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UWorld FACTOIDs > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Delusional disorder

A

Fixed, persistent, nonbizarre belief system lasting > 1 month. Functioning is otherwise not impaired.

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2
Q

Describe the hallmark feature of TB

A

Caseating granulomas of TB contain large epithelioid macrophages with pale pink granular cytoplasm and surface CD14 at the periphery. CD14 is a surface marker of monocyte-macrophage cell lineage

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3
Q

Diffuse pruritic papulopustular rash pustular fluid demonstrates oxidase-positive gram negative rods producing pigment

A

“Hot tub folliculitis” superficial and self-limited P. aeruginosa infection of hair follicles. Culture of pustule: Gram-negative, oxidase positive, non-lactose fermenting motile rod producing pigment

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4
Q

How are androgens produced in females?

A

LH stimulates theca interna cells of ovarian follicle to produce androgens. Aromatase within follicle’s granulosa cells convert these androgens to estradiol under FSH stimulation. Theca externa cells serve as a connective tissue support structure for the follicle

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5
Q

How is paranoid personality disorder different from delusional disorder

A

PPD is characterized by a pervasive pattern of suspiciousness or distrust. The paranoia typically permeates all interactions, in contrast to delusion disorder, where there is one fixed delusion. Delusional disorder harbor non-bizarre delusions but do not meet the criteria for schizophrenia and can function without significant impairment in day-to-day life.

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6
Q

Low-dose morphine is injected into the epidural space of a 44-year old female with severe back pain due to metastatic carcinoma. What is the MOA of morphine?

A

Mu receptors are G protein-linked receptors whose actions are mediated through various secondary messenger pathways. One pathway is ↑ potassium efflux. Binding of morphine to mu receptors -> G protein-coupled activation of potassium conductance -> ↑ Potassium efflux causes hyperpolarization of postsynaptic neurons and effectively blocks pain transmission

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7
Q

MOA streptokinase

A

protein synthesized by beta-hemolytic streptococci (foreign protein can induce hypersensitivity rxns) . Forms complex with plasminogen that cleaves plasminogen to form plasmin. Plasmin cleaves fibrin dissolving thrombi. Stretokinase-plasminogen complex also destroys fibrinogen and clotting factors V and VII. Most common side effect is hemorrhage

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8
Q

NCC migration is complete by week 12, if this process is interrupted during the final week of migration, which organs are most likely to be affected?

A

Rectum and anus involved 100% of the time, Sigmoid colon is involved 75% of the time;

Hirschprung disease is a result of abnormal migration of neural crest cells during embryogenesis. These cells are rpecursors of ganglion cells of tintestinal wall plexi. Since neural crest cells migrate caudally along the vagal nerve fibers, the rectum is ALWAYS affected in Hirschprug disease.

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9
Q

Nonbizarre vs. bizarre delusion

A

Nonbizarre - situations that are unlikely, but possible, like being followed, cheated or poisoned.

Bizzare delusion - suspicion of covert alien activity

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10
Q

Signs of intracerebral hemorrhage

A

asymmetric pupils, irregular breathing

(SE of streptokinase, why we prefer taking to cath lab if available)

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11
Q

4 primary features of Neuroleptic malignant syndrome

A

hyperthermia, extreme generalized rigidity, autonomic instability, altered mental status

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12
Q

Akathisia

A

subjective feeling of restlessness or objective motor restlessness

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13
Q

Body’s smallest striated muscle? Innervation?

A

stapedius, stabilizes stapes (body’s smallest bone), innervated by stapedius nerve (branch of facial nerve)

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14
Q

Causative agents in monospot-negative mononucleosis

A

CMV (90%), HHV-6, toxoplasmosis

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15
Q

Edwards’ syndrome

A

47, XX, +18 have small jaws (micrognathia), small eyes (microphthalmia), and malformed and low-set ears. Note that rocker-bottom feet are seen, as with Patau syndrome (trisomy 13). The presence of clenched hands with overlapping fingers is considered one of the distinguishing features of this syndrome. Trisomy 18 is the second most common autosomal trisomy, 90% result from nondisjunction

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16
Q

Ethambutol MOA, Treatment, What is an important side effect of ethambutol?

