BOOTCAMP Flashcards

1
Q

Is a fructose transporter chiefly found on the apical surface of intestinal epithelial cells and mature spermatocytes.

A

GLUT-5

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2
Q

Is primarily utilized in neuronal and placental glucose transport.

A

GLUT-3

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3
Q

Is found on the basement membrane of renal tubules and mucosa of the small intestine, hepatocytes, pancreatic β cells.

A

GLUT-2

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4
Q

Is a high-affinity transporter that contributes to basal glucose transporter in all cell types. However, it is highly expressed in erythrocytes and cells forming the blood-brain barrier (endothelial cells, astrocytes, pericytes, microglia).

A

GLUT-1

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5
Q

Is stored in vesicles predominately inside skeletal myocytes and adipocytes.

A

GLUT-4

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6
Q

Activation of ? can stimulate the translocation of GLUT-4 to the plasma membrane.

A

Phosphatidylinositol-3-kinase (PI3K)

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7
Q

The insulin receptor is a tetramer made from two ⍺ units and two β units joined together by

A

Disulfide bonds.

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8
Q

Breast malignancies typically arise from ducts or lobules, with both types originating from epithelial structures called

A

Terminal duct lobular units (TDLUs).

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9
Q

Typically presents as an irregular-shaped, adherent breast mass, with the upper outer quadrant of the breast being the most frequent site.

A

Invasive ductal carcinoma (IDC)

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10
Q

Code for proteins involved in repairing double-stranded DNA breaks (DSB).

A

BRCA1 and BRCA2

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11
Q

Lynch syndrome, or hereditary non-polyposis colorectal cancer, can increase the risk of endometrial and colorectal cancer. It is due to a germline mutation in DNA mismatch repair genes

A

Most commonly MHL1 and MHL2

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12
Q

Is a tumor suppressor gene located on the short arm of chromosome 9. This gene codes for the p16 protein, which normally induces cell cycle arrest at the G1 phase.

A

CDKN2A

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13
Q

CDKN2A: An inactivation mutation is associated with the development of various malignancies, including

A

Melanoma, pancreatic, and lung cancer.

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14
Q

Is a tumor suppressor gene located on the long arm of chromosome 18.

A

SMAD4

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15
Q

An inactivation mutation is found in over half of pancreatic adenocarcinomas.

A
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16
Q

Are tumor markers for melanoma.

A

HMB-45 and MART-1

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17
Q

Melanoma antigen recognized by T cells 1 (MART-1) is a protein found in ? molecules on melanoma cells.

A

MHC class I

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18
Q

Melanoma can be identified clinically using the “ABCDEs,” including:

A

Asymmetry
Border irregularity
Color variability
Diameter > 6 mm
Evolution over time

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19
Q

Is the most common skin malignancy and presents with a pearly nodule with telangiectasia and central ulceration or crusting.

A

Basal cell carcinoma

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20
Q

Is associated with BerEp4 on histological stains

A

Basal cell carcinoma

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21
Q

Kaposi sarcoma is a vascular tumor of the skin, gastrointestinal tract, or respiratory tract associated with

A

HHV-8 and HIV

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22
Q

Tumor markers associated with Kaposi sarcoma.

A

CD34, CD31, and D2-40

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23
Q

Is a rare, aggressive skin cancer that typically arises in the head, neck, or extremities.

A

Merkel cell carcinoma

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24
Q

Are tumor markers associated with Merkel cell carcinoma.

A

Chromogranin A, PAX5, and cytokeratin 20

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25
Q

Is the second most common skin cancer and presents with an ulcerative red lesion.

A

Squamous cell carcinoma

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26
Q

Is associated with actinic keratoses, immunosuppressive medications, and chronic wounds.

A

Squamous cell carcinoma

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27
Q

Is positive for cytokeratin on immunohistochemical staining.

A

Squamous cell carcinoma

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28
Q

Is a serine/threonine protein phosphatase that begins the helper T lymphocyte activation cascade.

A

Calcineurin

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29
Q

Antigen-presenting cells (e.g., macrophages, dendritic cells, and B lymphocytes) activate T lymphocyte receptors, triggering calcineurin-mediated dephosphorylation of

A

NFAT-P to NFAT (i.e., nuclear factor of activated T cells).

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30
Q

NFAT then activates ? transcription to stimulate the growth and differentiation of T lymphocytes.

A

IL-2

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31
Q

Are immunosuppressant medications that inhibit calcineurin, thereby preventing the propagation of this pathway. NFAT activates IL-2.

A

Cyclosporin and tacrolimus

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32
Q

IL-2 mRNA levels will decrease with tacrolimus usage, as this medication inhibits calcineurin binding to ? binding protein (FKBP) and prevents the dephosphorylation of NFAT.

A

FK506

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33
Q

Tacrolimus is used for immunosuppression following solid organ transplantation. Potential adverse effects include

A

Nephrotoxicity, hypertension, neurotoxicity, hyperlipidemia, and type II diabetes mellitus.

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34
Q

Binds to cyclophilin and calcineurin, forming a complex that renders calcineurin ineffective.

A

Cyclosporin

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35
Q

Interleukin-2 receptor availability would decrease with ? usage. ? is an IL-2R monoclonal antibody used in renal transplantation.

A

Basiliximab

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36
Q

Tumor necrosis factor-α levels would decrease with the administration of ?

A

Glucocorticoids

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37
Q

Glucocorticoids inhibit ?, decreasing cytokine transcription and preventing B and T lymphocyte activation and proliferation.

A

NF-κB

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38
Q

Xanthine monophosphate would decrease with ? usage.

A

Azathioprine

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39
Q

Inhibits PRPP (phosphoribosyl pyrophosphate) aminotransferase, reducing lymphocyte proliferation via blockade of nucleotide synthesis.

A

Azathioprine

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40
Q

Inosine monophosphate (IMP) levels would decrease with ? usage.

A

Mycophenolate mofetil

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41
Q

Mycophenolate inhibits ?, reducing purine levels and B and T lymphocyte production.

A

IMP dehydrogenase

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42
Q

Drug induced lupus syndrome

A

Hydralazine, procainamide, isoniazid

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43
Q

Add acetal groups to lysine. Relaxes chromatin to transcription.

A

Histone acetyltransferasas

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44
Q

SHIPPE (Sulfonamides, Hydralazine, Isoniazid, Phenytoin, Procainamide, Etanercept)

A

Drug induced lupus

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45
Q

Are seen in the diffuse form of scleroderma.

A

Anti-DNA topoisomerase I antibodies, also known as anti-Scl-70 antibodies

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46
Q

Are involved in Mixed Connective Tissue Disease (MCTD).

A

Anti-U1 ribonucleoprotein antibodies

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47
Q

Ribavirin (antiviral)

A

Inhibits IMP dehydrogenase

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48
Q

Are associated with celiac disease.

A

Anti-tissue transglutaminase antibodies

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49
Q

Mycophenolate (inmunosuppresant)

A

Inhibits IMP dehydrogenase of white cells

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50
Q

Added to PRPP by HGPRT = Thioinosinic acid.
Decreased level of IMP, AMP and GMP.

A

6-Mercaptopurine

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51
Q

Immunosuppressant used in inflammatory bowel disease, coverted to 6-MP

A

Azathioprine

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52
Q

Known to increase the risk of developing gastric carcinoma. Smoked meats.

A

Nitrosamines

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53
Q

Associated with metastatic gastric adenocarcinoma. Presence of bilateral round adnexal masses. Diffuse-type gastric carcinomas that have spread to the ovaries. They are most commonly bilateral at the time of diagnosis, distinguishing them from primary ovarian tumors.

A

Krukenberg tumors

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54
Q

Are the most common group of primary ovarian tumors. They most often derive from the coelomic epithelium that lines the ovary and are subclassified as serous or mucinous on histology. Less common types include endometrioid tumors composed of endometrioid-like glands and Brenner’s tumors composed of bladder (transitional)-like epithelium.

A

Epithelial tumors

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55
Q

Are a group of ovarian tumors derived from embryonic tissues. Are the second most common primary ovarian tumors, mainly occurring in females of reproductive age.

A

Germ cell tumors

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56
Q

Are common types of ovarian cysts.

A

Follicular cysts and theca-lutein cysts

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57
Q

Are typically unilateral. They arise from the distention of an unruptured Graafian follicle, occurring most often in young females.

A

Follicular cysts

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58
Q

Are often bilateral and multi-lesional. They arise due to hCG overstimulation and are associated with multiple gestations and trophoblastic disease.

A

Theca-lutein cysts

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59
Q

Do not typically present with fulminant abdominal and systemic symptoms.

A

Ovarian cysts

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60
Q

A rare group of primary ovarian tumors that arise from the structural connective tissue cells of the ovary or the sex cord. Examples include granulosa-theca cell tumors, Sertoli-Leydig cell tumors, and fibromas.

A

Sex cord-stromal tumors

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61
Q

Commonly presents with right upper quadrant pain, which can radiate to the back or right shoulder. Less commonly, individuals may present with abdominal fullness, distension, and reflux. His CT scan reveals hyperdensities within the gallbladder, confirming this diagnosis.

A

Symptomatic cholelithiasis

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62
Q

Parenteral feeding is accompanied by multiple complications, such as

A

Risk of bloodstream infection, metabolic effects, and gallstones.

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63
Q

The lack of normal oral gastrointestinal stimulation leads to biliary stasis, which encourages ? in a large proportion of individuals on long-term TPN.

A

Gallstone formation

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64
Q

Is a hormone that mediates bile production and release from the gallbladder.

A

Cholecystokinin

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65
Q

Represented by Th1 lymphocytes surrounding a core of multinucleated giant cells (Langhans giant cells) and epithelioid histiocytes engulfing mycobacterium.

A

Granuloma

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66
Q

An acid-fast bacillus that can elicit the formation of caseating granulomas in lung tissue.

A

MTB

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67
Q

Resident pulmonary macrophages engulf MTB and subsequently perform two actions:

A
  • Present various antigens (via MHC class II) to CD4+ T lymphocytes
  • Secrete IL-12

This induces differentiation of CD4+ T lymphocytes into Th1 lymphocytes, which then migrate and surround the inflammatory region (containing macrophages and MTB) and secrete interferon-γ. . This stimulates macrophages to release TNF-α in an autocrine fashion.

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68
Q

MTB: IFN-γ and TNF-α induce macrophage differentiation into ? — cells that can readily fuse to form multinucleated giant cells with enhanced phagocytic capabilities.

A

Epithelioid histiocytes

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69
Q

Are predominately involved in Th2 subtype responses (e.g., antibody production, especially IgE).

A

Interleukin-4 (IL-4) and interleukin-13 (IL-13)

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70
Q

Is predominately involved in Th2 subtype responses (e.g., antibody production, especially IgA) and eosinophil recruitment.

A

Interleukin-5 (IL-5)

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71
Q

Is an anti-inflammatory cytokine involved in fibrotic repair and angiogenesis.

A

Transforming growth factor β

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72
Q

Is an autosomal recessive disorder that most commonly results from an ∆F508 mutation in the cystic fibrosis transmembrane regulator (CFTR) gene.

A

Cystic fibrosis (CF)

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73
Q

Thick, viscous mucus accumulates in multiple organ systems, including the gastrointestinal and respiratory tract. Clinical manifestations include chronic, productive cough, recurrent sinopulmonary infections, pancreatic insufficiency (e.g., CF-related diabetes, malabsorption), biliary disease (e.g., bile duct obstruction), and male infertility (bilateral absence of vas deferens).

A

Cystic fibrosis (CF)

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74
Q

Can be used to determine the allelic and genotypic frequencies within a given population.

A

The Hardy-Weinberg principle

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75
Q

Hardy-Weinberg principle: This principle states that these frequencies will remain relatively constant from generation to generation if five contingencies are met:

A
  • Large population (major changes in the frequency of allele do not cause a genetic drift)
  • Random mating (mating will not favor a particular allele)
  • No genetic mutations (no DNA mutations for the alleles which may alter their function)
  • No natural selection (no evolutionary pressure will favor a particular allele)
  • No migration in and out of the population (new alleles are not introduced into the population)
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76
Q

The Hardy-Weinberg equation used to determine allelic frequencies is:
p + q = 1

A

p represents the dominant form of an allele
q represents the recessive form of an allele

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77
Q

The Hardy-Weinberg equation used to determine genotypic frequencies is:
p2 + 2pq + q2 = 1

A
  • p2 represents the frequency of the homozygous dominant genotype
  • 2pq represents the frequency of the heterozygous (carrier) genotype
  • q2 represents the frequency of the homozygous recessive genotype
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78
Q

Gastrointestinal hormones produced by enteroendocrine cells that stimulate insulin secretion from pancreatic β cells.

