A

Stimulated by IL5 from Th2 and Mast cells -> Fc receptors on Eo surface bind IgG and IgE coated parasites -> triggers degranulation of cytotoxic proteins (e.g. Major Basic Protein) and reactive oxygen species (this is antibody mediated cell cytotoxicity)

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25
Q

What is subacute granulomatous (de Quervain’s) thyroiditis?

A

-Occurs following viral infection
-Tenderness over thyroid gland, Increased ESR, and markedly reduced iodine uptake by thyroid
-Thyrotoxicosis from release of stored thyroid hormone, secondary to thyroid inflammation (new hormone is not formed)
Biopsy: Initial PMN infiltration followed by lymphocytes, histiocytes, and multi-nucleated giant cells which surround fragmented colloid

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26
Q

What are the presenting signs of congenital hypothyroidism?

A

Sx: Lethargic, poor feeding, prolonged jaundice, constipation, muscle hypotonia and a hoarse cry.

Physical: Pale, dry, cool skin, myxedema and macroglossia. Coarse facial features and umbilical hernia. Increased incidence for ASD/VSD

Will develop irreversible mental retardation (from low T4) if not screened and treated early

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27
Q

What is actinomycosis? Which patients are prone to get it, and what are the signs and sx of it?

A

Slowly progressive disease of gram+ anaerobic bacteria (actinomyces israelli)
-Often in patients with dental caries and poor dentition and alcoholics.
Sx: Pulmonary signs from aspiration (yellow sputum, coarse ronchi, apical lobe consolidation)
Biopsy: filamentous branching patterns and sulfur granules

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28
Q

Which portacaval anastamoses leads to the development of esophageal varices? Caput medusae? Hemorrhoids?

A

EV: Left gastric vein (portal circulation) and esophageal vein (systemic circulation)
CM: Paraumbilical veins and Superficial/inferior epigastric vessels
Hem: Superior rectal vein and Middle/inferior rectal veins

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29
Q

What conditions lead to renal papillary necrosis? What is the usual presentation?

A

Multiple systemic conditions causing ischemia:
-Sickle cell disease/trait, analgesic nephropathy (NSAIDs), Diabetes mellitus, Acute pyelonephritis

Present late in disease with gross hematuria

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30
Q

What is the usual presentation for ischemic tubular nechrosis?

A

Oliguria in hospitalized severely ill patients. Muddy brown granular casts in urine.

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31
Q

Which enzyme facilitates triglyceride break down? How about use of the byproducts of this reaction?

A
  • Lipase breaks Trigs into glycerol and Fatty acids.
  • Fatty acids undergo betaoxidation and ketogenesis
  • Glycerol is converted into Glycerol-3P in liver by GLYCEROL KINASE
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32
Q

What is the purpose of the enzyme ATP-citrate lyase?

A

Converts citrate in the cytoplasm back to oxaloacetate and acetyl CoA

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33
Q

What are the 3 methods to prevent Tumor lysis syndrome?

A
  1. Aggressive fluid hydration
  2. Allopurinol (XO inhibitor to decrease uric acid production)
  3. Rasburicase (recombinant urate oxidase which converts Uric acid to the 10x more soluble Allantoin)
34
Q

What is probenacid?

A

Uricosuric agent, which increases excretion of uric acid into urine.
-Used for gout and hyperuricemia, but ONLY effective in patients with good renal fxn (poor renal fxn = stones present, and this could worsen uric acid precipitation)

35
Q

What is denosumab?

A

Prevents osteoclast activation by binding RANK-L and preventing interaction with RANK. Decreases risk of bone loss and fracture in patients with bone metastasis.

36
Q

What diseases is carpal tunnel syndrome associated with?

A

Diseases that reduce carpal tunnel space, and classic CPS sx will occur bilaterally:
1. Pregnancy (fluid accumulation, 2. Hypothyroidism (glycosaminoglycan buildup), 3. Diabetes mellitus (connective tissue thickening), 4. Rheumatoid arthritis (tendon inflammation) 5. patients on long term hemodialysis (from deposition of beta2-microglobulin)

37
Q

What is the risk of giving blood products to a patient with a history of recurrent acute/chronic diarrhea and ear infections?

