BOOTCAMP

Question 1

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

Answer 1

GLUT-5

Question 2

Is primarily utilized in neuronal and placental glucose transport.

Answer 2

GLUT-3

Question 3

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

Answer 3

GLUT-2

Question 4

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).

Answer 4

GLUT-1

Question 5

Is stored in vesicles predominately inside skeletal myocytes and adipocytes.

Answer 5

GLUT-4

Question 6

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

Answer 6

Phosphatidylinositol-3-kinase (PI3K)

Question 7

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

Answer 7

Disulfide bonds.

Question 8

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

Answer 8

Terminal duct lobular units (TDLUs).

Question 9

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

Answer 9

Invasive ductal carcinoma (IDC)

Question 10

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

Answer 10

BRCA1 and BRCA2

Question 11

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

Answer 11

Most commonly MHL1 and MHL2

Question 12

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.

Answer 12

CDKN2A

Question 13

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

Answer 13

Melanoma, pancreatic, and lung cancer.

Question 14

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

Answer 14

SMAD4

Question 15

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

Question 16

Are tumor markers for melanoma.

Answer 16

HMB-45 and MART-1

Question 17

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

Answer 17

MHC class I

Question 18

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

Answer 18

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

Question 19

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

Answer 19

Basal cell carcinoma

Question 20

Is associated with BerEp4 on histological stains

Answer 20

Basal cell carcinoma

Question 21

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

Answer 21

HHV-8 and HIV

Question 22

Tumor markers associated with Kaposi sarcoma.

Answer 22

CD34, CD31, and D2-40

Question 23

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

Answer 23

Merkel cell carcinoma

Question 24

Are tumor markers associated with Merkel cell carcinoma.

Answer 24

Chromogranin A, PAX5, and cytokeratin 20

Question 25

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

Answer 25

Squamous cell carcinoma

Question 26

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

Answer 26

Squamous cell carcinoma

Question 27

Is positive for cytokeratin on immunohistochemical staining.

Answer 27

Squamous cell carcinoma

Question 28

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

Answer 28

Calcineurin

Question 29

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

Answer 29

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

Question 30

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

Answer 30

IL-2

Question 31

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

Answer 31

Cyclosporin and tacrolimus

Question 32

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.

Answer 32

FK506

Question 33

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

Answer 33

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

Question 34

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

Answer 34

Cyclosporin

Question 35

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

Answer 35

Basiliximab

Question 36

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

Answer 36

Glucocorticoids

Question 37

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

Answer 37

NF-κB

Question 38

Xanthine monophosphate would decrease with ? usage.

Answer 38

Azathioprine

Question 39

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

Answer 39

Azathioprine

Question 40

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

Answer 40

Mycophenolate mofetil

Question 41

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

Answer 41

IMP dehydrogenase

Question 42

Drug induced lupus syndrome

Answer 42

Hydralazine, procainamide, isoniazid

Question 43

Add acetal groups to lysine. Relaxes chromatin to transcription.

Answer 43

Histone acetyltransferasas

Question 44

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

Answer 44

Drug induced lupus

Question 45

Are seen in the diffuse form of scleroderma.

Answer 45

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

Question 46

Are involved in Mixed Connective Tissue Disease (MCTD).

Answer 46

Anti-U1 ribonucleoprotein antibodies

Question 47

Ribavirin (antiviral)

Answer 47

Inhibits IMP dehydrogenase

Question 48

Are associated with celiac disease.

Answer 48

Anti-tissue transglutaminase antibodies

Question 49

Mycophenolate (inmunosuppresant)

Answer 49

Inhibits IMP dehydrogenase of white cells

Question 50

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

Answer 50

6-Mercaptopurine

Question 51

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

Answer 51

Azathioprine

Question 52

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

Answer 52

Nitrosamines

Question 53

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.

Answer 53

Krukenberg tumors

Question 54

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.

Answer 54

Epithelial tumors

Question 55

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.

Answer 55

Germ cell tumors

Question 56

Are common types of ovarian cysts.

Answer 56

Follicular cysts and theca-lutein cysts

Question 57

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

Answer 57

Follicular cysts

Question 58

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

Answer 58

Theca-lutein cysts

Question 59

Do not typically present with fulminant abdominal and systemic symptoms.

Answer 59

Ovarian cysts

Question 60

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.

Answer 60

Sex cord-stromal tumors

Question 61

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.

Answer 61

Symptomatic cholelithiasis

Question 62

Parenteral feeding is accompanied by multiple complications, such as

Answer 62

Risk of bloodstream infection, metabolic effects, and gallstones.

Question 63

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

Answer 63

Gallstone formation

Question 64

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

Answer 64

Cholecystokinin

Question 65

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

Answer 65

Granuloma

Question 66

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

Answer 66

MTB

Question 67

Resident pulmonary macrophages engulf MTB and subsequently perform two actions:

Answer 67

• 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.

Question 68

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

Answer 68

Epithelioid histiocytes

Question 69

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

Answer 69

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

Question 70

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

Answer 70

Interleukin-5 (IL-5)

Question 71

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

Answer 71

Transforming growth factor β

Question 72

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

Answer 72

Cystic fibrosis (CF)

Question 73

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).

Answer 73

Cystic fibrosis (CF)

Question 74

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

Answer 74

The Hardy-Weinberg principle

Question 75

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

Answer 75

• 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)

Question 76

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

Answer 76

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

Question 77

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

Answer 77

• 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

Question 78

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

Answer 78

Incretins

Question 79

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

Answer 79

Incretins (examples)

Question 80

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

Answer 80

GIP

Question 81

GLP-1

Answer 81

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

Question 82

Increatins

Answer 82

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.