A

Incretins

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79
Q

Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1(GLP-1)

A

Incretins (examples)

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80
Q

Released by intestinal K cells located primarily in the duodenum and jejunum.

A

GIP

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81
Q

GLP-1

A

Secreted by intestinal L cells located primarily in the distal ileum and colon.

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82
Q

Increatins

A

Released in response to amino acids, fatty acids, and glucose-containing meals. Are released independent of plasma glucose levels, typically occurring before any elevation of plasma glucose levels following a meal.

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83
Q

Oral-administered glucose

A

Is metabolized faster than intravenous-administered glucose because oral intake triggers more robust insulin release via incretin production.

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84
Q

Intravenous glucose

A

Does not pass through the gastrointestinal tract, so it does not stimulate incretin release.

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85
Q

Is a hormone that stimulates appetite and promotes weight gain. It is primarily produced in the stomach; however, it is also secreted by pancreatic ε cells in response to fasting.

A

Ghrelin

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86
Q

Raise incretin levels. DPP-4 normally degrades GLP-1, so inhibitors increase GLP-1 levels. Incretins are directly responsible for stimulating insulin secretion from pancreatic β cells.

A

Gliptins or dipeptidyl peptidase-4 (DPP-4) inhibitors (sitagliptin, linagliptin)

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87
Q

Is a protein hormone synthesized by pancreatic ⍺ cells. Its release is chiefly stimulated by low plasma glucose levels, opposing the effects of insulin. It can rapidly correct hypoglycemia by increasing hepatic glycogenolysis. Can also induce gluconeogenesis and suppress glucose uptake by cells.

A

Glucagon

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88
Q

Is a hormone released from intestinal D cells through the gastrointestinal tract and peripheral nerves throughout the body. It inhibits the release of various gastrointestinal hormones, including secretin, gastrin, glucagon, and insulin.

A

Somatostatin

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89
Q

In the early stages of the disease, bone loss predominantly affects trabecular bone, leading to trabecular thinning and perforation with the loss of interconnecting bridges. Over time, cortical bone, which composes most of the appendicular skeleton, becomes involved.

A

Osteoporosis

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90
Q

Can be caused by medications such as corticosteroids, anticonvulsants, anticoagulants, and thyroid replacement therapy. Other causes include hyperparathyroidism, hyperthyroidism, multiple myeloma, anorexia, and malabsorption syndromes.

A

Secondary osteoporosis

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91
Q

Usually occurs secondary to excessive exogenous vitamin D intake over long periods of time but can also be associated with granulomatous diseases, such as sarcoidosis. Symptoms are due to secondary hypercalcemia and include nephrolithiasis, bone pain and weakness, constipation, and neuropsychiatric disturbances. The radiographic changes are highly variable.

A

Hypervitaminosis D

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92
Q

Is a disease of bone characterized by decreased mineralization of newly formed osteoid at sites of bone turnover, resulting in the development of soft bones. It is most commonly caused by vitamin D deficiency. On imaging, the bones of patients show poor corticomedullary differentiation and an “erased” or “fuzzy” appearance of cortical bone due to decreased mineralization.

A

Osteomalacia

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93
Q

Is a localized disorder of bone remodeling caused by increased osteoclast activity, followed by increased osteoblast activity, resulting in the formation of poor-quality bone. On imaging, Paget disease of the spine commonly manifests with cortical thickening and sclerosis that encases the vertebral margins, leading to a rectangular appearance of the vertebrae.

A

Paget’s disease of bone (osteitis deformans)

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94
Q

Typically affects postmenopausal females or those over age 65 and is caused by increased bone resorption associated with decreased estrogen levels and old age.

A

Primary osteoporosis

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95
Q

Is a depolarizing neuromuscular blocker that causes muscle relaxation. It acts as an acetylcholine receptor agonist but with a longer duration of action than acetylcholine (ACh). Binding of the ACh receptor on the motor endplate results in muscle cell depolarization. This depolarization is rapidly transmitted throughout the cell via a network of sarcolemmal (i.e., muscle plasma membrane) invaginations called T-tubules. These structures allow for synchronized muscle contraction by rapidly distributing the action potential.

A

Succinylcholine

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96
Q

Because succinylcholine remains bound to the receptor, these cells remain depolarized and cannot be further depolarized. ? is unable to degrade the drug, leading to a state of depolarized muscle block and flaccid paralysis.

A

Acetylcholinesterase

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97
Q

After membrane depolarization triggers calcium ion release from the sarcoplasmic reticulum, calcium binds to troponin C. This subsequently shifts tropomyosin from the myosin-binding sites on actin that it blocks, making them available for binding by myosin.

A

Myosin binds to actin at these sites, forming a cross-bridge that performs a “power slide” that causes the contraction of muscle fibers.

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98
Q

Is a specialized type of endoplasmic reticulum found in muscle cells. It primarily releases and stores calcium ions.

A

The sarcoplasmic reticulum

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99
Q

Are specialized sarcolemmal invaginations that help to rapidly distribute an action potential throughout the cell, allowing for synchronized contraction.

A

T-tubules

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100
Q

A first-generation antihistamine used to treat seasonal allergies.

A

Dimenhydrinate

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101
Q

Antagonism of histaminergic pathways; however, they can also act on cholinergic, α-adrenergic, and serotonergic receptors.

A

The primary mechanism of action of first-generation antihistamines

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102
Q

Elderly patients are especially at risk for CNS side effects due to age-related changes in the brain. Of note, they have a decreased number of cholinergic neurons, leaving them especially sensitive to anticholinergic effects. Significant neurological effects can include confusion, sedation, dizziness, hallucinations, and delirium. Additional anticholinergic effects include tachycardia, dry mouth, decreased sweating, constipation, and urinary retention.

A

Why the elderly patients are especially at risk for CNS side effects of antihistamines?

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103
Q

Can increase elderly patients’ risk of delirium, especially with the coadministration of benzodiazepines, beta-blockers, selective serotonin reuptake inhibitors (SSRIs), neuroleptics, and antihistamines.

A

Polypharmacy

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104
Q

Is a list that consists of medications and their potential interactions to avoid in the elderly due to significant potential for adverse effects.

A

Beers criteria

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105
Q

Is an angiotensin II receptor blocker used primarily to treat hypertension. Potential side effects include hyperkalemia, hypotension, and a decreased glomerular filtrate rate. Hypotension may lead to altered mental status but does not typically present as isolated agitation.

A

Losartan

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106
Q

Side effects of metformin include gastrointestinal upset, lactic acidosis, and B12 deficiency.

A

Metformin

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107
Q

Side effects are primarily myopathy and hepatotoxicity.

A

Atorvastatin

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108
Q

Is the probability that a particular disease (e.g., breast cancer) is present, given a positive result.

A

The positive predictive value (PPV)

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109
Q

It equals the number of individuals with a particular disease who test positive, true positives (TP), divided by every individual with a positive test result, TP + false positives (FP).

A

The positive predictive value (PPV)

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110
Q

PPV

A

= TP / (TP + FP)

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111
Q

Is the probability of an individual without a disease testing negative for that disease. It equals the true negatives (TN) divided by the true negatives + false positives.

A

Specificity

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112
Q

Specificity

A

= TN / (TN + FP)

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113
Q

As specificity increases, there will be fewer FP (less likely individuals with a positive test will be without the particular disease)—leading to an increase in the PPV.

A

↑ Specificity = TN / (TN + ↓ FP) and ↑ PPV = TP / (TP + ↓FP)

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114
Q

Increasing the specificity of a test,

A

will increase the PPV by decreasing the number of false positives (FP).

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115
Q

The negative likelihood ratio = (1 – sensitivity) / specificity. The positive likelihood ratio = sensitivity / (1 - specificity). A likelihood ratio above 1 indicates the test result is associated with the presence of the disease.

A

A likelihood ratio below 1 indicates the test result is associated with the absence of the disease. A likelihood ratio of 1 does not change the probability of having the disease despite a positive or negative test result.

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116
Q

The APOE ε4 gene allele (increased susceptibility.)

A

Alzheimer disease (AD)

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117
Q

AD: Decreased ability of the lipoprotein gene product to clear

A

Amyloid-beta protein

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118
Q

Is a neurodegenerative disorder resulting from a CAG trinucleotide expansion repeat. The condition manifests with motor, behavioral, and psychiatric findings. Dementia may develop.

A

Huntington disease

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119
Q

Are associated with familial hypercholesterolemia. This condition is characterized by accelerated atherosclerosis, myocardial infarction at a young age, and xanthomas.

A

LDLR gene mutations

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120
Q

Is associated with Gerstmann-Straussler-Scheinker Syndrome, a genetically inherited prion disease. Although dementia develops in this disorder, it is distinct from AD.

A

Mutation of the PRNP gene on chromosome 20p12

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121
Q

Trisomy 18 results in ?, characterized by multiple developmental abnormalities. Most individuals die before the age of 1.

A

Edward syndrome

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122
Q

Cardiac exam reveals an abnormal heart sound, representing the sudden deceleration of blood coming from the left atrium into the left ventricle. Which of the following best describes these findings?

A

An extra early diastolic sound occurring immediately after S2. This asymptomatic patient with no underlying medical problems and an abnormal heart sound most likely has an S3 gallop or a third heart sound.

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123
Q

This gallop is caused by rapid ventricular filling and the consequence of the blood suddenly decelerating against the ventricle wall during diastole. It is commonly described as an early diastolic gallop occurring immediately after S2 causing cardiac auscultation to resemble the cadence of “Kentucky” (Ken-TUC-ky).

A

S3 gallop or a third heart sound

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124
Q

In younger patients (< 40 years of age) without significant heart disease, an S3 sound may be physiologic and is more commonly seen in

A

Athletes or pregnant women

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125
Q

A third heart sound in patients with known cardiac disease is usually considered pathologic and may be caused by heart failure, aortic or mitral regurgitation, thyrotoxicosis, or dilated cardiomyopathy. In these patients, an S3 represents

A

Ventricular dysfunction or a hypervolemic state

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126
Q

A mid-systolic murmur occurs between S1 and S2 and is most likely physiologic, likely a

A

Pulmonary flow murmur

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127
Q

An early systolic click occurring directly after S1 describes a murmur caused by ?, which commonly presents with palpitations or shortness of breath.

A

Mitral valve prolapse

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128
Q

A late diastolic sound occurring directly before S1 describes an S4 gallop, or fourth heart sound. This sound is caused by the ? against a high-pressure ventricle and may cause cardiac auscultation to resemble the cadence of “Tennessee” (Ten-nes-SEE).

A

Atrial kick (late diastolic atrial contraction)

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129
Q

It is commonly heard in patients with reduced ventricular compliance, such as the elderly population, in ventricular hypertrophy, ischemic cardiomyopathy, and acute myocardial infarction.

A

S4 gallop or fourth heart sound

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130
Q

Assuming ischemic brain injury from vessel rupture, ptosis and miosis would result from sympathetic nerve involvement, while disturbances in pain and temperature sensation occur when ? are affected.

A

The spinothalamic tract and spinal trigeminal nucleus

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131
Q

Dizziness and ataxia reflect damage to the ?, respectively.

A

Vestibular nucleus and cerebellar peduncle

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132
Q

New-onset hoarseness is suspicious for vagal nerve involvement due to

A

Nucleus ambiguus damage

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133
Q

Symptoms such as hoarseness, dysphagia, and decreased gag response specifically indicate cranial nerve IX and X involvement, localizing the lesion to the lateral medulla.

A

Lateral medullary syndrome (i.e., Wallenberg syndrome) classically occurs due to damage of the posterior inferior cerebellar artery (PICA) from stroke, hemorrhage, or trauma.

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134
Q

Manifesting as dysphagia, hoarseness, decreased gag reflex, and/or hiccups are specific to these lesions. Other symptoms may include vomiting, vertigo, contralateral sensory loss of pain and temperature with ipsilateral facial sensory loss, ipsilateral Horner syndrome, ipsilateral ataxia, and dysmetria.

A

Nucleus ambiguus defects

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135
Q
  1. 4 cranial nerves above the pons, in the pons and in the medula.
  2. 4 cranial nerves are midline, 4 cranial nerves are lateral.
  3. 4 “M” structures are midline: the MLF, Motor nucleus, Motor pathway, Medial Lemniscus.
  4. 4 “S” structures are to the side: symphatetic, spinothalamic, sensory, and spinocerebellar.
A

RULE OF 4S

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136
Q

Trigeminal damage indicates ?; it doesn’t exclusively indicate pontine involment

A

Lateralization of the lesion

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137
Q

Only hearing loss can be localized in

A

CN VIII

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138
Q

Can originate from both medullary and pontine damage.