A

↓ carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase but has no effect on the creation of mycolic acid; Mycobacterium tuberculosis; Optic neuropathy (Red-Green Color Blindness) reversible

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17
Q

Facial nerve paralysis signs

A
  • ipsilateral hyperacusis,
  • inability to close the eye or smile on affected side,
  • ipsilateral increased salivation,
  • loss of taste on anterior 2/3 of tongue
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18
Q

How does wernicke syndrome manifest? What causes it?

A

classic triad - ophthalmoplegia, ataxia, confusion. Lethal in 10-20% of patients.

Chronic thiamine (B1) deficiency leads to the diminished ability of cerebral cells to utilize glucose. May cause hemorrhage and necrosis in mamillary bodies and periaqueductal gray matte. T*he mechanism is decreased function of the enzymes that use vitamin B1 as a cofactor (pyruvate dehydrogenase, alpha-keotglutartate dehydrogenase, and transketolase). *

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19
Q

How is Neuroleptic Malignant syndrome distinguished clinically from Serotonin syndrome?

A

NMS is distinguished by the absence of myoclonus and by the presence of rigidity. Dopamine agonists (bromocriptine) and/or direct muscle relaxants (dantrolene) have been used to decrease mortality rates associated with neuroleptic malignant syndrome (NMS), but there is no way to prevent NMS.

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20
Q

How is thiamine deficiency diagnosed?

A

measuring erythrocyte transketolase activity (increased activity upon addition of thiamine)

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21
Q

Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)

A
  • converts hypoxanthine to Inosinic acid (IMP); and
  • Guanine to Guanylic Acid (GMP)
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22
Q

Liver biopsy shows abundant pigment inclusions in lysosomes and electron spin resonance spectroscopy reveals pigment composed of polymers of epinephrine metabolites -

A

Dubin - Johnson characterized by defect in hepatic excretion of bilirubin glucuronides across canalicular membrane resulting in conjugated hyperbilirubinemia - black liver with dense pigment composed of epinephrine metabolites within lysosomes. Confirmation - high urinary coproporhyrin

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23
Q

MOA isoniazid

A

Antimycobacterial agent that specifically inhibits the synthesis of mycolic acids. Mycolic acids are essential components of the unique mycobacterial peptidoglycan cell wall. Without mycolic acids, the mycobacteria lose their acid-fastness and become unable to syntehsize new cell walls or multiply.

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24
Q

MOA Rifampin

A

inhibits DNA-dependent RNA polymerase - preventing transcription of DNA into RNA, halting protein synthesis. Does not cause mycobacteria to lose their acid-fastness

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25
Q

Neuroleptic malignant syndrome (NMS)

A

Specific anti-dopaminergic activity of antipsychotic medications (Haloperidol most common) particularly antagonism of the D2 receptor. Usually within 7-10 days after exposure to neuroleptic medication but may occur with chronic usage. Central dopaminergic systems are involved in thermoregulation and regulation of muscle tone and movement

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26
Q

What drug is used to raise HDL levels?

A

Niacin increase serum HDL levels an average of 25-35% (Diet and exercise 5-10%)

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27
Q

Patients with familial hypoalphalipoproteinemia have what problem? Rx?

A

Low HDL, increased risk for premature CAD. Niacin (Vitamin B3) is the best agent to increase HDL levels

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28
Q

Purine Synthesis requires what for carbon and nitrogen sources?

What enzyme catalyzes the first committed step in purine synthesis?

A

“pure GAG” Glycine (carbon source); Aspartate (nitrogen source); Glutamine (nitrogen source); Tetrahydrofolate (carbon donor); CO2;

the first committed step of de novo purine synthesis converts PRPP into 5-phosphoribosylamine then adds the carbon donor THF and 3 nitrogen sources (glycine, aspartate, glutamate) to make IMP via (Phosphoribosyl pyrophosphate amidotransferase)

29
Q

Rate-limiting step in purine synthesis

Rate-limiting step in pyrimidine synthesis?