Question 83

Oral-administered glucose

Answer 83

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

Question 84

Intravenous glucose

Answer 84

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

Question 85

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.

Answer 85

Ghrelin

Question 86

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.

Answer 86

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

Question 87

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.

Answer 87

Glucagon

Question 88

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.

Answer 88

Somatostatin

Question 89

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.

Answer 89

Osteoporosis

Question 90

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.

Answer 90

Secondary osteoporosis

Question 91

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.

Answer 91

Hypervitaminosis D

Question 92

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.

Answer 92

Osteomalacia

Question 93

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.

Answer 93

Paget’s disease of bone (osteitis deformans)

Question 94

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

Answer 94

Primary osteoporosis

Question 95

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.

Answer 95

Succinylcholine

Question 96

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.

Answer 96

Acetylcholinesterase

Question 97

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.

Answer 97

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

Question 98

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

Answer 98

The sarcoplasmic reticulum

Question 99

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

Answer 99

T-tubules

Question 100

A first-generation antihistamine used to treat seasonal allergies.

Answer 100

Dimenhydrinate

Question 101

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

Answer 101

The primary mechanism of action of first-generation antihistamines

Question 102

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.

Answer 102

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

Question 103

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

Answer 103

Polypharmacy

Question 104

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

Answer 104

Beers criteria

Question 105

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.

Answer 105

Losartan

Question 106

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

Answer 106

Metformin

Question 107

Side effects are primarily myopathy and hepatotoxicity.

Answer 107

Atorvastatin

Question 108

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

Answer 108

The positive predictive value (PPV)

Question 109

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).

Answer 109

The positive predictive value (PPV)

Question 110

PPV

Answer 110

= TP / (TP + FP)

Question 111

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.

Answer 111

Specificity

Question 112

Specificity

Answer 112

= TN / (TN + FP)

Question 113

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.

Answer 113

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

Question 114

Increasing the specificity of a test,

Answer 114

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

Question 115

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.

Answer 115

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.

Question 116

The APOE ε4 gene allele (increased susceptibility.)

Answer 116

Alzheimer disease (AD)

Question 117

AD: Decreased ability of the lipoprotein gene product to clear

Answer 117

Amyloid-beta protein

Question 118

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

Answer 118

Huntington disease

Question 119

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

Answer 119

LDLR gene mutations

Question 120

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

Answer 120

Mutation of the PRNP gene on chromosome 20p12

Question 121

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

Answer 121

Edward syndrome

Question 122

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?

Answer 122

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.

Question 123

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).

Answer 123

S3 gallop or a third heart sound

Question 124

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

Answer 124

Athletes or pregnant women

Question 125

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

Answer 125

Ventricular dysfunction or a hypervolemic state

Question 126

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

Answer 126

Pulmonary flow murmur

Question 127

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

Answer 127

Mitral valve prolapse

Question 128

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).

Answer 128

Atrial kick (late diastolic atrial contraction)

Question 129

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

Answer 129

S4 gallop or fourth heart sound

Question 130

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.

Answer 130

The spinothalamic tract and spinal trigeminal nucleus

Question 131

Dizziness and ataxia reflect damage to the ?, respectively.

Answer 131

Vestibular nucleus and cerebellar peduncle

Question 132

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

Answer 132

Nucleus ambiguus damage

Question 133

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

Answer 133

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

Question 134

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.

Answer 134

Nucleus ambiguus defects

Question 135

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.

Answer 135

RULE OF 4S

Question 136

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

Answer 136

Lateralization of the lesion

Question 137

Only hearing loss can be localized in

Answer 137

CN VIII

Question 138

Can originate from both medullary and pontine damage.

Answer 138

Vestibular signs

Question 139

Are the most common causes of gastric ulcers

Answer 139

Helicobacter pylori infection and NSAID use

Question 140

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.

Answer 140

Food intake

Question 141

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.

Answer 141

The right and left gastric arteries

Question 142

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

Answer 142

5%

Question 143

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

Answer 143

Greater curvature

Question 144

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

Answer 144

18%

Question 145

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.

Answer 145

Osteoporosis

Question 146

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.

Answer 146

Bone mineral density (BMD)

Question 147

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

Answer 147

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

Question 148

In secondary osteoporosis, BMD decreases are usually accompanied by

Answer 148

Abnormal lab values.

Question 149

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

Answer 149

Increased bone resorption

Question 150

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.

Answer 150

Type 1 primary osteoporosi

Question 151

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

Answer 151

Osteopetrosis

Question 152

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.

Answer 152

Paget disease of bone (osteitis deformans)

Question 153

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.

Answer 153

Osteomalacia

Question 154

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

Answer 154

Osteomalacia

Question 155

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

Answer 155

Hyperparathyroidism

Question 156

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

Answer 156

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

Question 157

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

Answer 157

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

Question 158

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.

Answer 158

Jarisch-Herxheimer reaction

Question 159

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).

Answer 159

Superantigen activation of immune cells

Question 160

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.

Answer 160

Release of preformed IgE

Question 161

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.

Answer 161

Circulating immune complex deposition

Question 162

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.

Answer 162

Granzyme release from CD8+ T lymphocytes

Question 163

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

Answer 163

Advanced glycation end products (AGEs).