A

Vestibular signs

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139
Q

Are the most common causes of gastric ulcers

A

Helicobacter pylori infection and NSAID use

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140
Q

Pain associated with gastric ulcers often worsens with ? as the presence of food in the stomach triggers acid secretion, further irritating the mucosa. This can lead to food aversion and weight loss.

A

Food intake

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141
Q

Gastric ulcers are most commonly located along the lesser curvature of the stomach, at the transitional zone between the gastric body and the antrum. If these ulcers erode through the gastric wall, there is a risk of bleeding from ?, coursing along the lesser curvature.

A

The right and left gastric arteries

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142
Q

Gastric ulcers occur in the proximal stomach, including the fundus and cardia, less than ? of the time.

A

5%

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143
Q

Gastric ulcers on the ? are extremely rare and, when they occur, are often malignant.

A

Greater curvature

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144
Q

The incidence of pyloric ulcers is about ? of the incidence of all other gastric ulcers combined.

A

18%

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145
Q

This patient’s T-score of -2.8 meets the diagnostic criteria for ?—a skeletal condition characterized by decreased bone mass, associated with reduced bone strength and an increased risk of fractures.

A

Osteoporosis

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146
Q

Osteoporosis is assessed via ?measurement by DEXA scan at the lumbar spine, total hip, and femoral neck. A diagnosis is made when the BMD value at the spine, hip, or femoral neck is 2.5 or more standard deviations below the young adult mean (T-score ≤ -2.5) or when a patient suffers a fragility fracture (e.g., fall from standing height, minimal trauma) of the hip or vertebra.

A

Bone mineral density (BMD)

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147
Q

In primary osteoporosis, trabecular and cortical bone lose mass despite normal bone mineralization and normal lab values for

A

Serum Ca2+, PO43-, parathyroid hormone (PTH), and alkaline phosphatase (ALP).

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148
Q

In secondary osteoporosis, BMD decreases are usually accompanied by

A

Abnormal lab values.

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149
Q

Primary osteoporosis typically affects postmenopausal females (type 1 primary osteoporosis) due to the ? associated with decreased estrogen levels.

A

Increased bone resorption

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150
Q

Patients are encouraged to incorporate regular weight-bearing exercise and adequate intake of Ca2+ and vitamin D into daily living. In addition, medications such as bisphosphonates, teriparatide, selective estrogen receptor modulators (SERMs), and denosumab are treatment options that increase bone mass.

A

Type 1 primary osteoporosi

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151
Q

Lab values often reveal decreased serum Ca2+ due to increased Ca2+ concentrations within bone.

A

Osteopetrosis

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152
Q

Patients present with a normal BMD and serum Ca2+ and PO43-. The high levels of ALP levels result from dysfunctional osteoclast activity. Clinical features include bone enlargement, facial deformities, and hearing loss.

A

Paget disease of bone (osteitis deformans)

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153
Q

Characterized by decreased mineralization of newly formed osteoid at sites of bone turnover, which results in the development of soft bones. It is most commonly due to vitamin D deficiency.

A

Osteomalacia

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154
Q

As a result, patients present with a low serum Ca2+and PO43- and an elevated serum PTH and ALP.

A

Osteomalacia

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155
Q

On laboratory testing, patients display hypercalcemia, hypophosphatemia, and increases in serum PTH and ALP.

A

Hyperparathyroidism

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156
Q

Patients with primary osteoporosis present with decreased bone mineral density (T-score ≤ -2.5) despite

A

Normal Ca2+, PO43-, PTH, and ALP serum values on laboratory testing

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157
Q

No pain, penile discharge, lymphadenopathy, or perianal lesions. This is most likely indicative of a

A

Chancre (due to primary syphilis, secondary to infection with Treponema pallidum.)

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158
Q

Following treatment of primary syphilis, the patient returns to the clinic with fever, chills, headache, and myalgias. This is most likely representative of a ? secondary to the rapid lysis of syphilitic spirochetes in the setting of recent antibiotic initiation (i.e., penicillin). This lysis results in the release of bacterial endotoxin-like substances and pyrogens, causing an acute, transient, systemic reaction (e.g., fever, chills, myalgias, headache) within hours of treatment initiation.

A

Jarisch-Herxheimer reaction

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159
Q

Describes the pathogenesis of toxic shock syndrome. This is secondary to the release of TSST-1 (S. aureus) or erythrogenic exotoxin A (S. pyogenes), leading to the inappropriate connection of T-cell receptors (TCRs) on T lymphocytes to MHC class II molecules on antigen-presenting cells outside of the normal binding sites. This leads to massive cytokine release and characteristic features such as high fever, rash, vomiting, diarrhea, shock, and end-organ dysfunction (e.g., hypotension, altered mental status).

A

Superantigen activation of immune cells

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160
Q

Describes a type I hypersensitivity reaction, which can manifest as an allergic (e.g., urticaria or pruritus) or anaphylactic (e.g., hypotension, respiratory arrest, wheezing, or shock) reaction. If the patient does not have a history of allergies, makes it less likely for this reaction to occur.

A

Release of preformed IgE

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161
Q

Describes the pathogenesis of a type III hypersensitivity reaction. Antigen-antibody complexes activate complement, which attracts and activates neutrophils to induce localized inflammation. Examples include systemic lupus erythematosus, poststreptococcal glomerulonephritis, and rheumatoid arthritis.

A

Circulating immune complex deposition

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162
Q

Would induce apoptosis in virally infected, graft, or neoplastic cells. Granzymes activate the mitochondria of these cells to release enzymes (e.g., caspases) that induce apoptosis. This process is not involved in a Jarisch-Herxheimer reaction.

A

Granzyme release from CD8+ T lymphocytes

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163
Q

Hyperglycemia can lead to the chemical attachment of glucose to amino acids without the involvement of enzymes (non-enzymatic glycation). These glycated-protein products can become cross-linked, leading to the formation of

A

Advanced glycation end products (AGEs).

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164
Q

AGEs contribute to various pathologies including renal failure. AGEs can decrease renal blood flow (from damage to the afferent arterioles), lead to mesangial proliferation and glomerular fibrosis (glomerulosclerosis), and can cause hyperfiltration (from damage to the efferent arterioles). This can ultimately result in

A

Diabetic nephropathy and nephrotic syndrome.

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165
Q

Glucose is predominately metabolized by the glycolytic pathway under normal metabolic conditions. However, prolonged hyperglycemia can saturate hexokinase, resulting in shunting to

A

The polyol pathway

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166
Q

Here glucose is converted to sorbitol via aldose reductase.

A

The polyol pathway

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167
Q

Sorbitol can then be converted to fructose via

A

Sorbitol dehydrogenase

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168
Q

Hyperglycemic states can cause oversaturation of sorbitol dehydrogenase, leading to sorbitol accumulation.

A

Cells of the peripheral nerves, retina, lens, and kidney lack significant amounts of sorbitol dehydrogenase, further contributing to sorbitol accumulation.

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169
Q

Sorbitol does not readily cross cellular membranes, and its accumulation can result in

A

Osmotic damage

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170
Q

Sorbitol accumulation has many potential manifestations, including

A

Neuropathy and ocular disorders (e.g., retinopathy, cataracts). It can accumulate in the epithelial and elongated fiber cells of the lens, causing fluid buildup and opacification over time (cataracts).

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171
Q

Fructose accumulation can occur in several metabolic disorders, including ?. Sorbitol can also be converted into fructose via sorbitol dehydrogenase. However, the accumulation of fructose is not the precipitating factor in either cataract formation or renal failure from hyperglycemia.

A

Essential fructosuria.

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172
Q

Glycogen accumulation can occur in glycogen storage disorders (e.g., Pompe’s Disease). However, the symptoms that arise (e.g., hypotonia, weakness, etc.) result from a state of

A

Hypoglycemia

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173
Q

Prolonged hyperglycemic states can lead to ?, resulting in neuropathy, retinopathy, and cataract formation.

A

Sorbitol accumulation from the polyol pathway

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174
Q

Occurs in familial hypertriglyceridemia (i.e., type IV hyperlipoproteinemia). Familial hypertriglyceridemia is an autosomal dominant disorder associated with the development of type II diabetes mellitus. Patients are also at risk for acute pancreatitis and early-onset atherosclerosis.

A

Hepatic overproduction of VLDL

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175
Q

Metabolic effects of thyroid hormone include

A

Increased basal metabolic rate, carbohydrate metabolism, and lipid metabolism

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176
Q

Thyroid hormone increases lipid metabolism in several ways. It increases

A

Lipolysis, biliary cholesterol secretion, and hepatic low-density lipoprotein (LDL) receptor expression

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177
Q

Consists of a small concentration of triglycerides and a high concentration of cholesterol and cholesteryl esters. It contains apolipoprotein B-100, a surface receptor for LDL receptors, and an enzyme cofactor.

A

LDL

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178
Q

LDL binds the hepatic LDL receptor via apolipoprotein B-100, clearing it from the plasma. T3 is responsible for upregulating LDL receptor gene activation. Consequently, patients with hypothyroidism are at risk for

A

High LDL plasma levels, hyperlipidemia, and hypercholesterolemia.

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179
Q

Is a rare autosomal recessive disorder caused by severe dysfunction of lipoprotein lipase (LPL). LPL is an extracellular enzyme found on the capillary walls that hydrolyzes triglycerides into fatty acids and glycerol, requiring the apolipoprotein C-II cofactor.

A

Familial hyperchylomicronemia (Type I hyperlipoproteinemia)

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180
Q

Familial hyperchylomicronemia is most commonly caused by a deficiency in ? but can also result from a deficiency in apolipoprotein C-II. Manifestations include recurrent acute pancreatitis, hypertriglyceridemia, eruptive xanthomas, and lipemia retinalis.

A

LPL

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181
Q

Is an autosomal recessive disorder caused by an abnormal subtype of apolipoprotein-E (i.e., E2). This results in the accumulation of chylomicron remnants and VLDL due to inadequate hepatic clearance. Patients classically develop hypercholesterolemia, hyperlipidemia, tuberoeruptive and palmar xanthomas, and early-onset atherosclerosis.

A

Familial dysbetalipoproteinemia (i.e., type III (remnant) hyperlipoproteinemia)

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182
Q

Dysuria and increased urinary frequency, indicative of urinary tract infection (UTI). Concomitant fever, unilateral costovertebral angle tenderness, and pyuria raise concern for

A

Acute pyelonephritis

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183
Q

The presence of white blood cells (pyuria) and bacteria in the urine are typical.

A

Acute pyelonephritis

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184
Q

Treatment of acute pyelonephritis is generally empiric, with considerations of the severity, setting, and individual patient risk factors. Before treatment is initiated, urinary cultures should be obtained to guide treatment antibiotic sensitivities once the causative pathogen is identified. Without treatment, ? may occur.

A

Bacteremia, sepsis, and renal failure

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185
Q

Represents acute inflammation of the renal interstitium and tubules. It can be asymptomatic or associated with fever, pyuria, hematuria, costovertebral angle tenderness, and azotemia. It is most commonly associated with the administration of drugs that act as haptens (e.g., diuretics, NSAID, sulfa drugs) and induce a type IV hypersensitivity reaction. The lack of known drug exposure in this patient makes AIN less likely.

A

Acute interstitial nephritis (AIN), also called tubulointerstitial nephritis

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186
Q

Is associated with localized findings, including dysuria, urinary frequency, hematuria, and suprapubic pain.

A

Cystitis

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187
Q

Comprises a spectrum of glomerular disorders that typically manifest with renal insufficiency, hematuria, and/or proteinuria. Depending on the etiology, systemic findings may be present.

A

Glomerulonephritis

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188
Q

Is a localized infection of the urethra that is typically associated with sexually transmitted infections. Individuals may also develop dysuria, pruritis, and urethral discharge.

A

Urethritis

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189
Q
  • Anatomic abnormality
  • Female sex
  • Pregnancy
  • Medical intervention (urinary catheter)
A

Epidemiology UTI

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190
Q
  • E. Coli
  • Staphylococcus saprophyticus (2do in sexually active women)
  • Klebsiella pneumoniae
  • Proteus Mirabilis (assoc. with strutive stones)
A

Etiology UTI

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191
Q
  1. First line:
    a) Nitrofurantoin (5 days)
    b) TMP/SMX (3 days)
    c) Fosfomycin (single dose)
  2. Beta-lactams (5-7 days)
  3. Flouroquinolones (varies)
    *Regimens in men should be longer usually to penetrate blood-testis barrier
A

Treatment UTI

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192
Q

Protein synthesis

A

Mechanism Nitrofurantoin

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193
Q

Folic acid synthesis

A

Mechanism TMP/SMX

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194
Q

Cell wall synthesis

A

Mechanism Fosfomycin, B-lactams

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195
Q

DNA gyrase

A

Mechanism Flouroquinolones

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196
Q

Intermittent abdominal pain, fatigue, and three episodes of coffee-ground emesis in the setting of three months of nausea and abdominal pain that worsens with meals. Physical exam is notable for conjunctival pallor and moderate epigastric tenderness to palpation.
This patient’s history is concerning for a

A

Gastric ulcer

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197
Q

Pain associated with gastric ulcers typically worsens with food intake as food stimulates the ?, further irritating the mucosa.

