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STEP 1: UWORLD > Microbiology > Flashcards

Microbiology Flashcards

1
Q

A virologist is researching acyclovir-resistant herpes simplex virus (HSV). Viral DNA analysis reveals a mutation in the thymidine kinase gene, resulting in a mutated enzyme that does not phosphorylate acyclovir to its active form. In an experiment, a resistant HSV type 2 strain containing this mutation is cultured in a cell line, and the cell culture is coinfected with a nonresistant HSV type 1 strain. It is found that some of the newly produced type 1 virions acquire resistance to acyclovir, and subsequent progeny continue to be resistant. Which of the following mechanisms best explains the observed findings?

A. Interference
B. Phenotypic mixing
C. Reassortment
D. Recombination
E. Transformation

A

D. Recombination

This scenario describes the exchange of genetic information between 2 virus strains that have nonsegmented, double-stranded DNA genomes. Recombination refers to the exchange of genes between 2 chromosomes via crossing over within homologous regions. The resulting progeny can have recombined genomes with traits from both parent viruses. In this case, the thymidine kinase genes in HSV type 1 and 2 virions are likely to have significant sequence similarity, allowing cross over to occur with relatively high frequency.

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2
Q

______ occurs when one virus inhibits replication and/or release of a second virus that is infecting the same cell. Simple interference would not result in recombinant progeny virions.

A. Interference
B. Phenotypic mixing
C. Reassortment
D. Recombination
E. Transformation

A

Interference

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3
Q

_____ can occur when a host cell is coinfected with 2 viral strains and progeny virions contain parental genome from one strain and nucleocapsid (or envelope) proteins from the other strain. This may result in progeny acquiring additional traits (eg, enhanced ability to infect new host cells due to different nucleocapsid proteins). However, as the genome is unchanged, subsequent progeny would not retain these traits.

A. Interference
B. Phenotypic mixing
C. Reassortment
D. Recombination
E. Transformation

A

Phenotypic mixing

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4
Q

_____ refers to changes in genomic composition that occur when host cells are coinfected with 2 segmented viruses that exchange whole genome segments. This process can cause sudden alterations in surface antigens of the viral progeny, as observed with the highly mutagenic influenza virus. However, because the herpesvirus genome is nonsegmented, it does not engage in reassortment.

A. Interference
B. Phenotypic mixing
C. Reassortment
D. Recombination
E. Transformation

A

Reassortment

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5
Q

_____ is the uptake of naked DNA by a prokaryotic or eukaryotic cell. In virology, transformation also describes incorporation of viral DNA into a host cell chromosome (lysogeny). Transformation alters the genetic composition of the host cell but typically causes no genomic change in progeny virions.

A. Interference
B. Phenotypic mixing
C. Reassortment
D. Recombination
E. Transformation

A

Transformation

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6
Q

_____ refers to gene exchange that occurs through the crossing over of 2 double-stranded DNA molecules

A. Interference
B. Phenotypic mixing
C. Reassortment
D. Recombination
E. Transformation

A

Recombination

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7
Q

____ describes the mixing of genome segments in segmented viruses that infect the same host cell.

A. Interference
B. Phenotypic mixing
C. Reassortment
D. Recombination
E. Transformation

A

Reassortment

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8
Q

A 26-year-old man comes to the office due to a 3-day-history of dysuria and urethral discharge. The symptoms developed about 2 weeks after he had unprotected sexual intercourse with a new partner. His temperature is 37.1 C (98.8 F). On physical examination, a mucoid discharge is expressed with gentle milking of the penis. Gram stain of the discharge reveals numerous neutrophils with intracellular diplococci. A sample of the discharge is placed on an antibiotic-containing medium, and bacterial colonies are cultured. Which of the following terms best describes the medium?

A. Differentiation
B. Enrichment
C. Reducing
D. Selective
E. Synthetic

A

D. Selective

This patient with dysuria and urethral discharge has gonococcal urethritis as indicated by the Gram stain showing gram-negative diplococci within leukocytes. Neisseria gonorrhoeae can be cultured on Thayer-Martin VCN selective medium, which contains vancomycin, colistin, nystatin, and trimethoprim. These antibiotics kill potential contaminants such as gram-positive organisms (vancomycin), gram-negative organisms other than Neisseria (colistin and trimethoprim), and fungi (nystatin).

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9
Q

This patient with dysuria and urethral discharge has ___ _____ as indicated by the Gram stain showing gram-negative diplococci within leukocytes.

A

gonococcal urethritis

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10
Q

__ ___ can be cultured on Thayer-Martin VCN selective medium, which contains vancomycin, colistin, nystatin, and trimethoprim. These antibiotics kill potential contaminants such as gram-positive organisms (vancomycin), gram-negative organisms other than Neisseria (colistin and trimethoprim), and fungi (nystatin).