A

Patient may have IgA deficiency (most common immunodeficiency and patients get recurrent sinopulmonary/GI infections)

  • Patient develops IgG antibodies against IgA, so if blood products contain small amounts of IgA -> patient may get fatal anaphylactic reaction
  • Also gamma-globulin preparations should not be given as these may increase anti-IgA Abs
38
Q

What is the effect of each class 1 anti-arrythmic class on inhibition of phase 0 depolarization and length of action potential?

A

1A -> intermediate inhibition of phase 0 and prolonged AP (big long pyramid slope)
1B -> Weak inhibition of phase 0, and Shortened AP (both parts of slope are shortened)
1C -> Strong inhibition of phase 0 and no change in AP (big old response to Na+ channels and nothing else)

39
Q

A patient is found to have antibodies against alpha3-chain of collagen type IV what are they at risk of?

A

Goodpasture syndrome - anti-glomerular basement membrane antibodies (anti-GBM) -> note GBM is made of collagen type IV!! -> patient will develop hemoptysis and oliguria (proteinuria and RBC casts)

40
Q

What are the three main features of sickle cell disease?

A
  1. Hemolysis -> Permanent sickling and premature RBC destruction -> increased indirect BR and decreased serum haptoglobin (because get bound to Hb and have very short half life in this form)
  2. Vasocclusive sx -> pain crisis, acute chest syndrome, dacytlitis (hand and foot, bone marrow occlusion), leg ulceration, priapism, autosplenectomy and stroke.
  3. Infections -> Encapsulated organisms
41
Q

What is the best treatment for cardiac abnormalities (QRS and QT prolongation) from TCA toxicity?

A

Sodium bicarbonate

42
Q

What is potassium solution a useful antidote for?

A

Digitalis toxicity when there is hypokalemia

43
Q

What deficiency develops in Hartnup disease?

A

Decreased absorption of Tryptophan -> decreased niacin (V. B3) -> Pellagra

Aminoaciduria of neutral AAs (excretion of proline, hydroxyproline, and arginine is unchanged)

44
Q

What disorder involves generalized aminoaciduria?

A

Fanconi Syndrome

45
Q

What 3 factors can decrease calcium stone formation in the kidneys? What would increase stone formation?

A

Decrease: Alkaline urine, increased urine flow and citrate (which binds free calcium)

Increase stone: High calcium, phosphate, oxalate, uric acid, acidic urine and low urine flow

46
Q

What is Laplace’s law and how does it apply to alveoli?

A

Pressure = 2 x Tension / radius

Therefore smaller alveoli have a higher pressure -> greater tendency to collapse -> surfactant prevents this by coming closer together as alveolus shrinks and keeping it open

47
Q

What are the liver findings associated with Reye syndrome?

A

Hepatic dysfunction -> increased AST, ALT, ammonia, bilirubin and prolonged PT & PTT

Light microscopy -> microvesicular steatosis (fat vacuoles in the cytoplasm)

EM -> Swelling and decreased mitochondria and glycogen

48
Q

Which factor is associated with increased morbidity and mortality from N. meningitidis infections? What effects will this factor have?

A

LIPOLIGOSACCHARIDE (LOS) -analogous to LPS of enteric gram negative rods

Causes sepsis and greater inflammatory response (TNF-alpha, IL6, IL8), petechiae and hemorrhagic bullae, and Waterhouse Freidrichson syndrome

49
Q

What leads to sorbitol build up in certain tissues of diabetic patients? What would normally happen to this excess sorbitol?

A
  • Excess glucose in tissues is converted into sorbitol by Aldose reductase.
  • Some tissues also have Sorbitol dehydrogenase which converts sorbitol into FRUCTOSE
  • Retina, Renal papilla and Scwhann cells have reduced SDH enzyme activity -> sorbitol build up -> osmotic damage to these cells (this will also occur in other tissues if there is enough excess sorbitol)
50
Q

What is the most effective long term treatment option in patients with HTN and chronic ischemic myocardial failure?

A

ACE inhibitors -> because they inhibit myocardial remodeling and deterioration of ventricular contractile function + reduce blood pressure (beta-blockers also a good option; but diuretics only used in isolated HTN or acute management of CHF, not long term)

51
Q

What prevents cerebral hypoperfusion upon standing?

A

alpha-1 adrenergic receptors which increase SANS tone and raise peripheral vascular resistance as venous blood pools upon standing -> alpha 1 blockade (Prazosin, Terazosin) can result in light-headedness and syncope

52
Q

What is ecthyma gangrenosum?