A

Secretion of gastric acid

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198
Q

Acute presentation of ? is concerning for upper gastrointestinal bleeding, likely due to a bleeding peptic ulcer.

A

Coffee-ground emesis

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199
Q

Coffee-ground emesis occurs due to the breakdown of red hemoglobin into ? by gastric acid. Esophagogastroduodenoscopy (EGD) reveals a gastric ulcer with a bleeding vessel, confirming this suspicion.

A

Brown hematin

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200
Q

The most common location of a gastric ulcer is at ?, at the transition zone between the gastric body and the antrum. The right and left gastric arteries course along this area and are at risk of bleeding if significant mucosal erosion occurs.

A

The lesser curvature

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201
Q

Courses posteriorly to the duodenum and is at risk of bleeding due to posterior duodenal ulcers.

A

The gastroduodenal artery

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202
Q

Is an extremely rare event with high morbidity and mortality. The pancreas sits between the stomach and the splenic artery, so to erode into the splenic vein, the ulcer must first erode through the pancreas.

A

Erosion of a gastric ulcer into the splenic artery

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202
Q

Courses along the greater curvature of the stomach. Gastric ulcers in this area are rare.

A

The left gastroepiploic artery

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203
Q

The short gastric arteries arise from the splenic artery and the left gastroepiploic artery to supply the ?. Fundal ulcers could damage the short gastric arteries; however, these are very rare.

A

Gastric fundus

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204
Q

Antiarrhythmic Drugs: Mechanism of Action: Class Ia

A

Na+ channel blockade (moderate)

205
Q

Antiarrhythmic Drugs: Mechanism of Action: Class Ib

A

Na+ channel blockade (weak)

206
Q

Antiarrhythmic Drugs: Mechanism of Action: Class Ic

A

Na+ channel blockade (strong)

207
Q

Antiarrhythmic Drugs: Mechanism of Action: Class II

A

β-adrenergic receptor blockade

208
Q

Antiarrhythmic Drugs: Mechanism of Action: Class III

A

K+ channel blockade

209
Q

Antiarrhythmic Drugs: Mechanism of Action: Class IV

A

Ca2+channel blockade

210
Q

Antiarrhythmic Drugs: Class Ia

A

Quinidine
Procainamide
Disopyramide

211
Q

Antiarrhythmic Drugs: Class Ib

A

Lidocaine
Phenytoin
Mexiletine

212
Q

Antiarrhythmic Drugs: Class Ic

A

Flecainide
Propafenone

213
Q

Antiarrhythmic Drugs: Class II

A

Metoprolol
Propranolol
Esmolol
Atenolol
Timolol
Carvedilo

214
Q

Antiarrhythmic Drugs: Class III

A

Amiodarone
Ibutilide
Dofetilide
Sotalol

215
Q

Antiarrhythmic Drugs: Class IV

A

Diltiazem
Verapamil

216
Q

Systolic heart failure for new-onset atrial fibrillation. The ECG shows the absence of discrete P waves between irregularly spaced QRS complexes. Atrial fibrillation can be treated with rate control (class II and IV antiarrhythmics), rhythm control (class I and III antiarrhythmics), or cardioversion. Additionally, these patients should be started on ? due to the risk of thromboembolic stroke originating in the left atrial appendage.

A

Anticoagulation

217
Q

After the initial episode of atrial fibrillation, this patient was started on rhythm control and began to develop symptoms of photodermatitis, hyperthyroidism (feeling warm, tachycardia, mild tremor, hyperreflexia, thyroid tenderness, and exophthalmos), and possibly hepatitis (right upper quadrant tenderness). These symptoms are adverse effects of ?, a K+ channel blocker (class III). This medication class inhibits the delayed rectifier K+ current (repolarization) during phase 3 of the cardiac action potential, thereby prolonging repolarization and total action potential time.

A

Amiodarone

218
Q

This medication class inhibits the delayed rectifier K+ current (repolarization) during phase 3 of the cardiac action potential, thereby prolonging repolarization and total action potential time.

A

Amiodarone

219
Q

Amiodarone can be used to treat atrial fibrillation, atrial flutter, and ventricular tachycardia. Possible adverse effects include

A

Pulmonary fibrosis, hepatoxicity, hypo or hyperthyroidism (as amiodarone is 40% iodine by weight), corneal deposits, photodermatitis, neurologic symptoms, constipation, and cardiovascular effects (e.g., heart block, bradycardia, heart failure).

220
Q

Activation of Gi proteins to block AV nodal activity describes the mechanism of

A

Adenosine

221
Q

Adenosine hyperpolarizes cardiac pacemaker cells by increasing potassium outflow leading to decreased AV nodal conduction. It is used in the management of supraventricular tachycardia. Possible adverse effects include

A

Flushing, hypotension, chest pain, extreme anxiety, and bronchospasm.

222
Q

Decreasing cyclic adenosine monophosphate (cAMP) levels to decrease SA and AV nodal activity describes the mechanism of

A

β-blockers

223
Q

β-blockers suppress cardiac pacemaker activity by reducing the slope of phase 4 and prolonging PR intervals. Possible adverse effects include

A

Bronchospasm (especially for asthma or COPD patients), bradycardia, CNS dysfunction, and masking signs of hypoglycemia.

224
Q

Inhibition of L-type Ca2+ channels describes the mechanism of

A

Ca2+ channel blockers

225
Q

These agents are used for rate control. Possible adverse effects include constipation, flushing, edema, and heart block.

A

Ca2+ channel blockers

226
Q

Moderate Na+ channel blockade describes the mechanism of class IA antiarrhythmics. These rhythm-controlling agents increase action potential, effective refraction period (ERP) duration, and the QT interval. Additionally, they have mild K+ channel-blocking effects (QT interval prolongation). Possible adverse effects include

A

Cinchonism, systemic lupus erythematosus (SLE)-like symptoms (procainamide), heart failure (disopyramide), and thrombocytopenia

227
Q

Pioglitazone is a ?, an oral glycemic control agent used as a second-line or third-line medication in patients with type II diabetes mellitus who have persistently elevated hemoglobin A1c despite appropriate medical and lifestyle management.

A

A thiazolidinedione (TZD)

228
Q

This patient is a good candidate for a TZD as her hemoglobin A1c has increased over the past three months despite management with

A

Metformin and liraglutide.

229
Q

Activate the gamma-isoform of the nuclear peroxisomal proliferator-activated receptors (PPAR-γ) present in the liver, muscle, and fat, upregulating the transcription of genes (lipoprotein lipase, glucokinase, fatty acyl-CoA synthase, etc.) involved in peripheral glucose and lipid metabolism.

A

TZDs (e.g., pioglitazone, rosiglitazone)

230
Q

TZDs improve peripheral insulin sensitivity by increasing levels of certain adipokines, such as adiponectin, increasing ?, and interfering with the deleterious effects of TNF-α in adipocytes. Overall, this leads to adipocyte maturation, storage of fatty acids, and depletion of free fatty acids from the serum. This enhances glucose uptake and utilization while decreasing hepatic gluconeogenesis.

A

GLUT4 expression

231
Q

Bind to K+ channels on pancreatic β-cells causing depolarization, influx of Ca2+, and endogenous insulin release.

A

Sulfonylureas (e.g., chlorpropamide, glipizide)

232
Q

Work similarly, either as an agonist at the GLP-1 receptor or to increase the availability of endogenous GLP-1. This patient is currently using liraglutide without adequate glycemic control, so prescribing an additional GLP-1 analog or a DPP-4 inhibitor likely would not influence glycemic control as much as adding another second-line agent like pioglitazone.

A

Glucagon-like peptide 1 (GLP-1) analogs (e.g., liraglutide) and dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g., linagliptin)

233
Q

Act on brush border cells to slow the hydrolysis of carbohydrates, thus decreasing the rate of glucose absorption.

A

α-glucosidase inhibitors (e.g., acarbose, miglitol)

234
Q

Thiazolidinediones increase insulin sensitivity by upregulating the transcription of

A

Adiponectin

235
Q

The treatment of invasive breast cancer most commonly consists of surgical resection followed by adjuvant chemotherapy. In cases of hormone receptor-positive (ER+/PR+) breast carcinoma, adjuvant therapy is prescribed as either

A

A selective estrogen receptor modulator (SERM)

An aromatase inhibitor.

236
Q

Are two commonly used SERMs, and exemestane and letrozole are two popular aromatase inhibitors. For this patient, each of these medications is a viable treatment option except for tamoxifen, as the patient’s history of endometrial cancer is a contraindication for its use.

A

Tamoxifen and raloxifene

237
Q

As a group, SERMs either function as estrogen receptor antagonists or partial estrogen receptor agonists, depending on the tissues they are acting on. For example, raloxifene acts as an estrogen receptor antagonist in both breast tissue and the uterus and as a partial agonist in bone. Tamoxifen has the same effects as raloxifene in breast tissue and bone but acts as a partial agonist in the uterus. The pro-estrogenic effects on the uterus are unfavorable as increased estrogen activity increases the risk of endometrial hyperplasia and uterine cancer. Therefore,

A

Tamoxifen is contraindicated for the treatment of ER+/PR+ breast carcinoma in patients with a previous history of uterine cancer.

238
Q

Is a GnRH analog that acts on the anterior pituitary. When administered continuously, leuprolide functions as a GnRH receptor antagonist through feedback inhibition. Suppression of the hypothalamic-pituitary-gonadal axis leads to a decrease in the release of FSH and LH and a subsequent reduction in sex hormone secretion.

A

Leuprolide

239
Q

In males, leuprolide is used to treat ?. In females, SERMs and aromatase inhibitors are better adjuvant treatment options for ER+ breast cancers.

A

Prostate cancer

240
Q

This pediatric patient presents with a lifelong history of extreme sun sensitivity, severe sunburns (dermatitis solaris) without significant exposure, and corneal ulcers. This is consistent with ?, an autosomal recessive disorder.

A

Xeroderma pigmentosum (XP)

241
Q

XP occurs due to a ?. The NER pathway is utilized to excise pyrimidine dimers and maintain DNA integrity. Patients present with extreme sensitivity to ultraviolet radiation (UVR) exposure and severe sunburn with vesiculation and desquamation. They are also at a high risk of skin cancer, including malignant melanoma, squamous cell carcinoma, and basal cell carcinoma. Ocular manifestations are also common. Patients may complain of painful sensitivity to sunlight, with exposure causing dryness and a bloodshot appearance with corneal clouding. More severe manifestations include conjunctivitis, corneal ulcers, and eye/eyelid cancers with vision loss.

A

Dysfunctional nucleotide excision repair (NER) system

242
Q

Is a disorder of heme synthesis due to a deficiency of the enzyme porphobilinogen deaminase [(PBGD), also known as hydroxymethylbilane synthase (HMBS)]. Symptoms include abdominal pain, dark-colored (port wine) urine, polyneuropathy, and psychiatric disturbances.

A

Acute intermittent porphyria

243
Q

Certain medications, such as ?, cause increased sensitivity to sunlight.

A

Tetracyclines

244
Q

Is a cell-mediated delayed hypersensitivity reaction that occurs in response to autoantigens released from exposure to UVR. It can cause rash with various morphologies, including erythema, papules, patches, lichenoid plaques, and vesicles. As a delayed reaction, symptoms typically appear a few hours or days after exposure and resolve within one week unless exposure persists.

A

Polymorphous light eruption (PMLE)

245
Q

Is a disorder of heme synthesis due to a deficiency of the enzyme uroporphyrinogen III decarboxylase (UROD). It causes blistering dermatologic lesions and hyperpigmentation in sun-exposed areas. This can be a familial or acquired (hepatitis C) disorder. Attacks are often triggered by increased alcohol consumption.

A

Porphyria cutanea tarda

246
Q

A young, sexually active female presenting with flank pain, dysuria, and increased urinary frequency likely has a urinary tract infection (UTI). This patient’s urinalysis revealed positive leukocyte esterase (evidence of leukocyte activity) and negative nitrites (no reduction of nitrates), indicating infection with a gram-positive organism. Of the options listed, ? is the most common gram-positive organism responsible for UTIs.

A

Staphylococcus saprophyticus

247
Q

Is a gram-positive, catalase-positive, coagulase-negative, urease-positive coccus that grows in clusters. It can be distinguished from S. epidermidis by its resistance to the antibiotic novobiocin. It is the second most common cause of UTIs overall after Escherichia coli.