A

Glutamine Phosphoribosyl pyrophosphate amidotransferase (PRPP aminotransferase)

Rate-limiting step for pyrimidine synthesis is Carbamoyl phosphate synthetase II (CPSII)

30
Q

Serotonin syndrome & treatment

Treatment?

A

Mental status changes, Autonomic instability, Neuromuscular abnormalities (myoclonus); Bronchospasm, flushing, Diarrhea, Right sided valve disease;

Treatment - cool down patient + benzodiazepines

31
Q

What are fibric acid derivatives mainly used to treat?

A

Fibric acid derivatives mainly used for hypertriglyceridemia. Activate peroxisomal proliferator-activated receptor alpha (PPAR-alpha)

also increase HDL by 10-25% (second best) Severe hypertriglyceridemia can cause pancreatitis.

32
Q

What does a nasal transepithelial potential difference measure?

A

Charge on the respiratory epithelial surface as compared to the interstitial fluid.

Individuals with CF have a significantly more negative nasoepithelial surface than normal. In cystic fibrosis, abnormalities of CFTR transmembrane protein reduce luminal chloride secretion and increase sodium and net water absorption, resulting in dehydrated mucus and _widened, negative transepithelial potential difference_. These electrolyte changes occur in most exocrine glands (other than sweat glands)

33
Q

What is hyperacusis? How can this happen?

A

** ↑ sensitivity to sound**

  • Paralysis of the stapedius muscle may allow the stapes to oscillate more widely leading to increased sensitivity to sound
  • Stapedius muscle is innervated by the stapedius nerve, a branch of facial nerve (CN VII)
34
Q

Which enzyme must increase in Lesch-Nyhan syndrome? Why?

A

Phosphoriosyl pyrophosphate amidotransferase

Lesch-Nyhanis an X-linked recessive disorder caused by a defect in hypoxanthine-guanine phosphoribosyltransferase (HGPRT). This results in failure of the purine salvage pathway. Because they are not recycled, increased amounts of purine bases hypoxanthine and guanine are degraded to uric acid. De novo purine synthesis must increase to replace the lost bases, hence PPRP amidotransferase activity increases.

35
Q

$ Main cells that express GLUT 4

A
  • Muscle cells, adipocytes
  • Insulin-mediated (only glucose transporter responsive to insulin)
36
Q

$What is a mutation?

What are the different types of mutations?

A

Mutation - changes in the DAN sequence

Types:

Base substitutions (point mutations) - one base is substituted with another base are the most common type, there are 3 types of point mutations:

  • Silent
  • Missense
  • Nonsense

$ Frameshift mutations - deletion or insertion of bases that are not a multiple of three. Alter reading frame of genetic code resulting in non-functional proteins. (If you ran a cDNA gel of the corresponding protein, you would see less base pairs ie 124 bp instead of 126 bp, ie a 2 pair base deletion of the CFTR protein.)

37
Q

Describe insulin synthesis. What happens to the portion removed from proinsulin?

A
  • Proinsulin is synthesized in pancreatic beta cells and deposited in RER
  • Proinsulin transported within membrane enclosed organelles from RER to sacs of golgi
  • Convertase cleaves proinsulin into insulin, C peptide, and 2 pairs of basic amino acids
  • C peptide and insulin are packaged together into secretory granules and released to extracellular space intact in equimolar concentrations
38
Q

Enoxaparin is a LWMH that functions like heparin by binding to and activating antithrombin III. What does antithrombin III do?

A
  • Binds to factor Xa and stops factor Xa from converting prothrombin to thrombin
  • Less thrombin is produces resulting in anticoagulation.
  • Enoxaparin shows a significant reduction in death and recurrent MI when used in acute treatment of MI as compared with unfractionated heparin (ESSENCE, TIMI-11 trials)
39
Q

Forms germ tubes (sprouts of true hyphae from yeast cells) if incubated in 37deg serum for 3 hours

A

C. albicans

40
Q

GLUT-1 major distribution and features

A
  • Red cells, CNS
  • Basal glucose transport
  • Insulin independent
41
Q

GLUT-2 major distribution and features

A
  • Hepatocytes, pancreatic beta-cells, kidney, SI
  • Regulation of insulin release
  • Insulin independent
42
Q

GLUT-3 major distribution and features

A
  • Placenta, brain, kidney
  • Placental glucose transport
  • Insulin independent
43
Q

GLUT-5 major cellular distribution, feature

A
  • Spermatocytes, GIT
  • Fructose transport
  • Insulin independent
44
Q

How can cryptococcus neoformans be Diagnosed?

