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UWORLD facts > random decks > Flashcards

random decks Flashcards

1
Q

which statistical test can evaluate if there is a significant difference between the means of multiple independent groups

A

analysis of variance (ANOVA)

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2
Q

which statistical test can evaluate if there is a significant difference between the means of 2 groups

A

t-test

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3
Q

how does a pt with a restrictive lung disease minimize the work of breathing

A

by increasing respiratory rate and decreasing tidal volume- rapid and shallow breathing

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4
Q

how do pts with an obstructive lung disease (high airflow resistance) minimize the work of breathing

A

by taking slow deep breaths

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5
Q

what are the 3 stop codons in mRNA sequence

A

UAG, UAA, UGA

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6
Q

what is the deficent enzyme in glycogen storage disease type II (Pompe disease)?

A

acid a-glucosidase (acid maltase) causes glycogen accumulation in the lysosomes

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7
Q

what are the major symptoms of glycogen storage disease type II (Pompe’s disease)?

A

Cardiomegaly and generalized hypotonia that presents in early infancy

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8
Q

what does a muscle biopsy show in polymyositis?

A

over-expression of MHC class I on the sarcolemma with CD8+ lymphocytic infiltration

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9
Q

cauda equina syndrome consists of damage to what nerve roots?

A

S2-S4

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10
Q

what are symptoms of cauda equina syndrome

A

saddle anesthesia and loss of the anocutaneous reflex

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11
Q

what are symptoms of untreated hydrocephalus in infants

A

hypertonicity and hyperreflexia (UMN injury due to stretching), developmental delay and seizures

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12
Q

what is the result of a t(14;18)

A

over-expression of Bcl-2 an anti-apoptotic protein (causes cellular immortality) causing follicular lymphoma

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13
Q

how do you treat lyme disease

A

doxycycline or penicillin type antibiotics (ceftriaxone)

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14
Q

what is terbinafines MOA and what is it used to treat

A

inhibits the enzyme squalene epoxidase to inhibit synthesis of ergosterol. used to treat dermatophytosis

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15
Q

what is etanercept’s MOA and what must be checked prior to initiation

A

its a TNF-a inhibitor therefore it impairs cell-mediated immunity. All pts should be checked for latent TB

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16
Q

what protein regulates transition from G1 to S phase and how is it activated

A 
Retinoblastoma protein (Rb)
active form is hypophosphorylated while inactive form is hyperphosphorylated. The inactive form allows for continuation of the cell cycle
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17
Q

what causes hemoglobin C disease

A

missense mutation which causes negtively charged glutamate residue being replaced by a positively charged lysine in the beta chain

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18
Q

rank HbA, HbS, HbC in order of speed of movement on gel electrophoresis

A

HbA> HbS>HbC

HbA is the most negatively charged

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19
Q

which cells are predominantly found in the paracortex of the lymph nodes

A

T lymphocytes and dendritic cells

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20
Q

what cardiac abnormalities are pts with turners syndrome at increased risk for

A

bicuspid aortic valve and aortic coarctation

valve without stenosis presents as an early systolic, high-frequency clink heard over the right second interspace. Is at higher risk for calcification and endocarditis

21
Q

what causes a trendelenburg sign

A

superior gluteal nerve injury (often do to trauma or damage during hip surgery or buttocks injections)

causing weakness of the gluteus medius and gluteus minimus and the pelvis to sag toward the unaffected side. the pt will lean toward the affected side when walking

22
Q

what are symptoms of primary hyperaldosteronism

A

hypertension, hypokalemia, metabolic alkalosis causing paresthesias and muscle weakness

23
Q

what is the most important mediator of sepsis? what produces it?

A

TNF-a produced by activated macrophages (IL-1 and 6 are also involved)

24
Q

what are the signs of McCune-Albright syndrome

A

fibrous dysplasia (multiple osteolytic lesions), endocrine abnormalities (precocious puberty), cafe-au-lait spots

25
Q

metabolism of what substance is defective in alkaptonuria and what is the clinical presentation

A

defective tyrosine metabolism (deficiency of homogentisic acid dioxygenase)

the presence of homogentisic acid in the urine turns it black if allowed to sit out

26
Q

what is the enzyme defect in Fabry disease

A

a-glalactosidase A (this is a lipid storage disorder)