A

S. saprophyticus

248
Q

Enterococcus spp., Klebsiella pneumoniae, Pseudomonas aeruginosa, and Serratia marcescens are all associated with ? and are often multidrug-resistant. Additionally, all of these except Enterococcus spp. are gram-negative and would demonstrate positive nitrites on urinalysis.

A

Hospital-acquired UTIs

249
Q

E. coli is a gram-negative organism and would show

A

Positive nitrites on urinalysis.

250
Q

Proteus mirabilis can be associated with UTIs involving

A

Struvite stones

251
Q

Long-standing joint pain and stiffness that improves throughout the day is a classic description of

A

Rheumatoid arthritis (RA)

252
Q

RA is an autoimmune inflammatory condition that causes progressive joint pain, erosion, and deformity. The disease demonstrates a predilection for multiple sites, including the

A

Metacarpophalangeal and proximal interphalangeal joints.

253
Q

RA: Chronic activation of the innate immune system results in damaging joint inflammation. Over time, this causes changes within the synovial space, most notably a reactive process within the synovial lining—referred to as a synovial pannus. This reflects

A

Hyperplasia of the synovial lining and an increase in fibroblast and mononuclear cell infiltration, contributing to the formation of granulation tissue.

254
Q

Cortical bone thickening is a common finding associated with ?. This is the second most common skeletal disease in patients aged 50 years or older and is more common in males. This condition is due to an increased rate of bone remodeling, with distinct osteoclast and osteoblast predominant phases.

A

Paget’s disease of bone (osteitis deformans)

255
Q

Multiple conditions are associated with granulomatous changes of the synovium, including ?.

A

Sarcoidosis

256
Q

Monosodium urate crystals are a pathologic finding associated with gouty arthritis. Gouty arthritis typically occurs in episodes, known as attacks or flares, which subside with interval asymptomatic periods. Over time, crystal deposition can result in ?, appearing as punched-out lesions on imaging—sometimes referred to as “rat-bite” erosions.

A

Erosive arthritis

257
Q

Is the thickening of the bone just below the cartilage zone of the affected joint. It is a typical finding in the later stages of osteoarthritis due to the degenerative wear and tear of the articular cartilage.

A

Subchondral sclerosis

258
Q

In rheumatoid arthritis is characterized by the formation of proliferative granulation tissue, fibroblastic and mononuclear cell infiltration, and subsequent release of cytokines and cellular enzymes, further worsening articular and connective tissue damage and erosion.

A

Synovial pannus

259
Q

A rare autosomal recessive disease caused by a mutation in the ATM gene.

A

Ataxia-telangiectasia

260
Q

Symptoms include early childhood cerebellar defects (e.g., ataxia), telangiectasia (e.g., spider angiomas), and recurrent sinopulmonary infections due to immunoglobulin deficiencies.Ataxia-telangiectasia

A

Ataxia-telangiectasia

261
Q

The presence of a third heart sound (S3), dry cough, and dyspnea indicates the patient may be displaying

A

Signs of fluid overload

262
Q

Auscultation of an S3 heart sound supports this, as S3 commonly results from increased blood turbulence. Although S3 can sometimes be normal in children, athletes, young adults, and pregnancy, it also occurs pathologically alongside mitral regurgitation (MR) and congestive heart failure.

A

Fluid overload

263
Q

Suspicion of fluid overload is further supported by dullness to percussion and the associated imaging, which displays diffuse pulmonary edema in both lobes of the lung and is likely responsible for the decreased oxygen saturation seen on room air. Furthermore, the presence of an ? is most indicative of a mitral murmur. The combined findings of an S3 heart sound, signs of fluid overload, and a mitral murmur makes MR the most likely cause of this presentation.

A

Axillary murmur

264
Q

Symptoms of MR include ?. Associated conditions include tuberous sclerosis, myocardial infarction, mitral valve prolapse, and rheumatic fever.

A

Fatigue, paroxysmal nocturnal dyspnea, and orthopnea

265
Q

Newly-onset MR is most commonly due to mitral valve insufficiency following

A

Trauma, infective endocarditis, or rupture of either the chordae tendinae or papillary muscles.

266
Q

MR: Resulting backflow from the left ventricle into the left atrium during systole increases left atrial pressure, as demonstrated by

A

An elevated pulmonary capillary wedge pressure.

267
Q

Increased left atrial pressure, increased volume overload and preload, and decreased cardiac output collectively increase left ventricular failure risk.

A

MR

268
Q

MR: Systolic pressure would ? in the aorta within acute mitral regurgitation, as blood would revert back to the left atrium.

A

Decrease

269
Q

MR: Left atrial pressures would ?rather than being depressed, as blood would revert back into the left atrium from the left ventricles.

A

Increase

270
Q

MR: Pulmonary venous pressure would be ? due to the fluid backup within mitral regurgitation, leading to the noted pulmonary edema.

A

Increased

271
Q

MR: Left ventricular diastolic volume would be ?, as more blood is accommodated from the pulmonary veins and mitral regurgitation.

A

Elevated

272
Q

MR causes an ?as blood flows from the left ventricle into the left atrium during systole.

A

Elevated pulmonary capillary wedge pressure

273
Q

The third heart sound, S3, occurs in early diastole during rapid ventricular filling and is associated with ?, such as in the case of mitral regurgitation (MR).

A

Increased filling pressures

274
Q

Is a psychotic disorder that mimics schizophrenia but does not persist longer than 6 months. Psychotic symptoms, including hallucinations, paranoia, and disorganized speech. Significant decline in functioning and social withdrawal.

A

Schizophreniform disorder

275
Q

Patients should have ≥ 2 psychotic symptoms causing significant functional impairment. At least 1 symptom should be a positive symptom (e.g., delusions, hallucinations, disorganized speech, formal thought disorders). A history of marijuana use, as seen in this patient, is a known risk factor for the development of schizophrenia spectrum disorders. If this patient’s symptoms continue to persist for > 6 months, his diagnosis would change to schizophrenia

A

Schizophreniform disorder

276
Q

First-line treatment for schizophreniform disorder includes atypical

A

Antipsychotics.

277
Q

Is characterized by < 1 month of ≥ 1 positive psychotic symptoms (e.g., delusion, hallucination, disorganized speech, bizarre behavior).

A

Brief psychotic disorder

278
Q

Is defined by ≥ 1 delusions that do not affect patient functioning and have no other identifiable medical causes or psychotic symptoms. This patient has multiple symptoms and a significant decline in functioning.

A

Delusional disorder

279
Q

Would have classic depressive symptoms (e.g., depressed mood, anhedonia, decreased motivation, changes in appetite) along with psychotic features (e.g., delusions, hallucinations).

A

Major depressive disorder with psychotic features

280
Q

Is a combination of psychotic features and mood symptoms.

A

Schizoaffective disorder

281
Q

Patients with ? disorder are often described as odd or eccentric with strange beliefs and behaviors. However, these symptoms do not cause a significant decrease in functioning and are not associated with psychotic symptoms.

A

Schizotypal personality

282
Q

Hives are pruritic wheals (transient smooth papules or plaques) categorized by superficial dermal edema and lymphatic channel dilation. Additionally, these lesions are erythematous and typically patchy. Urticaria is associated with a history of atopic diseases (asthma, allergic rhinitis, food allergies) and higher serum IgE levels. Atopic disease is a

A

Type 1 hypersensitivity reaction.

283
Q

This reaction is caused by allergen exposure, promoting antibody class switching to IgE(stimulated by IL-4). Subsequent exposures promote IgE-mediated activation of basophils and mast cells through receptor crosslinking, resulting in degranulation of histamine, leukotrienes, and many other inflammatory mediators. This leads to vasodilation that causes the redness and warmth of urticaria.

A

Type 1 hypersensitivity reaction.

284
Q

Activation of complement leading to Fc receptor-mediated inflammation describes the pathogenesis of the classic complement activation pathway. This pathway is activated by IgG or IgM when bound to antigens. This is the pathway by which the membrane attack ? forms to induce bacterial lysis.

A

Complex (MAC) (C5b-C9)

285
Q

Activation of neutrophils by immune complex formation describes the pathogenesis of a type III hypersensitivity. Antigen-antibody complexes activate complement, which attracts and activates neutrophils. Examples of type III hypersensitivities are

A

Systemic lupus erythematosus and rheumatoid arthritis.

286
Q

Direct CD8+ T lymphocyte-mediated cytotoxicity describes the immune mechanism against virally infected and tumor cells. Cytotoxic cells (CD8+) induce apoptosis in viral, tumor, and graft cells using

A

perforin and granzyme B.

287
Q

The release of inflammatory cytokines by CD4+ T lymphocytes describes the pathogenesis of cell-mediated immunity (type IV hypersensitivity). CD4+ cells are activated by an antigen and release cytokines that attract inflammatory cells (neutrophils and macrophages). An example of this hypersensitivity type is

A

A reaction to urushiol (poison ivy, poison sumac, poison oak) or graft rejection.

288
Q

Urticaria are pruritic wheals caused by IgE receptor crosslinking on the surface of mast cells and basophils. This crosslinking results in the degranulation of preformed

A

Vesicles containing histamine, leukotrienes, and other inflammatory mediators.

289
Q

As evidenced by an extensive history of cigarette smoking and classic clinical features (e.g., hypoxemia, barrel-shaped chest, tripod positioning, cachexia).

A

Chronic obstructive pulmonary disease (COPD)

290
Q

COPD is characterized by the spectrum of chronic bronchitis and emphysema, both of which progress in the presence of persistent pulmonary irritation and inflammation caused by the inhalation of the noxious particles in cigarette smoke. Emphysema occurs at the alveolar level and is characterized by

A

Alveolar destruction

291
Q

Emphysema results from an imbalance of proteases and antiproteases. Under normal conditions, neutrophils and macrophages release proteases (e.g., elastase) and reactive oxygen species to clear alveolar irritants. When the irritants are neutralized, antiproteases (e.g., ⍺1-antitrypsin) degrade proteases to prevent bystander tissue damage. Persistent alveolar inflammation overwhelms the neutralizing capabilities of antiproteases.

A

As a result, unchecked elastase activity and oxidative stress lead to alveolar destruction and increased lung compliance due to alveolar enlargement.

292
Q

In smokers, alveolar destruction typically occurs in the ?.
Additionally, because cigarette smoke interacts primarily with the pneumocytes that line the alveolar air sacs, inflammation is limited to the center of the acinus, where gas exchange occurs.

A

Upper lobes

293
Q

Classical asthma represents a ?characterized by smooth muscle hyperreactivity and reversible bronchoconstriction. Exacerbations occur in response to specific stimuli (e.g., allergens, exercise, cold temperatures) and are more common in childhood. In patients with asthma, histological specimens of the bronchi and bronchioles show smooth muscle hypertrophy, hyperplasia, and thickening of the reticular basement membrane. In addition, sputum samples may show whorled mucous plugs (i.e., Curschmann spirals) and eosinophilic, double-pointed crystals formed from degraded eosinophils (Charcot-Leyden crystals).

A

Type I hypersensitivity reaction

294
Q

Is an obstructive pulmonary disease associated with foreign bodies, cystic fibrosis, disorders of ciliary motility (e.g., primary ciliary dyskinesia), and allergic bronchopulmonary aspergillosis.

A

Bronchiectasis

295
Q

Patients with bronchiectasis typically develop

A

Foul-smelling, purulent sputum, hemoptysis, digital clubbing, and recurrent infections.

296
Q

Histologically, bronchiectasis is characterized by ?. In the alveoli, variable levels of inflammation and fibrosis can be observed.

A

Permanent bronchial dilation, necrotizing inflammation, and mucosal destruction

297
Q

Interstitial lung diseases are a group of restrictive lung conditions characterized by a thickened interstitium, decreased diffusion capacity, and an increased A-a gradient. Patients often present with

A

Dyspnea and short, shallow breathing due to reduced lung compliance. Various histologic findings can be observed, including common patterns of interstitial fibrosis and granulomatous inflammation

298
Q

Is an autosomal codominant, hepatopulmonary disease caused by deficient or absent levels of circulating antiproteases (e.g., ⍺1-antitrypsin).

