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Review / Wrong Answers > 6/19 UWorld > Flashcards

6/19 UWorld Flashcards

1
Q

Defect in Lynch syndrome

A
  • Defect in DNA mismatch repair (MMR) – e.g. MSH2, MLH1
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2
Q

Presentation of Neurofibromatosis type 1 vs type 2

A
  • Neurofibromatosis type 1
    • Caused by mutation in NF1 gene on chromosome 17
      • This gene is responsible for control of cell division
    • Neurocutaneous disorder characterized by café-au-lait spots, cutaneous neurofibromas, optic gliomas, pheochromocytomas, Lisch nodules (pigmented iris hamartomas)
    • Neurofibromas consist of proliferation of Schwann cells, fibroblasts, and neurites
  • Neurofibromatosis type 2
    • Due to mutation of NF2 gene on chromosome 22
    • Bilateral acoustic schwannomas, juvenile cataracts, meningiomas, and ependymomas
    • Presentation:
      • Hearing loss, tinnitus, balance problems, hyperpigmented skin lesions, cataracts
    • REMEMBER 2’s:
      • Chr 22
      • Bilateral hearing loss
      • NF Type 2
      • Cataracts
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3
Q

MOA and uses of Paclitaxel

A
  • MOA:
    • Hyperstabilization of polymerized microtubules in M phase so that mitotic spindle cannot break down and anaphase cannot occur
  • Uses:
    • Used to treat ovarian and breast carcinoma
    • Also prevents intimal hyperplasia, so can be used as coating in stent placement to prevent stent restenosis
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4
Q

Tumors associated with VHL

A
  • THINK: HIPA
    • Hemangioblastoma, Inreased risk for RCC, Pheochromocytoma, Angiomatosis
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5
Q

Describe deficiency in Medium-chain acyl CoA dehydrogenase deficiency (MCAD)

A
  • Deficient enzyme for beta-oxidation à decreased ability to breakdown fatty acids into acetyl-CoA à accumulation of fatty acyl carnitines in blood with hypoketotic hypoglycemia
  • Presentation:
    • Vomiting, lethargy, seizures, coma, liver dysfunction
    • Can lead to sudden death in infants or children
  • Treatment:
    • Avoid fasting
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6
Q

Adult derivatices of pros, mes, and rhombencephalon

A
  • Prosencephalon à forebrain
    • Telencephalon
      • Walls à cerebral hemisphere
      • Cavities à lateral ventricles
    • Diencephalon
      • Walls à thalamus, hypothalamus
      • Cavities à third ventricle
  • Mesencephalon à midbrain
    • Mesencephalon
      • Walls à midbrain
      • Cavity à aqueduct
  • Rhombencephalon à hindbrain
    • Metencephalon
      • Walls à pons, cerebellum
      • Cavity à upper 4th ventricle
    • Myelencephalon
      • Walls à medulla
      • Cavity à lower 4th ventricle
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7
Q

What cardiomyopathy is associated with chronic, excessive alcohol intake?

A

dilated cardiomyopathy

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8
Q

Describe chromosomes and hormone levels in Klinefelter syndrome (testosterone, estrogen, LH, FSH)

A

47, XXY

Atrophied/hyalinized seminiferous tubules -> decreased testosterone and inhibin B -> increased FSH and LH -> increased estrogen production

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9
Q

Will you see an increase or a decrease in the following values in obstructive lung disease:

  • Residual volume (RV)
  • Functional residual capacity (FRC)
  • Total lung capacity (TLC)
  • FEV1
  • FVC
  • FEV1:FVC
A

Residual volume (RV) - increased

Functional residual capacity (FRC) - increased

Total lung capacity (TLC) - increased

FEV1 - decreased

FVC - decreased

FEV1:FVC - decreased (< 80%)

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10
Q

Diagnostic criteria for chronic bronchitis

A
  • Chronic productive cough for > 3 months per year for > 2 consecutive years
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11
Q

Histology of chronic bronchitis

A
  • Characterized by hyperplasia of mucus-secreting glands in bronchi
    • Reid index (thickness of mucosal gland layer to thickness or wall) > 50%
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12
Q

What disease presents with “blue bloating” vs. “pink puffing”

A

Chronic bronchitis = blue bloater

Emphysema = pink puffer

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13
Q

Which is worse in upper vs. lower lobes?

Panacinar vs. centriacinar emphysema

A

Centriacinar = upper lobes (think: smoke rises)

Panacinat = lower lobes

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14
Q

Describe effects of A1ATD on liver

A
  • A1ATD due to misfolding of mutated proteins
  • Misfolded proteins accumulate in the endoplasmic reticulum of hepatocytes = liver cirrhosis
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15
Q

Describe basic premise and causes of bronchiectasis

A
  • Chronic infection of the bronchi causes permanent dilation of airways
  • Causes:
    • Cystic fibrosis, Kartagener syndrome, necrotizing infection, allergic bronchopulmonary aspergillosis
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16
Q

What are the effects of histamine?