27
Q

what are the clinical features of Fabry disease

A

neuropathic pain, angiokeratomas, telangiectasias, glomerular disease (proteinuria), cerebrovascular disease (TIA, stroke), Cardiac disease (LVH)

28
Q

where do very long chain fatty acids get metabolized

A

since they cannot undergo b-oxidation in the mitochondia they are oxidized in the peroxisome - diseases may result if the perioxisomes are absent or disfunctional

29
Q

what causes pigmented gallstones

A

unconjugated bilirubin accumulation usually secondary to bacterial or helminthic infection of the biliary tract cauing increased Beta-Glucuronidase which increases the amount of unconjugated bilirubin. Can also be seen in chronic hemolytic anemia

30
Q

what is the function of Phosphoribosyl pyrophosphate (PRPP) synthase? and what does an activating mutation increase the risk of?

A

PRPP synthase is involved in purine and pyrimidine synthesis therefore increased function could lead to gout (more purines being made –> more being broken down–> uric acid formation)

31
Q

how is achondroplasia inherited

A

it’s usually due to a sporatic mutation (advanced paternal age) but can also be Autosomal Dominant inheritance

32
Q

what are the signs and symptoms of opiod/heroin withdrawl

A

nausea, vomiting, abdominal cramping, muscle aches, dilated pupils, yawning, piloerection, lacrimation, hyperactive bowel sounds

33
Q

what does Acetyl CoA carboxylase do? and what does acyl CoA synthase do?

A

Acetyl CoA caboxylase - first step in fatty acid synthesis (requires biotin)

Acyl CoA synthase - activates fatty acids to acyl CoA in the cytoplasm, which are then combined with carnitine and transported to the mitochondria to undergo beta oxidation

34
Q

A pt has a ruptured aorta from a car accident, where is the injury most likely located?

A

aortic isthmus (just after the left subclavian vein comes off the arch, where the ligamentum arteriosum is located) this is due to the extreme stretching and torsional forces on an area that is relatively immobile

35
Q

what is heteroplasmy

A

the condition of having different mitochondrial genomes within a single cell - in mitochondrial disease the percent affected determines the severity of the disease

36
Q

what cell linage is the anterior pituitary derived from

A

surface ectoderm

37
Q

what are the signs of serotonin syndrome

A

confusion, agitation, tremor, tachycardia, hypertension, clonus, hypereflexia, hyperthermia, and diaphoresis

38
Q

what causes serotonin syndrome

A

any drug that increases serotonin levels including SSRIs, MAO inhibitors when taken together or high doses of SSRIs alone

39
Q

what is the treatment for serotonin syndrome

A

supportive care and a serotonin receptor antagonist in severe cases such as cyproheptadine

40
Q

what are the functions of the Smooth ER

A

steroid and phospholipid synthesis and detoxification of drugs (prominent SERs are seen in cells of the adrenal)

41
Q

what is ApoE responsible for

A

binding to hepatic lipoprotein receptors causing removal of VLDL and chylomicrons from the blood

42
Q

when are “red, dead” neurons seen after a stroke

A

12-24 hours (eosinophilic cytoplasm, pyknotic nuclei, loss of Nissl substance)

43
Q

to what lymph nodes do the testes drain? the penis? the scrotum?

A

testes - para-aortic nodes
penis - deep inguinal nodes
scrotum - superficial inguinal nodes

44
Q

what is Dactylitis and what disease is it associated with

A

painful swelling of the hands and feet associated with sickle cell disease

45
Q

what are common features of Patau syndrome and what causes them

A

midline defects including: holoprosencephally, microcephaly, microphthalmia, cleft lip/palete, omphalocele, intellectual disability and seizures, polydactyly and cutis aplasia

46
Q

what is I-cell disease

A

autosomal recessive lysosomal storage disorder, due to defect in protein targeting. defective phophotransferase enzyme prevents the phosphorylation of manose residues therefore instead of being transported to the lysosomes it

47
Q

how does SIADH normally present

A

euvolemic hyponatremia - low plasma sodium and osmolality, inappropriately concentrated urine, clinically normal body fluid levels

48
Q

what is milrinone’s MOA

A

PDE-3 inhibitor - acts as an inotropic agent in the heart by increasing cAMP but also acts as a vasodilator in smooth muscles

49
Q

what are characteristics of a drug with a low Vd?

A

large molecular weight, bound extensively to plasma proteins or highly charged (Vd= 3-5 L)

UWORLD facts (7 decks)

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