A

⍺1-antitrypsin deficiency (A1ATD)

299
Q

The pathophysiology of emphysema in A1ATD also results from an imbalance of proteases and antiproteases. As opposed to cigarette smoke-induced emphysema, unchecked elastase activity in the lungs of patients with A1ATD leads to diffuse alveolar destruction affecting the entirety of the acinus in all lung lobes. Thus, patients with A1ATD develop

A

Diffuse panacinar emphysema

300
Q

Patient’s sudden onset fever, dyspnea, chest pain, complete immunization schedule, bilateral pulmonary infiltrates on chest x-ray, and a peripheral blood smear containing abnormal sickle-shaped erythrocytes suggest acute chest syndrome—a severe manifestation of

A

Sickle cell anemia

301
Q

Sickle cell anemia is an autosomal recessive disorder caused by ?. This results in the non polar amino acid valine replacing the polar amino acid glutamate creating a hydrophobic portion of the β-globin chain. This new portion fits into a complementary site of the hemoglobin α-globin chain. These abnormal hemoglobin (HbS) molecules aggregate under hypoxic, acidic, and anhydrous conditions. Initially, a gel and then a fibrous meshwork of polymers forms, causing erythrocyte distortion into an abnormal sickle shape.

A

A single base substitution in the sixth codon (E6V) of the β-globin gene

302
Q

Sickle cell anemia: These “sickle” cells can cause both intravascular and extravascular hemolysis, vaso-occlusive symptoms, and an increased risk of infection. Acute chest syndrome occurs as a result of ?. Respiratory infections, such as pneumonia, can also exacerbate sickling due to local acidity and hypoxia.

A

Pulmonary microvascular vasoocclusion.

303
Q

Patients will complain of fever, various respiratory symptoms (chest pain and dyspnea), and have pulmonary infiltrates on chest x-ray.

A

Sickle cell anemia

304
Q

A deficiency or absent synthesis of α-globin or β-globin chains occurs in

A

Thalassemia

305
Q

Polycythemia vera is a form of myeloproliferative disorder that results from a mutation of ?.

A

JAK2

306
Q

Is a gene for a nonreceptor tyrosine kinase found on chromosome 9

A

JAK2

307
Q

Polycythemia vera, manifestations include

A

Aquagenic pruritis, hypertension, erythromelalgia, and deep vein thromboses.

308
Q

Is a genetic disorder, most commonly of autosomal dominant inheritance, that involves abnormal erythrocyte cytoskeletal proteins. These mutations most often affect spectrin and ankyrin (plasma-membrane scaffolding proteins). On peripheral blood smear, spherocytes will be seen. Spherocytes are approximately two-thirds of the diameter of normal erythrocytes and often lack of zone of central pallor.

A

Hereditary spherocytosis

309
Q

Acute Phase Reactants: positive (Upregulated): C-reactive protein

A

High levels indicate inflammation or infection.

310
Q

Acute Phase Reactants: positive (Upregulated): Ferritin

A

Binds and stores iron intracellularly to inhibit microbial iron scavenging.

311
Q

Acute Phase Reactants: positive (Upregulated): Fibrinogen

A

Promotes endothelial repair and correlates to erythrocyte sedimentation rate.

312
Q

Acute Phase Reactants: positive (Upregulated): Haptoglobin

A

Binds free hemoglobin to protect against oxidative stress.

313
Q

Acute Phase Reactants: positive (Upregulated): Hepcidin

A

Increases to reduce iron availability in the blood, which can inhibit the growth of certain pathogens.

314
Q

Acute Phase Reactants: positive (Upregulated): Procalcitonin

A

Increases in bacterial infections; decreases/normal in viral infections.

315
Q

Acute Phase Reactants: positive (Upregulated): Serum amyloid A

A

Increased levels can lead to secondary amyloidosis.

316
Q

Acute Phase Reactants: Negative (Downregulated): Albumin

A

Levels decrease in inflammation as resources are diverted to produce positive APRs.

317
Q

Acute Phase Reactants: Negative (Downregulated):Transferrin

A

Levels decrease during inflammation as the body attempts to reduce iron availability to pathogens.

318
Q

Acute Phase Reactants: Negative (Downregulated): Transthyretin
(Prealbumin)

A

Levels decrease as resources are diverted to produce positive APRs.

319
Q

This 70-year-old male, with a 25 pack-year smoking history, presents to the emergency department with fever, difficulty breathing, and a productive cough. This should raise suspicion for a pathologic lung process. These symptoms, in the presence of localized fremitus, dullness to percussion, and leukocytosis, are classic findings of

A

Pneumonia

320
Q

Acute phase reactants (APR) are laboratory markers commonly measured during periods of inflammation such as

A

Infection

321
Q

APRs are classified as either positive or negative depending on their serum concentration:

A
  • Positive APRs increase in concentration during inflammation. Positive APRs include C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), ferritin, fibrinogen, hepcidin, haptoglobin, and serum amyloid A
  • Negative APRs decrease in concentration during inflammation. Negative APRs include albumin, antithrombin, transferrin, and retinol-binding protein (RBP)
322
Q

Is a unique APR with positive and negative properties. PCT is normally produced as pre-procalcitonin by thyroid parafollicular cells and is later converted to PCT by prohormone convertase. Under regular physiologic conditions, PCT is produced at very low levels.

A

Procalcitonin (PCT)

323
Q

Endotoxins or cytokines (e.g., IL-1, TNF-α, IL-6) are usually increased during times of inflammation in bacterial infections and stimulate the production of

A

Extra-thyroid PCT

324
Q

Viral infection markers, such as interferon-γ, ? the production of PCT.

A

Down-regulate

325
Q

Since bacterial and viral sources can cause community-acquired pneumonia, PCT is an excellent laboratory value to assess this patient’s infection etiology

A

Increased PCT if bacterial, normal/decreased if viral.

326
Q

C-reactive protein (CRP) rises during inflammation but is less sensitive than PCT for bacterial infection. CRP is responsible for ?, making it a direct measure of the inflammatory response.

A

Complement fixation and the promotion of phagocytosis

327
Q

Erythrocyte sedimentation rate (ESR) and fibrinogen

A

Are nonspecific APRs.

328
Q

Fibrinogen promotes endothelial repair and can be elevated in times of inflammation. Additionally, it causes erythrocyte aggregation, which elevates ESR (i.e., the distance erythrocytes fall in a vertical tube over one hour). ESR and fibrinogen are likely to increase in community-acquired pneumonia but

A

Would not provide information about the underlying etiology

329
Q

Is a pro-inflammatory cytokine that induces the production of multiple APRs. Although IL-1 levels are likely elevated in this patient’s condition, the nonspecific APR production makes this test unhelpful in identifying the condition’s etiology.

A

Interleukin-1 (IL-1)

330
Q

Ferritin is an APR that increases as a nonspecific response to inflammation. It binds and sequesters iron to inhibit microbial iron scavenging. Many conditions (e.g., malignancy, infection) can cause ferritin levels to increase.

A

It binds and sequesters iron to inhibit microbial iron scavenging.

331
Q

Is the end product of glycolysis under anaerobic conditions.

A

Lactate

332
Q

Increased lactate levels are associated with ?. A case of community-acquired pneumonia may be associated with increased serum lactate secondary to bacteremia and underlying sepsis.

A

Impaired tissue oxygenation from impaired delivery or defective mitochondrial utilization.

333
Q

This patient’s symptoms of anxiety, palpitation, and unintentional weight loss after doubling her levothyroxine dose suggest

A

Thyrotoxicosis factitia (exogenous thyrotoxicosis).

334
Q

Excess thyroid hormone, whether due to endogenous entities or exogenous administration (e.g., levothyroxine over-replacement), can lead to

A

Increased metabolism (e.g., carbohydrates, lipids), β-adrenergic receptor expression (e.g., increased cardiac output, heart rate, stroke volume, contractility), and basal metabolic rate.

335
Q

Exogenous thyrotoxicosis will have low serum TSH levels and elevated serum thyroid hormone levels depending on the type of preparation

A

(e.g., levothyroxine, liothyronine).

336
Q

TSH binds to TSH receptors on thyroid follicular cells, leading to increased

A

Thyroglobulin synthesis, follicular cell growth, and T4 and T3 release.

337
Q

As levels of free T4 and T3 rise, TSH and TRH (thyrotropin-releasing hormone) secretion will be suppressed via negative feedback. This can also occur via exogenous thyroid hormone administration. Over time this can lead to ? from lack of TSH-mediated tropism.

A

Atrophy of thyroid follicular cells

338
Q

Is disordered cell proliferation

A

Dysplasia

339
Q

Mild dysplasia may resolve; however, severe dysplasia is often irreversible and may progress to malignancy. Dysplastic changes include

A

Cellular pleomorphism, hyperchromatic and enlarged nuclei, and chromatin clumping.

340
Q

Hypertrophy and hyperplasia are defined as increased cell size and number, respectively. TSH stimulation can lead to hypertrophy and hyperplasia of thyroid follicular cells. In Graves disease, overstimulation of TSH receptors on thyroid follicular cells can result in

A

A diffuse goiter.

341
Q

Can be defined as a change in the phenotype of a tissue bed, often as an adaptation to stress. It is potentially reversible if the stressor is removed but can lead to dysplasia/malignancy. For example, cigarette smoking can change columnar epithelium in the trachea and bronchi to squamous epithelium. Squamous epithelium is more durable; however, the loss of cilia increases the risk of respiratory tract infections.

A

Metaplasia

342
Q

Patient’s symptoms of headache, nausea, and vomiting, along with neck pain during passive flexion, suggest

A

Meningitis

343
Q

His age, occupation (working with cheeses and charcuterie), and the use of immunosuppressive medications (methotrexate and adalimumab) for rheumatoid arthritis increase his risk for

A

Listeria monocytogenes infection.

344
Q

L. monocytogenes is a ? that often displays a characteristic tumbling motility in culture. The organism can survive and reproduce in cold environments, which provides a route for bacterial growth in food and drinks stored at low temperatures.

A

Gram-positive facultative intracellular rod

345
Q

Ampicillin is effective against Listeria monocytogenes and several other gram-positive bacteria, while ? is an aminoglycoside antibiotic that is primarily effective against gram-negative bacteria. When used together, they provide synergistic effects that enhance their bactericidal activity and increase the likelihood of successfully treating the infection.

A

Gentamicin

346
Q

Although a variety of antibiotics have activity against L. monocytogenes, ? is the treatment of choice.

A

Ampicillin monotherapy, or in combination with gentamicin,

347
Q

Listeriosis can cause significant symptoms in at-risk groups, including very young and old, immunocompromised, and pregnant individuals. Immunocompromised patients are especially at increased risk of developing

A

Meningoencephalitis.

348
Q

Can cause foodborne illness, manifesting as either an emetic or diarrheal syndrome that typically has a self-limited course. It is associated with the consumption of starchy foods such as rice, with symptoms starting within six hours of consuming the contaminated food.

A

Bacillus cereus

349
Q

Causes botulism, which manifests as flaccid paralysis, double vision, difficulty speaking, and difficulty swallowing.

A

Clostridium botulinum

350
Q

In adults, botulism results from the ingestion of

A

Improperly canned foods.

351
Q

Was once a common cause of bacterial meningitis in children. However, the widespread use of the H. influenzae type b (Hib) vaccine has significantly reduced its incidence.

A

Haemophilus influenzae

352
Q

Is a contaminant found in raw poultry and eggs and typically causes gastroenteritis, with symptoms such as diarrhea, abdominal pain, and fever.

A

Salmonella enterica

353
Q

This patient presents with infertility due to cystic fibrosis-related

A

Congenital bilateral absence of the vas deferens

354
Q

Cystic fibrosis (CF) is an autosomal recessive protein trafficking disorder caused by a defect in the CFTR gene on

A

Chromosome 7

355
Q

CFTR encodes an ? that secretes Cl- in the lungs and gastrointestinal tract. Though several genotypes exist, the most common mutation is a Phe508 deletion.

A

ATP-gated chloride channel

356
Q

Most common mutation of CF

A

Phe508 deletion

357
Q

CF: Phe508 del: The missing amino acid results in a misfolded protein that undergoes improper protein trafficking and/or protein retention in the rough endoplasmic reticulum. Absence of the membrane ATP-gated chloride channels leads to deficient Cl- and H2O secretion. The rise in intracellular Cl- levels leads to a

A

Compensatory increase in Na+ reabsorption via epithelial Na+ channels (ENaC) and a subsequent increase in H2O reabsorption

358
Q

CF: Phe508 del: In the lungs and gastrointestinal tract, Na+ and H2O reabsorption from luminal contents leads to the formation of thick, dehydrated mucus. The mucus often becomes impacted, leading to a wide array of symptoms. In the lungs, mucus trapping leads to recurrent infections, chronic bronchitis, and bronchiectasis. Common manifestations in the upper respiratory tract include ? Effects on the gastrointestinal tract can include pancreatic insufficiency, malabsorption, fat-soluble vitamin deficiencies, biliary cirrhosis, and liver disease.

A

Opacification of the sinuses and nasal polyps.

359
Q

In males, CF also causes infertility. During early embryological development, P-gated chloride channels play an important role in vas deferens formation. Therefore, the absence of these channels leads to atrophy, ultimately resulting in congenital bilateral absence of the vas deferens. Because of this, nearly all males with cystic fibrosis have ?. Of note, spermatogenesis is often unaffected.