Effects on vessels and airways?

A
  • Increased nasal and bronchial mucus production
    • à dripping nose sap
  • Pain and pruritus, vasodilation, increased vascular permeability (which causes hives)
    • à red sap dripping from vascular branch (permeability)
  • Bronchoconstriction
    • à guy constricting lung branch
  • Functions as a neurotransmitter in the brain, where it regulates sleep and arousal
    • à brain tree
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17
Q

What are the 1st generation antihistamines

A
  • 1st generation H1-blockers
    • Are lipophilic and can cross the BBB
  • Diphenhydramine** and **Dimenhydrinate
    • à dragonfly fairy
  • Chorpheniramine
    • à color fairy
  • Hydroxysine, Meclizine, Promethazine
    • à fairy cuisine
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18
Q

What are the 2nd generation H1 blockers

A
  • 2nd generation H1-blockers:
    • Are less lipophilic and so do NOT cross the BBB (less central effects)
  • Fexofenadine
    • à fox
  • Cetirizine
    • à Satyr
  • Loratidine
    • à rat
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19
Q

What uses do 1st generation antihistamines have that 2nd generation do not?

A
  • Treats vestibular nausea or motion sickness
    • à seasick fairy sailors in front of the brain tree
    • Only 1st generation H1 blockers because they are lipophilic so can enter the CNS and act of the vestibular system and brainstem
    • Drowsiness (can be used to treat insomnia)
      • à guy sleeping
  • Antagonize peripheral and central muscarinic receptors (e.g. pupillary dilation, dry mouth, urinary retention, constipation, exacerbation of glaucoma, and delirium)
    • à anti-muscarinic tea party
  • Treat extrapyramidal side effects caused by antipsychotics (e.g. acute dystonia)
    • à falling “extra parking” cone
    • This is because the anti-muscarinic effects re-establish dopaminergic-cholinergic balance
  • Antagonize serotonin receptors in the CNS stimulating appetite and weight gain
    • à cut smiley face cake
    • à stuffed fairy next to cake
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20
Q

What are the two long-acting Beta-2 agonists (LABA) used for asthma

A
  • Salmeterol and Formoterol
    • = Salute
    • = formation
    • = ROL call
  • Used for prophylaxis of asthma
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21
Q

MOA of Montelukast and Zafilukast

A

Direct inhibitors of leukotriene receptors (CysLT1)

Causes broncodilation

Used for persistent asthma, espcially aspirin-induced asthma

22
Q

What drugs are substrates of CYP-450

A
  • Always Think When Outdoors:
    • A - Anti-epileptics
    • T - Theophylline (caffeine-like drug)
    • W - Warfarin
    • O - OCPs
23
Q

MOA of Omalizumab

A
  • Mechanism of action
    • Recall:
      • Mast cell degranulation is important to the pathogenesis of asthma
        • à bee hive
      • Antigen binding to IgE on mast cells causes degranulation and release of inflammatory mediators (e.g histamine)
        • à IgE gun shooting hive
    • Is an anti-IgE monoclonal antibody directed against the Fc portion of IgE (part that attaches IgE to mast cell), preventing mast cell sensitization
      • à limo guy grabbing end of IgE gun
  • Uses:
    • Adjunctive therapy for moderate-severe persistent asthma
24
Q

MOA of Cromolyn sodium

A
  • Cromolyn sodium à Lynn’s bee control in bottom R of image
    • Mechanism of action:
      • Inhibits mast cell degranulation, preventing the release of histamine
        • à bee sedating smoke
25
Q

What is used for emergent treatment of acute asthma exacerbation

A
  • Short-acting beta-2 agonists
    • à beta-2 tuba kid flying away
  • Systemic corticosteroids
    • à moon face balloon on kid flying away
    • Oral or IV administration
      • à ivy on wall behind moon balloon
  • Nebulized Ipratropium bromide (anticholinergic)
    • à cat-ipra-pillar balloon
  • Epinephrine
    • à EPIC!
26
Q

Will the following value be high or low in restrictive lung disease:

  • TLC
  • FEV1
  • FVC
  • FEV1:FVC
A

Decreased TLC

Decreased FEV1 and FVC, but FVC is decreased more

FEV1:FVC ratio is increased (> 80%)

27
Q

What disease presents with:

  • In children
  • Lytic bone lesions
  • Skin rash
  • Recurrent otitis media
  • Restrictive lung disease
A

Langerhans cell histiocytosis

  • Neoplastic proliferation of specialized dendritic cells (especially in skin)
  • Birbeck (“tennis racket”) granules seen on EM
  • S-100 (+) and CD1a (+)
28
Q

What type of HSR is hypersensitivity pneumonitis

A

Aka Pigeon breeder or Farmer’s lung

Mixed type III/IV HSR to environmental antigen

Presents with dyspnea, cough, chest tightness, and headache

Restrictive lung disease

29
Q

What pneumoconiosis is caused by aerospace and manufacturing industries

A

Berylliosis

30
Q

What pneumoconiosis is associated with shipbuilding and roofing

A

Asbestos

31
Q

Which pneumoconioses causes increased risk of cancer?