Question 164

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

Answer 164

Diabetic nephropathy and nephrotic syndrome.

Question 165

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

Answer 165

The polyol pathway

Question 166

Here glucose is converted to sorbitol via aldose reductase.

Answer 166

The polyol pathway

Question 167

Sorbitol can then be converted to fructose via

Answer 167

Sorbitol dehydrogenase

Question 168

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

Answer 168

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

Question 169

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

Answer 169

Osmotic damage

Question 170

Sorbitol accumulation has many potential manifestations, including

Answer 170

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).

Question 171

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.

Answer 171

Essential fructosuria.

Question 172

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

Answer 172

Hypoglycemia

Question 173

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

Answer 173

Sorbitol accumulation from the polyol pathway

Question 174

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.

Answer 174

Hepatic overproduction of VLDL

Question 175

Metabolic effects of thyroid hormone include

Answer 175

Increased basal metabolic rate, carbohydrate metabolism, and lipid metabolism

Question 176

Thyroid hormone increases lipid metabolism in several ways. It increases

Answer 176

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

Question 177

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.

Answer 177

LDL

Question 178

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

Answer 178

High LDL plasma levels, hyperlipidemia, and hypercholesterolemia.

Question 179

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.

Answer 179

Familial hyperchylomicronemia (Type I hyperlipoproteinemia)

Question 180

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.

Answer 180

LPL

Question 181

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.

Answer 181

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

Question 182

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

Answer 182

Acute pyelonephritis

Question 183

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

Answer 183

Acute pyelonephritis

Question 184

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.

Answer 184

Bacteremia, sepsis, and renal failure

Question 185

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.

Answer 185

Acute interstitial nephritis (AIN), also called tubulointerstitial nephritis

Question 186

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

Answer 186

Cystitis

Question 187

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.

Answer 187

Glomerulonephritis

Question 188

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

Answer 188

Urethritis

Question 189

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

Answer 189

Epidemiology UTI

Question 190

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

Answer 190

Etiology UTI

Question 191

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

Answer 191

Treatment UTI

Question 192

Protein synthesis

Answer 192

Mechanism Nitrofurantoin

Question 193

Folic acid synthesis

Answer 193

Mechanism TMP/SMX

Question 194

Cell wall synthesis

Answer 194

Mechanism Fosfomycin, B-lactams

Question 195

DNA gyrase

Answer 195

Mechanism Flouroquinolones

Question 196

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

Answer 196

Gastric ulcer

Question 197

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

Answer 197

Secretion of gastric acid

Question 198

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

Answer 198

Coffee-ground emesis

Question 199

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.

Answer 199

Brown hematin

Question 200

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.

Answer 200

The lesser curvature

Question 201

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

Answer 201

The gastroduodenal artery

Question 202

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.

Answer 202

Erosion of a gastric ulcer into the splenic artery

Question 202

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

Answer 202

The left gastroepiploic artery

Question 203

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.

Answer 203

Gastric fundus

Question 204

Antiarrhythmic Drugs: Mechanism of Action: Class Ia

Answer 204

Na+ channel blockade (moderate)

Question 205

Antiarrhythmic Drugs: Mechanism of Action: Class Ib

Answer 205

Na+ channel blockade (weak)

Question 206

Antiarrhythmic Drugs: Mechanism of Action: Class Ic

Answer 206

Na+ channel blockade (strong)

Question 207

Antiarrhythmic Drugs: Mechanism of Action: Class II

Answer 207

β-adrenergic receptor blockade

Question 208

Antiarrhythmic Drugs: Mechanism of Action: Class III

Answer 208

K+ channel blockade

Question 209

Antiarrhythmic Drugs: Mechanism of Action: Class IV

Answer 209

Ca2+channel blockade

Question 210

Antiarrhythmic Drugs: Class Ia

Answer 210

Quinidine
Procainamide
Disopyramide

Question 211

Antiarrhythmic Drugs: Class Ib

Answer 211

Lidocaine
Phenytoin
Mexiletine

Question 212

Antiarrhythmic Drugs: Class Ic

Answer 212

Flecainide
Propafenone

Question 213

Antiarrhythmic Drugs: Class II

Answer 213

Metoprolol
Propranolol
Esmolol
Atenolol
Timolol
Carvedilo

Question 214

Antiarrhythmic Drugs: Class III

Answer 214

Amiodarone
Ibutilide
Dofetilide
Sotalol

Question 215

Antiarrhythmic Drugs: Class IV

Answer 215

Diltiazem
Verapamil

Question 216

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.

Answer 216

Anticoagulation

Question 217

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.

Answer 217

Amiodarone

Question 218

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.

Answer 218

Amiodarone

Question 219

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

Answer 219

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).

Question 220

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

Answer 220

Adenosine

Question 221

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

Answer 221

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

Question 222

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

Answer 222

β-blockers

Question 223

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

Answer 223

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

Question 224

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

Answer 224

Ca2+ channel blockers

Question 225

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

Answer 225

Ca2+ channel blockers

Question 226

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

Answer 226

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

Question 227

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.

Answer 227

A thiazolidinedione (TZD)

Question 228

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

Answer 228

Metformin and liraglutide.

Question 229

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.

Answer 229

TZDs (e.g., pioglitazone, rosiglitazone)

Question 230

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.

Answer 230

GLUT4 expression

Question 231

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

Answer 231

Sulfonylureas (e.g., chlorpropamide, glipizide)

Question 232

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.