A

Multiple dark skin patches with an ulcerated appearance and occasional necrotic center -> strong association w/ P. aeruginosa bacteremia and can be seen in patients with febrile neutropenia (dalmatian in sketchy)

53
Q

What is Group A vs. B strep?

A

Group A = Strep Pyogenes

Group B = Strep agalactiae

54
Q

What comprises pre-eclampsia?

A

Triad of HTN, Proteinuria and Edema in pregnancy

55
Q

What is theophylline and what side effects can it cause, especially if overdosed? How can you counteract toxicity?

A

Methylzanthine drug (COPD/asthma) which causes bronchodilation via inhibition of phosphodiesterase -> increased cAMP

SE: GI sx (Ab pain, Vomiting diarrhea), Heart (arryhthmias) and Neurotox -> Seizures

Tx: GI lavage, Charcoal, and beta blockers for cardiotox

56
Q

What concurrent anomaly can make Berry aneurysms more prone to rupture?

A

Coarctation of the Aorta (which is associated with other heart abnormalities and Berry aneurysm) -> increased upper extremity pressure makes it more likely for aneurysm to rupture

57
Q

What are patients with ataxia-telangiectasia also prone to developing?

A

Repeated sinopulmonary infections (from severe immunodeficiency) and increased cancer risk (inefficient DNA repair)

58
Q

What is the most common benign liver tumor?

A

Cavernous hemangioma

59
Q

Which liver tumor can regress with the use of OCPs?

A

Hepatic adenoma

60
Q

What is DRESS syndrome and what causes it?

A

Drug Reaction w/ Eosinophilia and Systemic Symptoms - Fever, diffuse red rash, generalized LAD, symmetrical facial swelling -> serum has increased eosinophils, atypical lymphocytes, increased AST

Drugs -> anticonvulsants (phenytoin, Carbamaz.), Allopurinol, Sulfonamides (sulfasalazine), antibiotics (minocycline, vancomycin)

61
Q

What is SOB + hemoptysis, vaginal bleeding, enlarged uterus and increased beta-hcg 8 weeks post pregnancy indicative?

A

Choriocarcinoma (tumor of cytotrophoblasts and syncytiotrophoblasts) that has metastasized to lungs

62
Q

Which enzyme is affected in acute intermittent porphyria, and what conditions can worsen this disease? How can you reverse acute attacks?

A

HMB synthase (uroporphyrinogen 1 synthase) which converts porphobilinogen into HMB (or uroporphyrinogen I).

Hypoxia, Alcohol, barbiturates, phenytoin, griseofulvin can increase activity of ALA synthase and because of downstream HMB synthase deficiency -> Aminolevulinic acid builds up causing symptoms

Heme inhibits ALA synthase -> decreases symptoms

63
Q

How and where is insulin-like growth factor 1 (IGF1) produced?

A

Growth hormone binds receptors on hepatocytes -> Jak -STAT signaling pathway activated -> dimerization and translocation to nucleas -> increased transcription and release of IGF1

64
Q

What is displacement? What is projection?

A

DISP = Redirecting unacceptable thoughts, feelings, and impulses from one person to another. e.g. wife who is mad at her husband, redirects anger to kids

PROJ = Misattributing one’s own unconscious thoughts or feelings to another person. e.g. husband who has unconscious feelings to cheat on wife, thinks wife is cheating on him

65
Q

What fetal defects would lead to polyhydramnios?

A
  1. Anything that inhibits swallowing -> anencephaly, or GI obstruction (esophageal, duodenal or intestinal atresia)
  2. Increased urine output -> high cardiac output (alloimmunization, parvovirus infection, fetomaternal hemorrhage)
66
Q

What defects can lead to oligohydramnios?

A

Fetal uirnary tract obstructions -> renal agenesis (POTTER sequence), posterior urethral valves, bladder or urethra blockages of any kind

67
Q

What major factor contributes to the virulence of group A strep and how?

A

Protein M -> inhibits phagocytosis and activation of complement & cytotoxic to PMNs in serum & mediates bacterial attachment

68
Q

In organophosphate poisoning, what symptoms cannot be reversed by treatment with atropine? How can you treat?

A

Atropine takes care of all muscarinic effects but has no effect on nicotinic receptors -> muscle paralysis may persist -> Pralidoxime given early can reverse this

69
Q

What feature worsens the cyanosis of tetralogy of fallot?

