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Review / Wrong Answers > 5/2 - UWorld > Flashcards

5/2 - UWorld Flashcards

1
Q

What are the proteins involved in and function of gap junctions?

A

§ Proteins - Connexins

§ Function - Intercellular communication

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2
Q

o What are the proteins involved in and function of tight junctions?

A

§ Proteins - claudins, occludin

§ Function - paracellular barrier

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3
Q

o What are the proteins involved in and function of adherins junctions?

A

§ Proteins - cadherins

§ Function - cellular anchor

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4
Q

o What are the proteins involved in and function of desmosomes?

A

§ Proteins - cadherins (e.g. desmoglein)

§ Function - cellular anchor

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5
Q

What are the proteins involved in and function of hemidesmosomes?

A

§ Proteins - integrins

§ Function - cellular anchor

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6
Q

Describe the geographic locations associated with histoplasmosis, blastomycosis, coccidiomycosis, and paracoccidiomycosis

A

Histo - Mississippi and Ohio river valleys (central US)

Blasto - Eastern and central US

Coccidio - Southwestern US

Para-coccidio - Latin America

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7
Q

Describe the histologic appearance of histoplasmosis

A

Smaller than RBCs

Macrophage filled with ovoid cells

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8
Q

Describe histologic appearance of blastomycosis

A

Round yeast with single broad based bud

Same size are RBCs

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9
Q

Describe the histologic appearance of coccidiomycosis

A

Spherule filled with endospores

Much larger than RBCs

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10
Q

Describe histology of para-coccidiomycosis

A

Budding yeast with “captain’s wheel formation”

Much larger than RBCs

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11
Q

Describe the mechanism behind glucagon as a treatment for beta blocker toxicity

A
  • Glucagon acts on G-protein coupled receptors, increasing intracellular cAMP, and thus increasing release of intracellular calcium during muscle contraction
  • This increases heart rate and cardiac contractility
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12
Q

Enzyme used to create ribose-5-phosphate in HMP shunt

A

Transketolase

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13
Q

Causes and basic premise behind phenylketonurie (PKU)

A

Tyrosine deficiency

Due to:

o Deficiency in phenylalanine hydroxylase, or

o Deficiency in tetrahydrobiopterin cofactor (BH4)

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14
Q

Basic premise behind maple syrup urine disease

A

THINK: I Love Vermont maple syrup from branched maple trees

§ Branches - blocked degradation of branched amino acids

§ I - Isoleucine

§ Love - leucine

§ Vermont - Valine

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15
Q

Presentation of maple syrup urine disease

A

CNS defects, intellectual disability, and death

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16
Q

Basic premise behind Alkaptonuria

A

Inability to degrade tyrosine due to defect of homogentisate oxidase

17
Q

Presentation of phenylketonuria

A
  • Tyrosine becomes an essential amino acid
  • Presentation:
    • Intellectual disability
    • Growth retardation
    • Seizures
    • Fair skin à inability to make melanin
    • Eczema
18
Q

Causes of homocysteinuria

A

o Cystathionine synthase deficiency

o Decreased affinity of cystathionine synthase for B6

o Methionine synthase deficiency

19
Q

Presentation of homocysteinuria

A

o Homocysteine in urine

o Marfanoid habitus

o Ocular changes (downward and inward lens subluxation – vs. Marfan which is upward)

o CV effects (thrombosis and atherosclerosis)

o Kyphosis

o Intellectual disability

20
Q

Cause of cystinuria

A

Defect in proximal convoluted tubule of the kidney in the COLA transporter (Cysteine, Ornithine, Lysine, Arginine)

Defect prevents reabsorption of COLA amino acids

21
Q

Presentation of cystinuria

A

Excess cysteine in urine can lead to hexagonal cysteine stones

22
Q

What is CREST syndrome?