Answer 232

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

Question 233

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

Answer 233

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

Question 234

Thiazolidinediones increase insulin sensitivity by upregulating the transcription of

Answer 234

Adiponectin

Question 235

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

Answer 235

A selective estrogen receptor modulator (SERM)

An aromatase inhibitor.

Question 236

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.

Answer 236

Tamoxifen and raloxifene

Question 237

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,

Answer 237

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

Question 238

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.

Answer 238

Leuprolide

Question 239

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

Answer 239

Prostate cancer

Question 240

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.

Answer 240

Xeroderma pigmentosum (XP)

Question 241

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.

Answer 241

Dysfunctional nucleotide excision repair (NER) system

Question 242

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.

Answer 242

Acute intermittent porphyria

Question 243

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

Answer 243

Tetracyclines

Question 244

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.

Answer 244

Polymorphous light eruption (PMLE)

Question 245

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.

Answer 245

Porphyria cutanea tarda

Question 246

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.

Answer 246

Staphylococcus saprophyticus

Question 247

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.

Answer 247

S. saprophyticus

Question 248

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.

Answer 248

Hospital-acquired UTIs

Question 249

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

Answer 249

Positive nitrites on urinalysis.

Question 250

Proteus mirabilis can be associated with UTIs involving

Answer 250

Struvite stones

Question 251

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

Answer 251

Rheumatoid arthritis (RA)

Question 252

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

Answer 252

Metacarpophalangeal and proximal interphalangeal joints.

Question 253

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

Answer 253

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

Question 254

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.

Answer 254

Paget’s disease of bone (osteitis deformans)

Question 255

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

Answer 255

Sarcoidosis

Question 256

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.

Answer 256

Erosive arthritis

Question 257

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.

Answer 257

Subchondral sclerosis

Question 258

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.

Answer 258

Synovial pannus

Question 259

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

Answer 259

Ataxia-telangiectasia

Question 260

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

Answer 260

Ataxia-telangiectasia

Question 261

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

Answer 261

Signs of fluid overload

Question 262

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.

Answer 262

Fluid overload

Question 263

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.

Answer 263

Axillary murmur

Question 264

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

Answer 264

Fatigue, paroxysmal nocturnal dyspnea, and orthopnea

Question 265

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

Answer 265

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

Question 266

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

Answer 266

An elevated pulmonary capillary wedge pressure.

Question 267

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

Answer 267

MR

Question 268

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

Answer 268

Decrease

Question 269

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

Answer 269

Increase

Question 270

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

Answer 270

Increased

Question 271

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

Answer 271

Elevated

Question 272

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

Answer 272

Elevated pulmonary capillary wedge pressure

Question 273

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).

Answer 273

Increased filling pressures

Question 274

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.

Answer 274

Schizophreniform disorder

Question 275

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

Answer 275

Schizophreniform disorder

Question 276

First-line treatment for schizophreniform disorder includes atypical

Answer 276

Antipsychotics.

Question 277

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

Answer 277

Brief psychotic disorder

Question 278

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.

Answer 278

Delusional disorder

Question 279

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

Answer 279

Major depressive disorder with psychotic features

Question 280

Is a combination of psychotic features and mood symptoms.

Answer 280

Schizoaffective disorder

Question 281

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.

Answer 281

Schizotypal personality

Question 282

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

Answer 282

Type 1 hypersensitivity reaction.

Question 283

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.

Answer 283

Type 1 hypersensitivity reaction.

Question 284

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.

Answer 284

Complex (MAC) (C5b-C9)

Question 285

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

Answer 285

Systemic lupus erythematosus and rheumatoid arthritis.

Question 286

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

Answer 286

perforin and granzyme B.

Question 287

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

Answer 287

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

Question 288

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

Answer 288

Vesicles containing histamine, leukotrienes, and other inflammatory mediators.

Question 289

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

Answer 289

Chronic obstructive pulmonary disease (COPD)

Question 290

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

Answer 290

Alveolar destruction

Question 291

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.

Answer 291

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

Question 292

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.

Answer 292

Upper lobes

Question 293

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).

Answer 293

Type I hypersensitivity reaction

Question 294

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

Answer 294

Bronchiectasis

Question 295

Patients with bronchiectasis typically develop

Answer 295

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

Question 296

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

Answer 296

Permanent bronchial dilation, necrotizing inflammation, and mucosal destruction

Question 297

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

Answer 297

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

Question 298

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

Answer 298

⍺1-antitrypsin deficiency (A1ATD)

Question 299

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

Answer 299

Diffuse panacinar emphysema

Question 300

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

Answer 300

Sickle cell anemia

Question 301

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.

Answer 301

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

Question 302

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.

Answer 302

Pulmonary microvascular vasoocclusion.

Question 303

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

Answer 303

Sickle cell anemia

Question 304

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

Answer 304

Thalassemia

Question 305

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

Answer 305

JAK2

Question 306

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

Answer 306

JAK2

Question 307

Polycythemia vera, manifestations include

Answer 307

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

Question 308

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.

Answer 308

Hereditary spherocytosis

Question 309

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

Answer 309

High levels indicate inflammation or infection.

Question 310

Acute Phase Reactants: positive (Upregulated): Ferritin

Answer 310

Binds and stores iron intracellularly to inhibit microbial iron scavenging.

Question 311

Acute Phase Reactants: positive (Upregulated): Fibrinogen

Answer 311

Promotes endothelial repair and correlates to erythrocyte sedimentation rate.