A

Neisseria gonorrhoeae

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11
Q

____ media help identify cultured organisms based on their metabolic and biochemical properties. Examples of _____ media include the MacConkey and eosin methylene blue (EMB) agars used to culture enteric organisms. Organisms that ferment lactose will appear pink on MacConkey agar and black on EMB agar.

A. Differentiation
B. Enrichment
C. Reducing
D. Selective
E. Synthetic

A

Differential

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12
Q

_____ media contain special growth factors required for some organisms. Examples include the X and V factors required by Haemophilus or the anaerobic conditions needed by Clostridium species.

A. Differentiation
B. Enrichment
C. Reducing
D. Selective
E. Synthetic

A

Enrichment

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13
Q

____ media (eg, thioglycolate broth) remove oxygen and are used to culture anaerobic organisms.

A. Differentiation
B. Enrichment
C. Reducing
D. Selective
E. Synthetic

A

Reducing

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14
Q

A ____ medium is any chemically-defined medium for which all of the chemical contents are known

A. Differentiation
B. Enrichment
C. Reducing
D. Selective
E. Synthetic

A

synthetic

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15
Q

Lipopolysacharide: mechanism

A

Activates macrophages —> widespread release of IL-1, IL-6, and TNF-a

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16
Q

Lipopolysacharide: Presentation

A

Bacteremia and septic shock

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17
Q

K1 Capsular Polysaccharide: Mechanism

A

Prevents phagocytosis and complement-mediated lysis

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18
Q

K1 Capsular Polysaccharide: Presentation

A

Neonatal meningitis

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19
Q

Shiga toxin: Mechanism

A

Inactivates 60S ribosomal subunit, halting protein synthesis and causing cell death

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20
Q

Shiga toxin: Presentation

A

Gastroenteritis (Bloody)

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21
Q

Heat-stable/heat-labile enterotoxins: Mechanism

A

promotes fluid and electrolyte secretion from intestinal epithelium

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22
Q

Heat-stable/heat-labile enterotoxins:: presentation

A

gastreoenteritis (watery)

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23
Q

P-Fimbriae: mechanism

A

allows adhesion to uroepithelium

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24
Q

P-Fimbriae: presentation

A

urinary tract infection

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25
Q

A patient has _____ diarrhea due to Escherichia coli O157:H7, or Shiga toxin–producing E coli (STEC). The transmission of STEC occurs primarily via consumption of contaminated beef products, but isolated cases without a clear source can occur.

A

bloody

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26
Q

After colonization and adherence to intestinal epithelial cells, STEC elaborates Shiga toxin (virtually identical to that produced by Shigella dysenteriae). Enterocytes bind to Shiga toxins, which then inactivate the 60S ribosomal subunit within the host cells by cleaving an adenine nucleobase from the integrated 28S RNA. This leads to inhibition of protein synthesis and apoptosis of intestinal epithelial cells. Clinical manifestations include:

A

Watery diarrhea that becomes bloody within 1-3 days.

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27
Q

Shiga toxin can spread through the damaged intestinal epithelium to the bloodstream and capillary endothelial cells in the kidney, leading to ___ ___ ___ approximately a week after gastrointestinal symptoms. Manifestations include thrombocytopenia, microangiopathic hemolytic anemia, and renal insufficiency.

A

Hemolytic uremic syndrome

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28
Q

Clostridioides difficile produces 2 exotoxins, one of which is a cytotoxin (toxin _) that disrupts the cytoskeleton by ____ actin and causing cell death.

A

Clostridioides difficile produces 2 exotoxins, one of which is a cytotoxin (toxin B) that disrupts the cytoskeleton by depolymerizing actin and causing cell death.

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29
Q

___ produced by Corynebacterium diphtheriae (diphtheria toxin) inactivate elongation factor 2 via ribosylation, which leads to the inhibition of protein synthesis and cell death

A

Exotoxins

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30
Q

Enterotoxigenic E coli produces heat-labile toxin (LT) and heat-stable toxin (ST). LT ____ (increases/decreases_ intracellular cyclic AMP in intestinal mucosal cells, which leads to the ___ (increased/decreased) absorption and increased secretion of sodium, chloride, and water; ST increases intracellular cyclic guanosine monophosphate (GMP), also contributing to diarrhea and electrolyte loss. Watery, not bloody, diarrhea occurs.

A

Enterotoxigenic E coli produces heat-labile toxin (LT) and heat-stable toxin (ST). LT increases intracellular cyclic AMP in intestinal mucosal cells, which leads to the decreased absorption and increased secretion of sodium, chloride, and water; ST increases intracellular cyclic guanosine monophosphate (GMP), also contributing to diarrhea and electrolyte loss. Watery, not bloody, diarrhea occurs.