A
  • India ink stain of CSF
  • Latex agglutination of CSF (if (+) then soluble polysaccharide antigen present)
  • Culture (Sabouraud’s agar)
  • Methenamine (GMS), mucicarmine stains of tissue
45
Q

How can Meckel diverticulum present? What causes it?

A
  • Melena from Lower GI bleeding is the most common manifestation and occurs due to acid secretion by ectopic gastric mucosa presenting in the diverticulum
  • RLQ pain due to inflammation similar to acute appendicitis.
  • Diverticulum may predispose intestine to intussuception, manifesting as colickly abdominal pain and “currant jelly” (strawberry jam) stools.
  • $ Cause: Failure of obliteration of the omphalomesenteric duct
46
Q

Major determinant of virulence among strains of I. coli that cause neonatal meningitis?

A
  • K-1 capsular antigen is a virulence factor that allows bacteria to survive hematogenous spread and establish meningeal infection
  • Present in 20-40% of intestinal E. coli isolates
  • Inhibits complement, phagocytosis and other host response
  • Capsule is immunogenic and anticapsular antibodies are protective
47
Q

Most common cause of neonatal meningitis in the United States?

A
  1. Group B Streptococcus
  2. E. coli
  3. Listeria monocytogenes
  4. Klebsiella pneumoniae
    Haemophilus influenzae type b remains an important cause in non-immunized infants
48
Q

Nonseptate hyphae that branch at wide angles

A

Mucor and Rhizopus

49
Q

Order the severity of damage that results from the 3 types of point mutations.

A

From most severe to least:

Nonsense > missense> silent

50
Q

Reduced visual acuity, color blindness and central scotoma from this anti-TB drug?

A

Ethambutol

51
Q

SE of Lithium

A

Nephrogenic diabetes insipidus (ADH antagonist)
Hypothyroidism
Teratogenic - causes ebstein’s anomaly

52
Q

Treatment for C. neoformans?

A
  • Amphotericin B and flucytosine (acute meningitis)
  • Fluconazole for lifelong prophylaxis
53
Q

What are the causes of acute Mitral regurgitation?

A
  • Spontaneous rupture of chordae tendinae
  • Infective endocarditis with destruction of valve leaflets or chordal rupture
  • Ischemia or rupture of papillary muscle
  • Failure of prosthetic valve
54
Q

What are the primary sources of alkaline phosphatase? How do you clarify the importance of moderately elevated alkaline phosphatase?

A
  • Bone and liver are the primary sources of alkaline phosphatase, with 3-fold elevation relatively nonspecific finding in many liver diseases
  • γ-glutamyl transpeptidase should be evaluated, (enzyme present in hepatocytes and biliary epithelia) to determine if elevated alkaline phosphatase is due to liver or bone.
55
Q

What causes Graft-versus-host disease? What organs are most commonly involved? What transplantation most often results in GVHD? What is the time frame?

A
  • GVHD is mediated by T-lymphocytes of the donor tissue that are sensitized against MHC antigens of the recipient
  • Mechanism: Immunocompetent donor T-cells (both CD4+ and CD8+ cells) participate in destryoing host cells
  • Skin, liver and intestine are commonly involved
  • Most commonly occurs after allogeneic bone marrow transplantation but also with organs rich in lymphocytes (liver or non-irradiated blood)
  • Timeframe varies but acute GVHD develops within one week
56
Q

What diagnostic screen is used to diagnose Meckel Diverticulum?

A
  • _ 99mmTc-pertechnetate_ scan detects ectopic gastric epithelium and helps diagnose Meckel diverticulumn
  • Accumulatin of pertechnetate in the RLQ is diagnostic of meckel diverticulum
  • Meckel’s diverticulum often contains ectopic gastric mucosa that produces acid causing possible ulceration and bleeding
57
Q

What is a complication of acute mitral regurgitation? Why does this occur and how does the body compensate?