Question 312

Acute Phase Reactants: positive (Upregulated): Haptoglobin

Answer 312

Binds free hemoglobin to protect against oxidative stress.

Question 313

Acute Phase Reactants: positive (Upregulated): Hepcidin

Answer 313

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

Question 314

Acute Phase Reactants: positive (Upregulated): Procalcitonin

Answer 314

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

Question 315

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

Answer 315

Increased levels can lead to secondary amyloidosis.

Question 316

Acute Phase Reactants: Negative (Downregulated): Albumin

Answer 316

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

Question 317

Acute Phase Reactants: Negative (Downregulated):Transferrin

Answer 317

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

Question 318

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

Answer 318

Levels decrease as resources are diverted to produce positive APRs.

Question 319

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

Answer 319

Pneumonia

Question 320

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

Answer 320

Infection

Question 321

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

Answer 321

• 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)

Question 322

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.

Answer 322

Procalcitonin (PCT)

Question 323

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

Answer 323

Extra-thyroid PCT

Question 324

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

Answer 324

Down-regulate

Question 325

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

Answer 325

Increased PCT if bacterial, normal/decreased if viral.

Question 326

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.

Answer 326

Complement fixation and the promotion of phagocytosis

Question 327

Erythrocyte sedimentation rate (ESR) and fibrinogen

Answer 327

Are nonspecific APRs.

Question 328

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

Answer 328

Would not provide information about the underlying etiology

Question 329

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.

Answer 329

Interleukin-1 (IL-1)

Question 330

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.

Answer 330

It binds and sequesters iron to inhibit microbial iron scavenging.

Question 331

Is the end product of glycolysis under anaerobic conditions.

Answer 331

Lactate

Question 332

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.

Answer 332

Impaired tissue oxygenation from impaired delivery or defective mitochondrial utilization.

Question 333

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

Answer 333

Thyrotoxicosis factitia (exogenous thyrotoxicosis).

Question 334

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

Answer 334

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

Question 335

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

Answer 335

(e.g., levothyroxine, liothyronine).

Question 336

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

Answer 336

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

Question 337

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.

Answer 337

Atrophy of thyroid follicular cells

Question 338

Is disordered cell proliferation

Answer 338

Dysplasia

Question 339

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

Answer 339

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

Question 340

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

Answer 340

A diffuse goiter.

Question 341

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.

Answer 341

Metaplasia

Question 342

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

Answer 342

Meningitis

Question 343

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

Answer 343

Listeria monocytogenes infection.

Question 344

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.

Answer 344

Gram-positive facultative intracellular rod

Question 345

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.

Answer 345

Gentamicin

Question 346

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

Answer 346

Ampicillin monotherapy, or in combination with gentamicin,

Question 347

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

Answer 347

Meningoencephalitis.

Question 348

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.

Answer 348

Bacillus cereus

Question 349

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

Answer 349

Clostridium botulinum

Question 350

In adults, botulism results from the ingestion of

Answer 350

Improperly canned foods.

Question 351

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.

Answer 351

Haemophilus influenzae

Question 352

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

Answer 352

Salmonella enterica

Question 353

This patient presents with infertility due to cystic fibrosis-related

Answer 353

Congenital bilateral absence of the vas deferens

Question 354

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

Answer 354

Chromosome 7

Question 355

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

Answer 355

ATP-gated chloride channel

Question 356

Most common mutation of CF

Answer 356

Phe508 deletion

Question 357

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

Answer 357

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

Question 358

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.

Answer 358

Opacification of the sinuses and nasal polyps.

Question 359

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.

Answer 359

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

Question 360

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.

Answer 360

Classical-type Ehlers-Danlos syndrome

Question 361

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.

Answer 361

COL3A1

Question 362

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

Answer 362

Infertility.

Question 363

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.

Answer 363

Marfan syndrome

Question 364

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.

Answer 364

Fragile X syndrome

Question 365

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

Answer 365

Subfertility

Question 366

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

Answer 366

The PKHD1 gene

Question 367

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.

Answer 367

Polycystic kidney disease (ARPKD)

Question 368

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

Answer 368

Malignancy

Question 369

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.

Answer 369

Renal cell carcinoma (RCC)

Question 370

RCC is associated with several risk factors, including

Answer 370

Male sex, smoking, and obesity.

Question 371

RCC: Individuals may present with various findings, including an

Answer 371

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

Question 372

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.

Answer 372

Nephroblastomas (Wilms tumor)

Question 373

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

Answer 373

Renal oncocytoma

Question 374

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.

Answer 374

Renal oncocytoma

Question 375

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

Answer 375

Squamous cell carcinoma

Question 376

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.

Answer 376

Transitional cell carcinoma (urothelial carcinoma)

Question 377

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

Answer 377

PCT of the nephron.

Question 378

Of all RCC subtypes, ? is the most prevalent.

Answer 378

Clear cell RCC

Question 379

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

Answer 379

Hematuria, flank pain, and a palpable abdominal mass.

Question 380

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.

Answer 380

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

Question 381

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.

Answer 381

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

Question 382

Highly adaptive defense mechanisms include

Answer 382

Altruism
Anticipation
Humor
Sublimation
Suppression

Question 383

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.

Answer 383

Suppression

Question 384

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.

Answer 384

Rationalization

Question 385

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.

Answer 385

Displacement

Question 386

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.

Answer 386

Repression

Question 387

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

Answer 387

Intellectualization

Question 388

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

Answer 388

Intellectualization

Question 389

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

Answer 389

Lisinopril

Question 390

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).