A

Obstructive azoospermia despite normal levels of FSH, LH, and testosterone.

360
Q

Is caused by mutations in the COL5A1/3 genes on chromosome 9. This is characterized by defective type V collagen, leading to hyperextensible skin and hypermobile joints.

A

Classical-type Ehlers-Danlos syndrome

361
Q

Vascular-type Ehlers-Danlos is caused by mutations in the ? gene on chromosome 2. It is characterized by defective type III procollagen synthesis, leading to the formation of fragile vessels, muscles, and organs that are prone to rupture.

A

COL3A1

362
Q

Ehlers-Danlos syndrome and Marfan syndrome is not a cause of

A

Infertility.

363
Q

Is an autosomal dominant connective tissue disorder caused by a mutation in the FBN1 gene on chromosome 15. The mutation results in a defective glycoprotein that forms a sheath around elastin called fibrillin-1, leading to laxity of the skeleton, heart, and eyes. Phenotypic features include tall stature, long extremities, chest wall deformities, hypermobile joints, and arachnodactyly. Patients are also at increased risk of aortic root aneurysm, rupture, or dissection and risk of spontaneous pneumothorax.

A

Marfan syndrome

364
Q

Is an X-linked dominant disease caused by trinucleotide CGG repeats in the FMR1 gene that encodes the shuttle protein, FMRP, that aids in the transport of mRNA within cells of many tissues throughout the body. Trinucleotide repeats in the FMR1 gene lead to hypermethylation of cytosine residues and decreased expression of FMRP.

A

Fragile X syndrome

365
Q

Patients with Fragile X syndrome typically have intellectual disability, behavioral instability, and autism. In males, typical phenotypic features include a long face, large jaw, large everted ears, and macroorchidism. Fragile X may cause

A

Subfertility

366
Q

Found on chromosome 6, encodes a protein called fibrocystin that is present in fetal and adult kidney cells.

A

The PKHD1 gene

367
Q

Fibrocystin plays a role in cellular adhesion, repulsion, and proliferation. Mutations in the PKHD1 gene result in autosomal recessive ?. ARPKD presents in infancy and is characterized by cystic dilation of collecting ducts. Patients often present in infancy with renal failure and concurrent hepatic fibrosis. In many cases, ARPKD causes renal failure in utero and results in the Potter sequence.

A

Polycystic kidney disease (ARPKD)

368
Q

A renal mass along with hematuria and abdominal pain, all of which raise suspicion for

A

Malignancy

369
Q

The kidney biopsy demonstrates polygonal cells with clear cytoplasm. This is most consistent with the clear cell subtype of ?. This subtype represents approximately 80% of all RCCs.

A

Renal cell carcinoma (RCC)

370
Q

RCC is associated with several risk factors, including

A

Male sex, smoking, and obesity.

371
Q

RCC: Individuals may present with various findings, including an

A

Abdominal mass, flank pain, hematuria, or paraneoplastic syndromes (EPO, renin, PTHrP, ACTH).

372
Q

Arise with embryonic glomerular structures on histology. These malignant tumors are most common in children and present with hematuria and a unilateral flank mass that does not cross the midline.

A

Nephroblastomas (Wilms tumor)

373
Q

Large eosinophilic cells with abundant mitochondria are histologic findings associated with ?

A

Renal oncocytoma

374
Q

This rare renal tumor arises from the collecting ducts of the nephron and is considered benign. Clinical presentation is similar to RCC; therefore, these masses are typically resected to rule out malignancy.

A

Renal oncocytoma

375
Q

Is an extremely rare renal tumor. This condition is most often associated with chronic nephrolithiasis.

A

Squamous cell carcinoma

376
Q

Is a tumor arising from the transitional cells of the urinary system, including the renal pelvis and lower urinary tract. Affected individuals classically present with painless hematuria as the only clinical sign of disease.

A

Transitional cell carcinoma (urothelial carcinoma)

377
Q

Renal cell carcinoma is the most common primary renal neoplasm, arising from the?.

A

PCT of the nephron.

378
Q

Of all RCC subtypes, ? is the most prevalent.

A

Clear cell RCC

379
Q

RCC: Histology demonstrates polygonal cells with clear cytoplasm. Individuals may present with the classic triad of

A

Hematuria, flank pain, and a palpable abdominal mass.

380
Q

This patient with a past medical history of chronic low back pain is seeing a new physician and requesting documentation for disability benefits. He is uncooperative and refuses a physical exam. Physicians are legally required to perform thorough physical examinations of all patients seeking disability benefits, regardless of pain level or other extraneous factors.

A

The appropriate response is to disclose the physician’s legal obligation and explain why the physical exam is an essential aspect of the encounter.

381
Q

Addressing the legal responsibility of the physician to perform a physical exam is the best response, but the question regarding referral makes this choice incorrect.

A

The question implies other physicians would sign the documentation without performing a physical exam.

382
Q

Highly adaptive defense mechanisms include

A

Altruism
Anticipation
Humor
Sublimation
Suppression

383
Q

Is a mature, highly adaptive defense mechanism in which an individual intentionally and temporarily withholds negative emotions, ideas, or experiences until a more optimal time. A student who focuses on practicing basketball to distract himself from his parent’s divorce is using this mature defense mechanism. He is allowing himself to temporarily withhold negative emotions related to the divorce to focus his attention on something productive. It is entirely healthy for him to allow himself to feel these negative emotions at an appropriate time.

A

Suppression

384
Q

This musician who was cut from the orchestra and said he never liked playing the violin is using ?, an immature defense mechanism. This occurs when an individual develops an extrinsic explanation to justify a negative situation, often one’s own behavior or a related outcome.

A

Rationalization

385
Q

This teenager who is teasing her little brother after being picked on at school is using ?, an immature defense mechanism. This occurs when an individual redirects a negative impulse or emotion to a neutral party (i.e., her brother) that is not involved in the situation.

A

Displacement

386
Q

This teenager who has a fear of cats despite having no recollection of the incident is using ?, an immature defense mechanism. It is easily mistaken for suppression, although repression involves involuntarily withholding negative emotions or experiences.

A

Repression

387
Q

This woman who begins reading medical journals to distract herself from her mother’s recent stroke is using ?, an immature defense mechanism.

A

Intellectualization

388
Q

Differs from simply learning about a stressful situation as it involves emotionally distancing oneself from the situation through facts and reasoning.

A

Intellectualization

389
Q

Evidence of bilateral renal artery stenosis on imaging and an acute kidney injury (i.e., doubling of serum creatinine) following initiation of a new medication. This is likely an adverse effect of the antihypertensive medication

A

Lisinopril

390
Q

Renal artery stenosis is a condition characterized by the narrowing of one or both renal arteries, which can lead to renal hypoperfusion in the affected kidney(s) with subsequent physiologic compensation of renal perfusion via the renin-angiotensin-aldosterone system (RAAS).

A

Angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril) can cause acute kidney decompensation in patients with bilateral renal artery stenosis by further impairing renal blood flow.

391
Q

The hypoperfusion due to renal artery stenosis forces the efferent arterioles to constrict (i.e., angiotensin II-induced vasoconstriction) to maintain the glomerular filtration rate (GFR).

A

This is accomplished via activation of the RAAS, which maintains blood pressure by causing vasoconstriction via angiotensin II and sodium retention via aldosterone.

392
Q

ACE inhibitors are contraindicated in the setting of bilateral renal artery stenosis, as they block the conversion of angiotensin I to angiotensin II,

A

Causing a precipitous drop in the GFR and a subsequent rise in serum creatinine.

393
Q

Patients with renal artery stenosis may present clinically with ?. Over time, the condition can lead to chronic kidney disease if both kidneys are affected, as one kidney is often sufficient for maintaining homeostatic blood pressure.

A

Abdominal bruits and treatment-resistant hypertension.

394
Q

Are often considered in managing hypertension, including in patients with renal artery stenosis. They work by inhibiting calcium influx into vascular smooth muscle cells, leading to vasodilation and a consequent reduction in blood pressure.

A

Calcium channel blockers (e.g., amlodipine)

395
Q

Do not significantly interfere with renal autoregulation mechanisms, making them safer to use when maintaining renal perfusion is critical

A

Calcium channel blockers

396
Q

A widely used HMG-CoA reductase inhibitor, is primarily indicated for managing hyperlipidemia. By inhibiting HMG-CoA reductase (the rate-limiting step) in the cholesterol synthesis pathway, ? effectively reduces low-density lipoprotein (LDL) cholesterol levels. While it offers cardiovascular benefits by stabilizing atherosclerotic plaques and reducing the risk of cardiovascular events, it does not have a direct effect on renal function or the maintenance of GFR.

A

Atorvastatin

397
Q

A thiazide-like diuretic, is often used to treat hypertension and may be beneficial in cases of resistant hypertension where volume overload contributes to elevated blood pressure. It reduces intravascular volume by promoting sodium and water excretion, thereby counteracting the sodium retention associated with RAAS activation. Although the use of diuretics in bilateral renal artery stenosis may potentially exacerbate kidney injury due to volume depletion, this would likely be evidenced by decreased blood pressure and/or signs of dehydration on physical exam.

A

Chlorthalidone

398
Q

A thiazolidinedione, acts as an agonist for peroxisome proliferator-activated receptor gamma (PPAR-γ) and is primarily used to improve insulin sensitivity in patients with type 2 diabetes mellitus.

A

Pioglitazone

399
Q

By enhancing insulin action, pioglitazone aids in improving glucose control. While a known adverse effect is fluid retention, which can exacerbate heart failure and worsen renal function,

A

It is not contraindicated in renal artery stenosis and does not cause an acute drop in GFR.

400
Q

Are contraindicated in patients with renal artery stenosis because they inhibit the renin-angiotensin-aldosterone system (RAAS). This inhibition can lead to a decrease in glomerular filtration rate (GFR) and an increase in serum creatinine levels.

A

Angiotensin-converting enzyme (ACE) inhibitors

401
Q

HSV-2

A

Is an enveloped, double-stranded DNA virus, typically contracted through sexual intercourse or perinatal transmission.

402
Q

While HSV-1 often affects the perioral region and may cause genital lesions in some cases, HSV-2

A

Is more likely to cause genital lesions.

403
Q

Presents as painful inguinal lymphadenopathy with a painful vesicular genital rash and an associated fever.

A

Primary HSV-2

404
Q

Consists of vesicular lesions on an erythematous background—“dew drops on a rose petal.” After primary infection, HSV-2 remains dormant within sacral dorsal root ganglia and can become reactivated to cause recurrent genital lesions. Diagnosis is often made based on the clinical exam, but the virus displays distinct features on pathologic analysis. Though no longer used, Tzanck smears of vesicles show multinucleated giant cells, indicative of HSV. Intranuclear eosinophilic Cowdry A inclusions are also seen.

A

The genital rash caused by HSV-2

405
Q

Though not all patients experience relapses, ? can be used to treat the genital lesions caused by HSV-2.

A

Acyclovir, famciclovir, and valacyclovir

406
Q

Is the bacteria that causes chancroid, a sexually transmitted infection characterized by the presence of a painful genital ulcer with exudate and inguinal adenopathy. Chancres are single sores that arise at the site where the bacteria enter the body. Multiple vesicular genital lesions are more suggestive of HSV-2 infection.

A

Haemophilus ducreyi

407
Q

HSV-1 is an enveloped, double-stranded DNA virus. However, it is primarily transmitted via respiratory secretions and saliva, causing perioral lesions and often presents as ?. Other manifestations include keratoconjunctivitis, herpetic whitlow, temporal lobe encephalitis, and esophagitis, especially in patients with HIV.

A

Gingivostomatitis

408
Q

Is the bacteria that causes syphilis. Primary syphilis is characterized by a painless chancre.

A

Treponema pallidum

409
Q

Belongs to the herpesvirus family. Primary ? infection causes varicella (chickenpox), with reactivation of the virus causing zoster (shingles). Chickenpox is a common childhood exanthem that presents with a headache, fever, and rash that appears similar to the rash caused by HSV but affects the entire body. In patients with shingles, the rash is also vesicular, painful, and typically involves a single dermatome.

A

Varicella-zoster virus (VZV)

410
Q

What antibiotic prevents the removal of RNA primers from strands of DNA in bacteria?

A

Inhibits DNA polymerase I, which is responsible for removing RNA primers and replacing them with DNA nucleotides.

411
Q

What is the primary function of DNA polymerase III during DNA replication?

A

DNA polymerase III synthesizes the majority of new DNA strands, beginning replication at the 3’ end of an RNA primer and proceeding in a 5’ to 3’ direction until it encounters another RNA primer.