A
  • Marked pulmonary hypertension –> pulmonary edema
  • Patients with acute MR have near-normal left atrial (LA) compliance (compliance is dV/dP) and regurgitant volume overload occurs –> LA, pulmonary venous and pulmonary artery pressures rise significantly.
  • Patients with chronic mitral regurgitation (due to myxomatous degeneration or MVP) acquire an adaptive increase in LA volume and compliance. Thus, they are less prone to pulmonary hypertension/edema but more prone to atrial fibrillation and mural thromboembolism
58
Q

What is a missense mutation?

A

A type of point mutation resulting in the placement of an incorrect aa in protein sequence (and a new aa is introduced into similar chemical structure)

59
Q

What is a Nonsense mutation?

A

A type of point mutation that introduce a stop codon within the gene sequence, resulting in shorter, truncated protein.

60
Q

What is a silent mutation?

A

Type of point mutation that result from codon base substitution which code for the same amino acid

61
Q

What is the morphology and main virulence factor for C. neoformans?

A
  • Morphology: Yeast form only; round or oval encapsulated cells with narrow-based buds
  • VF: Thick polysaccharide capsule
62
Q

What is the most common mutation seen in CF?

A
  • 70% of cases, a Codon (3-base pair) deletion (one or more entire codons (genetic triplet codes) of the phenylalaine at position 508 in the CFTR protein. Usually result in the formation of a shorter, potentially nonfunctional protein.
  • Mutation impairs posttranslational processing of the CFTR gene stranscript and results in degradation of the gene product before it can be transported to the cell surface
  • Results in complete absence of the CFTR protein from the apical membrane of exocrine duct epithelial cells
63
Q

What is the purpose of insulin?

A

Allows glucose to enter adipose and skeletal muscles via GLUT-4 glucose transporters so they can use it for energy

64
Q

What is verotoxin?

A

Shiga-like toxin (SLT) synthesized by enterohemorrhagic E. coli (EHEC) enhances cytokine release and inactivate the 60S ribosome by cleaving rRNA, EHEC does not invade host cells

65
Q

What is winter’s formula?

A
  • Used to evaluate respiratory compensation when there is metabolic acidosis (DKA)
  • Metabolic acidosis is normally partially compensated for by respiratory alkalosis ie hyperpnea (kussmaul respirations).
  • When the steady-state PaCO2 persists above the range by Winter’s formula
  • ** (PaCO2 = [1.5*HCO3-] +8 ± 2)**, the patient has a superimposed degree of respiratory acidosis and respiratory failure.
  • Example: DKA = Metabolic acidosis, we use winter’s formula and this formula indicates he should compensate to a PaCO2 of 26, yet he is still at 40. HE IS NOT COMPENSATING because his LUNGS FAILED
66
Q

Which laboratory tests should be used to evaluate liver function? Liver structural integrity and cellular intactness of liver and biliary tract?

A
  • Liver function: PT, bilirubin, Albumin, Cholesterol
  • Liver structure: transaminases
  • Biliary tract: Alkaline phosphatase, gamma-glutamyl transferase
67
Q

Which organs don’t need insulin for glucose uptake?

A

BRICK L

  • Brain
  • RBC
  • Intestine
  • Cornea
  • Kidney
  • Liver
68
Q

Why does a vitamin B12 deficiency result in homocystinemia and megaloblastic anemia?

A
  • Cobalamin (Vitamin B12) deficiency results in homocystinemia due to imparied methionine re-synthesis
  • Homocystinuria occurs in B12 deficiency because homocysteine methyltransferase, the enzyme that converts homocystine and methyltetrahydrofolate to methionine and tetrahydrofolate requires B12 as a cofactor
69
Q

What metabolic reactions is Vitamin B12 involved?

A
  • Homocysteine & methyl-THF –> methionine & THF (required fro SAM to function)
  • Methylalonyl CoA (coenzyme A) -> Succinyl CoA

UWorld FACTOIDs (10 decks)

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