Answer 390

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.

Question 391

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).

Answer 391

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

Question 392

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

Answer 392

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

Question 393

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.

Answer 393

Abdominal bruits and treatment-resistant hypertension.

Question 394

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.

Answer 394

Calcium channel blockers (e.g., amlodipine)

Question 395

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

Answer 395

Calcium channel blockers

Question 396

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.

Answer 396

Atorvastatin

Question 397

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.

Answer 397

Chlorthalidone

Question 398

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.

Answer 398

Pioglitazone

Question 399

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,

Answer 399

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

Question 400

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.

Answer 400

Angiotensin-converting enzyme (ACE) inhibitors

Question 401

HSV-2

Answer 401

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

Question 402

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

Answer 402

Is more likely to cause genital lesions.

Question 403

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

Answer 403

Primary HSV-2

Question 404

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.

Answer 404

The genital rash caused by HSV-2

Question 405

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

Answer 405

Acyclovir, famciclovir, and valacyclovir

Question 406

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.

Answer 406

Haemophilus ducreyi

Question 407

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.

Answer 407

Gingivostomatitis

Question 408

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

Answer 408

Treponema pallidum

Question 409

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.

Answer 409

Varicella-zoster virus (VZV)

Question 410

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

Answer 410

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

Question 411

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

Answer 411

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.

Question 412

How does DNA ligase function in the DNA replication process?

Answer 412

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.

Question 413

Where do DNA polymerase enzymes bind when synthesizing DNA?

Answer 413

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

Question 414

What is the role of DNA helicase in DNA replication?

Answer 414

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

Question 415

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

Answer 415

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.

Question 416

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

Answer 416

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

Question 417

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

Answer 417

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)

Question 418

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

Answer 418

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.

Question 419

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

Answer 419

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

Question 420

What potential cardiovascular effect can fluoroquinolone antibiotics cause?

Answer 420

Prolong the QT interval on an ECG.

Question 421

Why are fluoroquinolone antibiotics considered unsafe in pregnancy?

Answer 421

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

Question 422

What is the role of dihydrofolate reductase in bacterial metabolism?

Answer 422

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

Question 423

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

Answer 423

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

Question 424

What role does DNA ligase play in DNA replication?

Answer 424

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

Question 425

What happens if DNA ligase is inhibited during DNA replication?

Answer 425

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

Question 426

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

Answer 426

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

Question 427

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

Answer 427

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

Question 428

What is the consequence of inhibiting telomerase in cells?

Answer 428

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

Question 429

What are telomeres?

Answer 429

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

Question 430

What is the most common adult renal malignancy?

Answer 430

Renal cell carcinoma (RCC).

Question 431

What is the most common subtype of renal cell carcinoma?

Answer 431

Clear cell renal cell carcinoma.

Question 432

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

Answer 432

Polygonal cells with clear cytoplasm.

Question 433

How is renal cell carcinoma often discovered?

Answer 433

Incidentally on imaging studies, such as CT scans.

Question 434

What percentage of renal cell carcinomas may be found incidentally?

Answer 434

Up to 50%.

Question 435

What is a major complication of renal cell carcinoma?

Answer 435

Metastatic disease.

Question 436

To which locations does renal cell carcinoma commonly metastasize?

Answer 436

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

Question 437

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

Answer 437

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

Question 438

What is the function of the internal capsule?

Answer 438

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

Question 439

What structures are adjacent to the internal capsule?

Answer 439

The basal ganglia.

Question 440

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

Answer 440

Upper motor neuron syndrome.

Question 441

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

Answer 441

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

Question 442

What is clasp knife spasticity?

Answer 442

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

Question 443

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

Answer 443

Contralateral deficits (motor and/or sensory loss).

Question 444

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

Answer 444

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

Question 445

What does “clasp knife spasticity” refer to

Answer 445

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

Question 446

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

Answer 446

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

Question 447

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

Answer 447

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

Question 448

How does LMN syndrome differ from upper motor neuron syndrome?

Answer 448

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

Question 449

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

Answer 449

Flaccid paralysis of the affected muscle groups.

Question 450

What causes fasciculations in LMN lesions?

Answer 450

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

Question 451

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

Answer 451

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

Question 452

What are common causes of SVC syndrome?

Answer 452

Mediastinal malignancies, particularly small-cell bronchogenic carcinoma.

Question 453

Why is the SVC vulnerable to compression and obstruction?

Answer 453

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

Question 454

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

Answer 454

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

Question 455

What classic physical signs are associated with SVC syndrome?

Answer 455

Jugular venous distention, edema, and upper body blanching.

Question 456

How can SVC syndrome affect intracranial pressure?

Answer 456

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

Question 457

What condition might localized findings in a single limb suggest?

Answer 457

Compression of a brachiocephalic vein.

Question 458

Which embryonic structures give rise to the SVC?

Answer 458

The right common cardinal and anterior cardinal veins.

Question 459

What does the truncus arteriosus develop into?

Answer 459

The ascending aorta and the pulmonary trunk.

Question 460

What is a common pathology of the ascending aorta?

Answer 460

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

Question 461

Which genetic condition is associated with ascending aortic aneurysms?

Answer 461

Marfan syndrome.

Question 462

How does Marfan syndrome affect the aortic walls?

Answer 462

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

Question 463

What condition results from the persistence of the truncus arteriosus?

Answer 463

Right to left cyanotic congenital heart disease.

Question 464

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

Answer 464

Cyanosis due to right to left shunting.