A

· Calcinosis / anti-centromere antibody

· Raynoud

· Esophageal dysmotility

· Sclerodactyly (tightening of skin with loss of wrinkles)

· Telangiectasias

23
Q

Cause and presentation of Hyper-IgE Syndrome (aka Job)

A

o Deficiency in IFN-y lead to impaired neutrophil recruitment

o Presentation - FATED

§ F – coarse Facies

§ A – Abscesses

§ T – retained primary Teeth

§ E – increased IgE (all other immunoglobulins are normal)

§ D – dermatologic problems (eczema)

24
Q

Infliximab

A
  • TNF-a inhibitor
    • Recall: TNF-a is an acute phase reactant produced by activated macrophages to mediate inflammation by accelerating neutrophil migration, and facilitate lymphocyte proliferation; TNF-a is responsible for fever, anorexia, corticotropin releasing hormone, septic shot, and cachexia
  • Mechanism of action:
    • Is a monoclonal antibody to TNF-a
  • Uses:
    • Used for autoimmune conditions due to anti-inflammatory effect
    • Rheumatoid arthritis, psoriasis, ankylosing spondylitis
25
Q

Etanercept

A
  • TNF-a inhibitor
    • Recall: TNF-a is an acute phase reactant produced by activated macrophages to mediate inflammation by accelerating neutrophil migration, and facilitate lymphocyte proliferation; TNF-a is responsible for fever, anorexia, corticotropin releasing hormone, septic shot, and cachexia
  • Mechanism of action:
    • Mimics TNF-a receptor (aka it intercepts TNF-a before it can reach its target)
  • Uses:
    • Used for autoimmune conditions due to anti-inflammatory effect
    • Inflammatory bowel disease, rheumatoid arthritis, ankylosing spondylitis, psoriasis
26
Q

Cyclosporine

A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Binds cyclophilin (protein within cytosol of T-cells)
    • Inhibits calcineurin (which stimulates IL-2) à prevention of IL-2 transcription
  • Uses:
    • Transplant rejection
    • Psoriasis
    • Rheumatoid arthritis
  • Toxicity
    • Nephrotoxicity
27
Q

Tacrolimus

A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Binds FK506 binding protein
    • Inhibits calcineurin à prevention of IL-2 transcription
  • Uses:
    • Transplant rejection prophylaxis
  • Toxicity:
    • Nephrotoxicity
28
Q

Sirolumus

A
  • (aka Rapamycin)
    • Immunosuppressant
      • Blocks lymphocyte activation and proliferation
    • MOA:
      • Binds FKBp12 à inhibition of mTOR
      • Prevents response to IL-2
29
Q

Dacluzimab

A
  • Immunosuppressant
    • Blocks lymphocyte activation and proliferation
  • MOA:
    • Binds CD25 (IL-2 receptor) à preventing response to IL-2
30
Q

Describe Wiskott Aldrich syndrome

A

o X-linked recessive immunodeficiency - due to T cells unable to reorganize actin skeleton

o WATER - Wiskott Aldrich, Thrombocytopenia, Eczema (especially truncal), Recurrent infections

31
Q

Antibody associated with mixed connective tissue disease

A

Anti-U1 RNP (ribonucleoprotein)

32
Q

Antibody associated with polymositis and dermatomyositis

A

Anti-Jo-1

33
Q

Defective enzyme and presentation of fructose intolerance

A

§ Defect in aldolase B (Fructose-1-phosphate -> Glyceraldehyde or DHP)

§ F1P will accumulate, decreasing the available phosphate, and inhibiting glycogenolysis and gluconeogenesis

§ Symptoms: hypoglycemia, jaundice, cirrhosis, vomiting

· THINK: Boyfriend giving present of heels (Aldo shoes) + chocolate covered strawberries (fructose)

34
Q

What are the classic immunologic cells found in sarcoidosis

A

Elevated CD4+/CD8+ T-cell ration in bronchoalveolar lavage

35
Q
A

Review / Wrong Answers (140 decks)

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