412
Q

How does DNA ligase function in the DNA replication process?

A

Acts after DNA polymerase I has replaced RNA primers with DNA nucleotides, linking DNA portions synthesized by DNA polymerase III with those synthesized by DNA polymerase I.

413
Q

Where do DNA polymerase enzymes bind when synthesizing DNA?

A

DNA polymerase enzymes bind to the 3’ end of nucleic acid primers, which are composed of RNA, not DNA.

414
Q

What is the role of DNA helicase in DNA replication?

A

DNA helicase separates paired DNA strands to initiate replication. Single-stranded binding proteins then bind to these separated strands to prevent re-annealing.

415
Q

In which direction does DNA replication proceed and how does it read the template strand?

A

DNA replication proceeds in the 5’ to 3’ direction and reads the template strand in the 3’ to 5’ direction to ensure correct base pairing.

416
Q

What is the difference between RNA primers and DNA in terms of nitrogenous bases?

A

In RNA primers, uracil (U) is used in place of thymine (T) found in DNA.

417
Q

What are the base pairing rules between RNA primers and DNA template strands?

A

Correct base pairing between the DNA template strand and the RNA primer is:

Guanine (G) pairs with Cytosine (C)
Adenine (A) pairs with Uracil (U)

418
Q

What would be the sequence of an RNA primer that pairs with a DNA template strand?

A

The RNA primer would have a sequence in the 5’ to 3’ direction that appropriately pairs with the template strand in the 3’ to 5’ direction.

419
Q

What is the mechanism of action of fluoroquinolone antibiotics like levofloxacin?

A

Inhibit bacterial (prokaryotic) topoisomerase, which is essential for DNA replication and repair.

420
Q

What potential cardiovascular effect can fluoroquinolone antibiotics cause?

A

Prolong the QT interval on an ECG.

421
Q

Why are fluoroquinolone antibiotics considered unsafe in pregnancy?

A

Associated with an increased risk of birth defects in animal studies, making them unsafe for use during pregnancy.

422
Q

What is the role of dihydrofolate reductase in bacterial metabolism?

A

Dihydrofolate reductase is an enzyme in the folic acid synthesis pathway, and it is inhibited by the antibiotic trimethoprim.

423
Q

How do beta-lactam antibiotics function in bacterial cell walls?

A

Beta-lactam antibiotics prevent the cross-linking of peptidoglycan in bacterial cell walls, weakening the structural integrity of the bacteria.

424
Q

What role does DNA ligase play in DNA replication?

A

DNA ligase forms the final bonds between the multiple Okazaki fragments on the lagging strand, connecting them into a continuous DNA strand

425
Q

What happens if DNA ligase is inhibited during DNA replication?

A

Inhibition of DNA ligase will prevent the joining of Okazaki fragments, resulting in incomplete lagging strand synthesis.

426
Q

What is the effect of inhibiting DNA polymerase III on DNA replication?

A

Inhibition of DNA polymerase III prevents the synthesis of both the leading strand and the lagging strand of bacterial DNA.

427
Q

How would inhibition of helicase or single-stranded binding proteins affect DNA replication?

A

Inhibition of helicase or single-stranded binding proteins would prevent the opening of the chromosome, thereby stopping DNA replication from occurring.

428
Q

What is the consequence of inhibiting telomerase in cells?

A

Inhibition of telomerase would lead to the shortening of chromosomes after multiple generations of replication, as telomerase is responsible for maintaining telomere length.

429
Q

What are telomeres?

A

Telomeres are nucleotide sequences located at the ends of chromosomes that protect them from deterioration or fusion with neighboring chromosomes.

430
Q

What is the most common adult renal malignancy?

A

Renal cell carcinoma (RCC).

431
Q

What is the most common subtype of renal cell carcinoma?

A

Clear cell renal cell carcinoma.

432
Q

What are the typical histological features of clear cell RCC on biopsy?

A

Polygonal cells with clear cytoplasm.

433
Q

How is renal cell carcinoma often discovered?

A

Incidentally on imaging studies, such as CT scans.

434
Q

What percentage of renal cell carcinomas may be found incidentally?

A

Up to 50%.

435
Q

What is a major complication of renal cell carcinoma?

A

Metastatic disease.

436
Q

To which locations does renal cell carcinoma commonly metastasize?

A

Lungs (hemoptysis and dyspnea) and bones (pathologic fractures and bone pain).

437
Q

What is the likely mechanism of metastasis for renal cell carcinoma?

A

Hematogenous spread, particularly via the renal vein and inferior vena cava.

438
Q

What is the function of the internal capsule?

A

The internal capsule transmits afferent and efferent nerve fibers between the cortex and the body.

439
Q

What structures are adjacent to the internal capsule?

A

The basal ganglia.

440
Q

What syndrome results from damage to the efferent motor fibers in the internal capsule?

A

Upper motor neuron syndrome.

441
Q

What are the characteristic changes observed in upper motor neuron syndrome?

A

Muscle weakness, hyperreflexia, increased muscle tone, and spastic paresis.

442
Q

What is clasp knife spasticity?

A

Increased resistance to joint extension observed in upper motor neuron syndrome.

443
Q

What type of deficits do upper motor neuron lesions present as?

A

Contralateral deficits (motor and/or sensory loss).

444
Q

What are the “HYPER” signs associated with upper motor neuron lesions?

A

Clasp knife spasticity, hyperreflexia, hypertonicity, and upgoing plantar reflex.

445
Q

What does “clasp knife spasticity” refer to

A

A condition where there is increased resistance to passive movement, often seen in upper motor neuron lesions.

446
Q

What is the significance of the upgoing plantar reflex in upper motor neuron lesions?

A

It indicates upper motor neuron dysfunction and is a sign of neurological damage.

447
Q

What are the characteristic signs of a lower motor neuron (LMN) lesion?

A

Hyporeflexia, fasciculations, muscle atrophy, decreased tone, and flaccid paralysis.

448
Q

How does LMN syndrome differ from upper motor neuron syndrome?

A

LMN syndrome presents with decreased reflexes and muscle tone, whereas upper motor neuron syndrome presents with increased reflexes and tone.

449
Q

What is a common physical manifestation of muscle atrophy in LMN lesions?

A

Flaccid paralysis of the affected muscle groups.

450
Q

What causes fasciculations in LMN lesions?

A

Fasciculations are caused by spontaneous contractions of motor units due to denervation or damage to lower motor neurons.

451
Q

What symptoms should raise suspicion for SVC syndrome in a patient with a significant smoking history?

A

Identifiable chest mass, diffuse venous distention, double vision when leaning forward.

452
Q

What are common causes of SVC syndrome?

A

Mediastinal malignancies, particularly small-cell bronchogenic carcinoma.

453
Q

Why is the SVC vulnerable to compression and obstruction?

A

It is a low-pressure, thin-walled vessel.

454
Q

What acute symptoms do patients with SVC syndrome typically present with?

A

Face, neck, and bilateral upper extremity swelling, stridor, and cyanosis.

455
Q

What classic physical signs are associated with SVC syndrome?

A

Jugular venous distention, edema, and upper body blanching.

456
Q

How can SVC syndrome affect intracranial pressure?

A

It can increase intracranial pressure, leading to neurological symptoms like headaches, vision abnormalities, and altered mental status.

457
Q

What condition might localized findings in a single limb suggest?

A

Compression of a brachiocephalic vein.

458
Q

Which embryonic structures give rise to the SVC?

A

The right common cardinal and anterior cardinal veins.

459
Q

What does the truncus arteriosus develop into?

A

The ascending aorta and the pulmonary trunk.

460
Q

What is a common pathology of the ascending aorta?

A

Ascending aortic aneurysms, which are the majority of thoracic aneurysms.

461
Q

Which genetic condition is associated with ascending aortic aneurysms?

A

Marfan syndrome.

462
Q

How does Marfan syndrome affect the aortic walls?

A

It weakens the aortic walls, causing them to bulge out and increasing the risk of rupture.

463
Q

What condition results from the persistence of the truncus arteriosus?

A

Right to left cyanotic congenital heart disease.

464
Q

What are the immediate signs of persistent truncus arteriosus following birth?

A

Cyanosis due to right to left shunting.

465
Q

What structures do the endocardial cushions form?

A

Atrial septum, membranous interventricular septum, and AV and semilunar valves.

466
Q

Why do endocardial cushion defects often affect multiple cardiac chambers?

A

Because their derivatives are centrally positioned, leading to continuity between both sides of the heart.

467
Q

What is a specific type of defect associated with endocardial cushion defects?

A

Atrioventricular (AV) septal defects.

468
Q

In which condition are AV septal defects most notably observed?

A

Down syndrome.

469
Q

What does the right sixth pharyngeal arch provide?

A

The recurrent laryngeal branch of CN X (vagus nerve).

470
Q

What symptom may occur if the recurrent laryngeal branch of CN X is damaged?

A

Impaired speech.

471
Q

To what structure is the right sixth pharyngeal arch related?

A

The aorta.

472
Q

What cranial nerve is associated with the left fourth pharyngeal arch?

A

CN X (Vagus nerve)

473
Q

What branch does the left fourth pharyngeal arch grant?

A

Superior laryngeal branch

474
Q

What issues can arise if the superior laryngeal branch of CN X is damaged?

A

Issues with swallowing

475
Q

Which major blood vessel is related to the left fourth pharyngeal arch?

A

The aorta

476
Q

Is compression of the aorta indicated for patients with issues related to the left fourth pharyngeal arch?

A

No, it is not indicated.

477
Q

What are mature cystic teratomas commonly known as?

A

Dermoid cysts

478
Q

In which demographic are mature cystic teratomas most commonly found?

A

Young females

479
Q

What type of tumors are mature cystic teratomas classified as?

A

Germ cell tumors

480
Q

What three germ layers do mature cystic teratomas contain elements from?

A

Ectoderm, mesoderm, and endoderm

481
Q

Name three common tissue elements found in mature cystic teratomas

A

Teeth, hair, and sebaceous glands

482
Q

What is the rare monodermal form of mature cystic teratomas that contains thyroid tissue called?

A

Struma ovarii

483
Q

Are most mature cystic teratomas symptomatic or asymptomatic?

A

Asymptomatic

484
Q

When symptoms are present, what are some common symptoms of mature cystic teratomas?

A

Weight gain, abdominal pain, pelvic fullness, and urinary frequency

485
Q

How are mature cystic teratomas treated?

A

Surgically with oophorectomy

486
Q

What is ligated during oophorectomy to prevent uncontrolled intraoperative bleeding?

A

The ovarian vessels

487
Q

What is the major blood supply to the ovaries?

A

Ovarian arteries (gonadal arteries)

488
Q

Where do the ovarian arteries arise from?

A

The abdominal aorta, just below the renal arteries

489
Q

What structure connects the ovaries to the lateral pelvic wall?

A

Infundibulopelvic ligament (suspensory ligament)

490
Q

What structures does the broad ligament contain?

A

Fallopian tubes, uterus, and ovaries

491
Q

What does the broad ligament connect to?

A

The pelvic sidewall

492
Q

Is the broad ligament a fibrous ligament?

A

No, it is a fold of parietal peritoneum.

493
Q

What are the three components of the broad ligament?

A

Mesosalpinx, mesometrium, and mesovarium

494
Q

Which two fibrous ligaments run within the broad ligament?

A

Round ligament and ovarian ligament

495
Q

Do the round and ovarian ligaments require ligation during oophorectomy?

A

No, they do not require ligation.

496
Q

What is another name for the ovarian ligament?

A

Utero-ovarian ligament

497
Q

Where does the ovarian ligament connect the ovary?

A

From the medial pole of the ovary to the lateral uterine horn

498
Q

What is the origin of the ovarian ligament?

A

It is derived from the gubernaculum.

499
Q

Within which ligament does the ovarian ligament run?

A

The broad ligament

500
Q

What types of blood vessels are found in the ovarian ligament?

A

Nonmajor blood vessels, such as ovarian branches of the uterine artery

501
Q

Does the ovarian ligament require ligation during surgical procedures?

A

No, it does not require ligation.

502
Q

What does the round ligament of the uterus connect?

A

The uterine horn to the labia majora

503
Q

What is the origin of the round ligament?

A

It is a derivative of the gubernaculum.

504
Q

Through which canal does the round ligament travel?

A

The inguinal canal

505
Q

Which artery does the round ligament travel above?

A

The artery of Sampson

506
Q

What type of vessels does the round ligament contain?

A

Lymphatic vessels that drain the uterine horn

507
Q

Does the round ligament contain any major blood vessels?

A

No, it does not contain any major blood vessels.

508
Q

Does the round ligament require ligation during gynecologic surgeries?

A

No, it does not require ligation.

509
Q
A