Question 465

What structures do the endocardial cushions form?

Answer 465

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

Question 466

Why do endocardial cushion defects often affect multiple cardiac chambers?

Answer 466

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

Question 467

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

Answer 467

Atrioventricular (AV) septal defects.

Question 468

In which condition are AV septal defects most notably observed?

Answer 468

Down syndrome.

Question 469

What does the right sixth pharyngeal arch provide?

Answer 469

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

Question 470

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

Answer 470

Impaired speech.

Question 471

To what structure is the right sixth pharyngeal arch related?

Answer 471

The aorta.

Question 472

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

Answer 472

CN X (Vagus nerve)

Question 473

What branch does the left fourth pharyngeal arch grant?

Answer 473

Superior laryngeal branch

Question 474

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

Answer 474

Issues with swallowing

Question 475

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

Answer 475

The aorta

Question 476

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

Answer 476

No, it is not indicated.

Question 477

What are mature cystic teratomas commonly known as?

Answer 477

Dermoid cysts

Question 478

In which demographic are mature cystic teratomas most commonly found?

Answer 478

Young females

Question 479

What type of tumors are mature cystic teratomas classified as?

Answer 479

Germ cell tumors

Question 480

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

Answer 480

Ectoderm, mesoderm, and endoderm

Question 481

Name three common tissue elements found in mature cystic teratomas

Answer 481

Teeth, hair, and sebaceous glands

Question 482

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

Answer 482

Struma ovarii

Question 483

Are most mature cystic teratomas symptomatic or asymptomatic?

Answer 483

Asymptomatic

Question 484

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

Answer 484

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

Question 485

How are mature cystic teratomas treated?

Answer 485

Surgically with oophorectomy

Question 486

What is ligated during oophorectomy to prevent uncontrolled intraoperative bleeding?

Answer 486

The ovarian vessels

Question 487

What is the major blood supply to the ovaries?

Answer 487

Ovarian arteries (gonadal arteries)

Question 488

Where do the ovarian arteries arise from?

Answer 488

The abdominal aorta, just below the renal arteries

Question 489

What structure connects the ovaries to the lateral pelvic wall?

Answer 489

Infundibulopelvic ligament (suspensory ligament)

Question 490

What structures does the broad ligament contain?

Answer 490

Fallopian tubes, uterus, and ovaries

Question 491

What does the broad ligament connect to?

Answer 491

The pelvic sidewall

Question 492

Is the broad ligament a fibrous ligament?

Answer 492

No, it is a fold of parietal peritoneum.

Question 493

What are the three components of the broad ligament?

Answer 493

Mesosalpinx, mesometrium, and mesovarium

Question 494

Which two fibrous ligaments run within the broad ligament?

Answer 494

Round ligament and ovarian ligament

Question 495

Do the round and ovarian ligaments require ligation during oophorectomy?

Answer 495

No, they do not require ligation.

Question 496

What is another name for the ovarian ligament?

Answer 496

Utero-ovarian ligament

Question 497

Where does the ovarian ligament connect the ovary?

Answer 497

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

Question 498

What is the origin of the ovarian ligament?

Answer 498

It is derived from the gubernaculum.

Question 499

Within which ligament does the ovarian ligament run?

Answer 499

The broad ligament

Question 500

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

Answer 500

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

Question 501

Does the ovarian ligament require ligation during surgical procedures?

Answer 501

No, it does not require ligation.

Question 502

What does the round ligament of the uterus connect?

Answer 502

The uterine horn to the labia majora

Question 503

What is the origin of the round ligament?

Answer 503

It is a derivative of the gubernaculum.

Question 504

Through which canal does the round ligament travel?

Answer 504

The inguinal canal

Question 505

Which artery does the round ligament travel above?

Answer 505

The artery of Sampson

Question 506

What type of vessels does the round ligament contain?

Answer 506

Lymphatic vessels that drain the uterine horn

Question 507

Does the round ligament contain any major blood vessels?

Answer 507

No, it does not contain any major blood vessels.

Question 508

Does the round ligament require ligation during gynecologic surgeries?

Answer 508

No, it does not require ligation.

Question 509

What is the likely complication causing fatigue and mild normocytic anemia in an 84-year-old female with chronic kidney disease (CKD)?

Answer 509

Decreased erythropoietin (EPO) production.

Question 510

Where is erythropoietin (EPO) produced in the body?

Answer 510

In the renal peritubular interstitial cells.

Question 511

What triggers the production of EPO?

Answer 511

Hypoxia-inducible factors (HIFs) respond to hypoxia and anemia, leading to EPO stimulation.

Question 512

How does hypoxia affect the degradation of HIFs?

Answer 512

In hypoxic conditions, the normal degradation of HIFs is reduced, leading to increased EPO production.

Question 513

How does hypoxia affect the degradation of HIFs?

Answer 513

In hypoxic conditions, the normal degradation of HIFs is reduced, leading to increased EPO production.

Question 514

What happens after EPO is released into the bloodstream?

Answer 514

EPO travels to the bone marrow and stimulates Jak/STAT pathways in erythrocyte precursors.

Question 515

How does tissue oxygenation affect EPO production?

Answer 515

Improved oxygenation relieves hypoxia in the peritubular interstitium, increasing HIF degradation and decreasing EPO production.

Question 516

What is the effect of EPO stimulation in the bone marrow?

Answer 516

It increases erythrocyte division, improving oxygen-carrying capacity and tissue oxygenation.