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31
Q

____ means pain in a joint

A

Arthralgia

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32
Q

____ infection is marked by the presence of HBsAg, HBeAg, and anti-HBc, and a lack of anti-HBs.

A

Acute hepatitis B virus (HBV)

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33
Q

____ Infections are often asymptomatic, but many patients have a few months of jaundice, fatigue, nausea, and right upper–quadrant discomfort.

A

Acute hepatitis B virus (HBV)

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34
Q

___ infection: Perinatal transmission is most common in high-prevalence countries (eg, Sub-Saharan Africa); in low-prevalence regions (eg, United States), most cases occur due to unprotected sex or intravenous drug use.

A

Acute hepatitis B virus (HBV)

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35
Q

HBV is a hepadnavirus composed of:

  1. an __ __ envelope that contains viral-encoded proteins (HBsAg) and host lipid components.
  2. an ___ _____ core that contains a circular, partially double-stranded DNA genome and a DNA polymerase with reverse transcriptase activity.
A
  1. an outer lipid envelope that contains viral-encoded proteins (HBsAg) and host lipid components.
  2. an icosahedral nucleocapsid core that contains a circular, partially double-stranded DNA genome and a DNA polymerase with reverse transcriptase activity.
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36
Q

____ binds to a bile salt transporter on the surface of hepatocytes and enters the cell.

A

HBV

37
Q

HBV:
After the virus is uncoated in the host cytoplasm, the single-stranded DNA portion of the viral genome is completed (repaired) by cellular DNA polymerases. This generates ____-_____ viral DNA, which is subsequently transcribed by host RNA polymerase into a ____ ___ _ ___. The +RNA template is then translated into the proteins that compose the virus (eg, envelope, core, polymerase); it is also converted by viral DNA polymerase/reverse transcriptase into the partially __-__ ___ progeny of developing viral particles.

A

After the virus is uncoated in the host cytoplasm, the single-stranded DNA portion of the viral genome is completed (repaired) by cellular DNA polymerases. This generates double-stranded viral DNA, which is subsequently transcribed by host RNA polymerase into a +single-stranded RNA pregenome. The +RNA template is then translated into the proteins that compose the virus (eg, envelope, core, polymerase); it is also converted by viral DNA polymerase/reverse transcriptase into the partially double-stranded DNA progeny of developing viral particles.

38
Q

The ______ virus replicates via the following sequence: double-stranded DNA → +RNA template → partially double-stranded DNA progeny.

A

hepatitis B virus (HBV)

39
Q

Although it is a DNA virus, ____ uses reverse transcription to generate new viral DNA from a positive-sense RNA template.

A

HBV

40
Q

Epidermal growth factor receptor (EGFR) is stimulated in a paracrine or autocrine fashion by its ligands, leading to the downstream activation of ___

A

KRAS

41
Q

____, a membrane-bound GTP-binding protein that stimulates cellular growth and proliferation.

A

KRAS

42
Q

Many cancers (eg, colorectal, pancreas) leverage this system to drive unchecked cellular growth by overexpressing ____ and its ligands or by developing constitutive activating mutations in the KRAS proto-oncogene.

A

EGFR

43
Q

The EGFR signaling system can be targeted for cancer treatment through the use of monoclonal antibodies (eg, cetuximab, panitumumab) that block ____, leading to reduced KRAS stimulation and decreased cellular growth. However, this treatment is only effective for tumors with wild-type (___) KRAS.

A

EGFR

normal

44
Q

Tumors with KRAS-activating mutations are resistant to ___-___ agents as they have a constitutive activation of a downstream signal that is independent of EGFR stimulation or blockade. Prior to the use of anti-EGFR agents, genetic testing of tumor tissue is performed to see if KRAS is wild-type (eligible for treatment) or mutated (noneligible).

A

anti-EGFR

45
Q

Adenomatous polyposis coli is a tumor suppressor protein that helps degrade ___-_____, preventing uncontrolled cell growth. Inherited inactivating gene mutations are responsible for familial adenomatous polyposis.

A

Adenomatous polyposis coli is a tumor suppressor protein that helps degrade beta-catenin, preventing uncontrolled cell growth. Inherited inactivating gene mutations are responsible for familial adenomatous polyposis.

46
Q

____ is a tumor suppressor protein involved in DNA repair, apoptosis, and cell cycle control; mutations or deletions are present in a large percentage of human tumors.

A

p53

47
Q

____-_____ growth factor stimulates formation of new blood vessels and proliferation of fibroblasts and smooth muscle cells by binding to a receptor tyrosine kinase; mutations resulting in overexpression encourage tumor growth by promoting uncontrolled angiogenesis.