A

Asbestos

  • Causes fibrosis of lung or pleura; cancer of lung or pleura (mesothelioma)
    • Lung carcinoma more common than mesothelioma
32
Q

Describe presentation of Berylliosis

A

Noncaseating granulomas in lung, hilar lymph nodes, and systemic organs

Looks similar to sarcoidosis

33
Q

Which pneumoconioses is associated with increased risk for TB and why

A

Silicosis

Silica impairs phagolysosome formation (increased risk for TB)

34
Q

Describe the pathogenesis behind acute respiratory distress syndrome (ARDS)

A

Due to diffuse damage to alveolar-capillary interface

Caused by neutrophil activation inducing protease- and free radical-mediated damage of type I and type II pneumocytes

Endothelial damage = increased capillary permeability = protein-rich leakage into alveoli = diffuse alveolar damage and noncardiogenic pulmonary edema

Results in intra-alveolar hyaline membrane

35
Q

Causes of ARDS

A

Sepsis, Pancreatitis, Pneumonia, Aspiration, Uremia, Trauma, Amniotic fluid embolism, Shock, Infection

36
Q
A
37
Q

What is the function of smooth ER, and where is a lot of it found

A

o Site of steroid synthesis and detoxification of drugs and poisons

o A lot of smooth ER found in adrenal cortex and hepatocytes

38
Q

2 functions of Golgi apparatus

A

Post-translational protein modification

Distribution center for proteins and lipids from ER to secretory vesicles, lysosomes, or plasma membrane

39
Q

Describe the amino acids that can be modified in the golgi apparatus

A

o Asparagine (modifies N-oligosaccharide)

o Serine (adds O-oligosaccharide)

o Threonine (adds O-oligosaccharide)

40
Q

How does Golgi apparatus mark a protein to be sent to lysosome

A

Adds mannose-6-phosphate to proteins destined for lysosomes

41
Q

What is I-cell diseaase

A
  • o I-cell disease = deficiency in mannose phosphorylation
    • No mannose to target lysosomal proteins = proteins are secreted extracellularly instead of into lysosome
    • Corneal clouding, coarse facies, HSM, skeletal abnormalities, restricted joint movement, +/- intellectual disability
    • Death by age 8
42
Q

What are the 3 most imporant vesicular trafficking protiens

A

Coat protein I and II (COPI and COPII)

Clathrin

43
Q

Describe the origin and destination of each of the trafficking protiens: COPI, COPII, Clathrin

A
  • COPI
    • retrograde
    • from Golgi to rough ER
  • COPII
    • anterograde
    • from rough ER to golgi
  • Clathrin
    • from golgi to lysosomes
    • from cell membrane into cell
44
Q

What are the function of chaperones

A

Intracellular protein involve in facilitating and/or maintaining protein folding

45
Q

What is heat shock protein

A

A type of chaperone

Heat shock protein (e.g. HSP60) are expressed at high temperatures in yeast to prevent protein denaturing/misfolding

46
Q

Which cyclin-CDK complexes assist in the progression from G1 to S phase

A

Cyclin D + CDK4

Cylcin E + CDK 2

47
Q

What are the exclusively ketogenic amino acids, and in what disorder are they important

A

Lysine and leucine

Patients with pyruvate kinase deficiency should stick to a ketogenic diet in order to prevent the buildup of pyruvate

48
Q

What are the negatively charged amino acids

A

The acidic ones

Aspartate and glutamate

49
Q

What are the positive charged amino acids (make up histone since they bind to neg. DNA)

A

Are the basic amino acids

  • THINK: His lies are basic
    • His = histidine, lies = lysine, are = arginine, basic
      • o Lysine
      • o Arginine
      • o Histidine
  • Arginine and lysine are within histones
    • THINK: the only + charged AA that sounds like histone is not in histones
50
Q

Can cholinesterase inhibitors be used to reverse the effects of depolarizing or non-depolarizing neuromuscular blockade

A

Non-depolarizing (e.g. Rocuronium) - MOA is competitive inhibition of ACh receptor, so increasing ACh will undo effects

Depolarizing agents (e.g. Succinylcholine) are ACh agonist which cause contant depolarization so that the receptor cannot respond to subsequent impulses

Can only be reversed by AChE inhibitors during phase 2

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