Question 517

What complications can arise in end-stage renal disease related to EPO?

Answer 517

Renal interstitial damage and fibrosis, which impair EPO production and release.

Question 518

What are potential treatments for anemia related to CKD?

Answer 518

EPO supplementation and blood transfusions in unstable patients.

Question 519

Various hormones function through G protein-coupled receptors, including

Answer 519

Catecholamines, glucagon, and anterior pituitary hormones (e.g., ACTH, LH, FSH, TSH).

Question 520

Certain neurotransmitters (e.g., ?) bind to and activate ligand-activated ion channels, changing the membrane potential of the postsynaptic membrane to exert their effects.

Answer 520

Acetylcholine, GABA, glutamate

Question 521

Function through receptor tyrosine kinase/MAP kinase pathways.

Answer 521

Insulin and other growth factors (e.g., IGF-1, TGF, FGF, EGF)

Question 522

Is a signaling pathway involved in cell-cell communication, regulating multiple processes found during development, such as neurogenesis.

Answer 522

The notch pathway

Question 523

What are the common symptoms of gastroesophageal reflux disease (GERD)?

Answer 523

Heartburn, regurgitation, dysphagia, hoarseness, sore throat, and chronic cough.

Question 524

What physical exam finding is associated with GERD in this patient?

Answer 524

Widespread dental erosion.

Question 525

What can cause dental erosion in patients with GERD?

Answer 525

Gastric acid damaging dental enamel due to reflux.

Question 526

What is the first-line treatment for GERD?

Answer 526

Proton pump inhibitors (PPIs).

Question 527

How do proton pump inhibitors work?

Answer 527

They irreversibly inhibit the H+/K+-ATPase pump to prevent gastric acid secretion.

Question 528

Which receptors stimulate gastric acid secretion?

Answer 528

M3 receptor (via acetylcholine), H2 receptor (via histamine), and CCKB receptor (via gastrin).

Question 529

What role does the vagus nerve play in gastric acid secretion?

Answer 529

It increases gastric acid secretion through parasympathetic activity.

Question 530

What role do prostaglandins and somatostatin play in gastric acid secretion?

Answer 530

They inhibit gastric acid secretion by blocking the effects of histamine.

Question 531

Which hormone, secreted from duodenal S cells, inhibits gastric acid release?

Answer 531

Secretin

Question 532

Does vasoactive intestinal polypeptide (VIP) directly affect gastric acid production or secretion?

Answer 532

No, it does not have a direct effect on gastric acid production or secretion.

Question 533

What are the primary functions of vasoactive intestinal polypeptide (VIP)?

Answer 533

Increasing intestinal water and electrolyte secretion and relaxing intestinal smooth muscle.

Question 534

What are tendinous xanthomas, and where are they commonly found?

Answer 534

Tendinous xanthomas are lipid deposits found in tendons, commonly located in the calcaneal (Achilles) tendon or fingers.

Question 535

What are xanthomas composed of?

Answer 535

Xanthomas are composed of cholesterol and lipid-containing histiocytes.

Question 536

What condition is associated with the presence of xanthomas?

Answer 536

Hyperlipidemia.

Question 537

What family history detail raises concern for familial dyslipidemia in this patient?

Answer 537

A familial history of early-onset heart disease.

Question 538

What are common presentations of familial dyslipidemias?

Answer 538

Xanthomas, early-onset atherosclerosis, and pancreatitis.

Question 539

What are some complications of hyperlipidemia?

Answer 539

Coronary artery disease, stroke, peripheral arterial disease, and other ischemic conditions.

Question 540

What are the key components of managing hyperlipidemia?

Answer 540

Exercise, diet modification, and medications.

Question 541

Xanthomas are nodules composed of ? and are a clinical sign of hyperlipidemia.

Answer 541

Lipid-laden histiocytes

Question 542

What are the classic presenting symptoms of a pulmonary embolism (PE)?

Answer 542

Sudden onset dyspnea, pleuritic chest pain, tachycardia, tachypnea, and hypoxemia.

Question 543

What is the most common cause of pulmonary embolism?

Answer 543

Most pulmonary embolisms arise from deep venous thromboembolism (DVT) in the lower extremities.

Question 544

What are the components of Virchow’s triad that predispose to DVT?

Answer 544

Blood stasis, hypercoagulable state, and endothelial damage.

Question 545

How does a pulmonary embolism affect alveolar dead space?

Answer 545

It increases alveolar dead space due to decreased blood flow to ventilated areas.

Question 546

What are some significant causes of pulmonary embolism besides thrombus formation?

Answer 546

Fat embolism, air embolism, septic emboli, amniotic fluid embolism.

Question 547

How does the body compensate for hypoxemia in pulmonary embolism?

Answer 547

By increasing the respiratory rate, leading to lower tidal volumes and a higher proportion of dead space ventilation.

Question 548

What happens to tidal volume in response to pulmonary embolism?

Answer 548

Tidal volume decreases due to inefficient respiration, as the patient takes smaller breaths.

Question 549

What is the primary treatment for pulmonary embolism?

Answer 549

Anticoagulation (e.g., heparin), thrombolysis (tPA), thrombectomy, or an IVC filter.

Question 550

Why is there respiratory alkalosis in pulmonary embolism?

Answer 550

Due to excess exhalation of carbon dioxide from increased respiratory rate.

Question 551

What imaging study is used to diagnose a pulmonary embolism?

Answer 551

CT pulmonary angiogram, which shows intraluminal filling defects.