A

Greatest factor is degree of RV outflow obstruction (i.e. worse pulmonary stenosis can put more back pressure -> increased R->L shunting of deoxy blood)

70
Q

What is one of the major limiting factors of coronary blood flow during exercise and how can this be overcome?

A

Most coronary blood flow occurs during diastole -> during exercise diastole is much shorter therefore impeding greater levels of perfusion needed -> ATP vasodilates coronary vessels -> significantly increasing flow in this state

71
Q

What is required for Isoniazid to be effective in bacteria? What other anti-mycobacterial drug depends on a similar mechanism?

A
  • Must be processed by mycobacterial catalase peroxidase to get activated in bacteria -> thus non-expression or mutation of this enzyme -> Isoniazid resistance
  • Pyrazinamide also requires pyrazinamidase to get activated
72
Q

What would occur with epinephrine treatment with propranalol?

A

Epi -> Activation of alpha 1 (increased TPR -> increased diastolic BP at high doses) and beta 1 (increased heart rate) and beta 2 (vasodilation only at low doses)
-> now giving Propranalol will block beta signaling so HR will decrease and unopposed Epi action on alpha 1 -> increased blood pressure

73
Q

What are the features of orotic aciduria? How do you treat?

A

Disorder of pyrimidine metabolism w/ mutation of orotate phosphoribosyl transferase & OMP decarboxylase -> hypochromic megaloblastic anemia, Neuro abnormalities, growth retardation, excretion of excess orotic acid

Tx: Uridine -> converted to UMP by nucleoside kinases -> UMP inhibits Carbamoyl phosphate synthetase II (first enzymatic step of this process) -> decreasing orotic acid production

74
Q

What are the distinguishing features of 11-beta hydroxylase deficiency?

A
  • Increased androgen production -> ambiguous genitalia in females
  • Decreased cortisol -> more ACTH -> making this #2 cause of adrenal hyperplasia
  • Low levels of weak mineralcorticoid (11-deoxycorticosterone) produced -> low-renin hypertension and hypokalemia
75
Q

How can you differentiate 21hydroxylase deficiency from 11-betahydroxylase def?

A
  • In 21-hydroxylase def there is no mineralocorticoid produced -> w/o Aldosterone production K+ and H+ are not excreted as much -> Hyperkalemia
  • 11bhydroxy has weak mineralocorticoid production which builds up -> Hypokalemia
76
Q

What is the most notable side effect of ethambutol?

A

Optic neuritis (check visual acuity)

77
Q

The use of which antibiotics require frequent monitoring of hearing and vestibular function?

A

Aminoglycosides and Vancomycin -> ototoxicity direct on CN VIII -> vertigo, tinnitus, deafness
(aminoglcyosides also known for renal tox)

78
Q

What is the main reason patients with silicosis have a high incidence of TB infection?

A

Impaired macrophage killing (perhaps from disruption of phago-lysosome by silica particles) -> macrophage can also get disrupted and autolyse -> TB spread and destruction of surrounding tissues by lysosomal enzymes

79
Q

A patient presents with arthralgias and migratory arthritis, proteinuria, RBC casts, and pancytopenia. What is the cause of these symptoms and why?

A

LUPUS (SLE)

  1. Type II hypersensitivity reaction -> warm body IgGs against RBCs -> autoimmune hemolysis
  2. Antibody mediated destruction of platelets and PMNs -> Leukopenia/Thrombocytopenia
  3. Type III hypersens rxn -> immune complex deposition in mesangium, subendothelial and/or subepithelial spaces of kidney -> Proteinuria and RBC casts
80
Q

What physical organ finding do the majority of the patients with myastenia gravis have?

A

Thymus abnormalities -> Thymoma, thymic hyperplasia (anterior mediastinal mass)

81
Q

What conditions can cause compression of the transverse portion of the duodenum?

A

This part has the SMA coming over it, thus anything that causes decrease of the underlying fat pad can cause the SMA/aortic angle to decrease -> leading to compression of the duodenum
e.g. major fat loss, low body weight, severe burns, or other inducers of prolonged catabolism and bed rest

82
Q

What are the three manifestations of ADPCKD?

A

Cysts in the kidney, liver and brain (aneurysms)

USMLE Wrong Answer Facts (9 decks)

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