A

Platelet-derived

48
Q

___ ___ ____ is the dominant growth factor involved in angiogenesis and lymph vessel development. Overexpression of VEGF promotes tumor vascularization, facilitating the growth and metastasis of cancers.

A

Vascular endothelial growth factor (VEGF)

49
Q

The ______-_____ ____ gene is a product of translocation of genetic material from chromosome 9 to chromosome 22 [t(9;22)]. It codes for a protein with tyrosine kinase activity. The bcr-abl translocation is the Philadelphia chromosome found in chronic myelogenous leukemia.

A

bcr-abl fusion

50
Q

The _______ codes a protein that participates in signal transduction (MAP-kinase associated pathway). Over-expression of this gene leads to increased sensitivity of cells to mitogenic stimuli. This mutation occurs in a large number of cancers.

A

ras proto-oncogene

51
Q

The ____ gene encodes a protein with tyrosine kinase activity related to the epidermal growth factor receptor. Over-expression of this proto-oncogene is associated with breast and ovarian cancers.

A

Erb-B2

52
Q

Expression of the N-myc proto-oncogene is amplified in ______.

A

neuroblastoma

53
Q

_____ is a commonly used immunohistochemical marker forepithelial-derivedtumors, such as breast cancer. Keratin is also the major protein component of hair and nails.

A

cytokeratin

54
Q

____ is a marker used to identify B lymphocytes, and CD3 is used to identify T lymphocytes.

A

CD20

55
Q

____ is an intermediate filament present in mesenchymal tissue and can be used to detect sarcomas.

A

Vimentin

56
Q

______ is a peroxidase enzyme that can be used as a marker for myeloid cells such as those in acute myeloid leukemia.

A

Myeloperoxidase

57
Q

___ and ____ are markers used for neuroendocrine tumors.

A

Chromogranin A and synaptophysin are markers used for neuroendocrine tumors.

58
Q

The ___ ___ codes for a human epidermal growth factor receptor with tyrosine kinase activity in the intracellular domain. It is known to play a role in the activation of transduction pathways that control epithelial growth and differentiation.

A

HER2 oncogene

59
Q

Epithelial cell carcinomas that ____ HER2 demonstrate increased proliferation and resistance to apoptosis.

A

Epithelial cell carcinomas that overexpress HER2 demonstrate increased proliferation and resistance to apoptosis.

60
Q

HER2-____ breast cancers have a higher risk of disease recurrence and worse prognosis compared to HER2-___ breast cancers

A

HER2-positive breast cancers have a higher risk of disease recurrence and worse prognosis compared to HER2-negative breast cancers

61
Q

____ (a monoclonal antibody against HER2) is used to treat women who test positive for overexpression of the HER2 oncogene.

A

Trastuzumab

62
Q

Estrogen and progesterone receptors are intracellular receptors that are frequently overexpressed in patients with breast cancer. Stimulation of these hormone receptors increases cellular proliferation, and patients with hormone-receptor-positive breast cancer are treated with ___ medications to suppress tumor growth.

A

antiestrogen

63
Q

Intercellular binding is mediated by cell surface proteins such as intercellular adhesion molecules (ICAMs), selectins, and numerous others. Many adhesion proteins, including ICAMS, also play a role in signal ____.

A

Intercellular binding is mediated by cell surface proteins such as intercellular adhesion molecules (ICAMs), selectins, and numerous others. Many adhesion proteins, including ICAMS, also play a role in signal transduction.

64
Q

____ is an intracellular protein that helps form rounded vesicles in the cytoplasm. Clathrin-coated vesicles help mediate intracellular trafficking and endocytosis.

A

Clathrin

65
Q

Blood in your urine is called

A

hematuria

66
Q

Interleukin-2 (IL-2) is a cytokine produced endogenously by activated ___ cells, ____ cells, and natural killer (NK) cells. High-dose IL-2 infusions can also be administered to patients with advanced renal cell carcinoma or metastatic melanoma in order to ___ (increase/decrease) antitumor lymphocyte activity

A

Interleukin-2 (IL-2) is a cytokine produced endogenously by activated CD4 cells, CD8 cells, and natural killer (NK) cells. High-dose IL-2 infusions can also be administered to patients with advanced renal cell carcinoma or metastatic melanoma in order to increase antitumor lymphocyte activity

67
Q

CD4 cells: IL-2 converts activated CD4 cells into type _ T-helper cells, which then secrete inflammatory cytokines (eg, IFN-gamma, TNF-alpha, IL-2) that drive an antitumor response.

A

CD4 cells: IL-2 converts activated CD4 cells into type 1 T-helper cells, which then secrete inflammatory cytokines (eg, IFN-gamma, TNF-alpha, IL-2) that drive an antitumor response.

68
Q

CD8 cells: IL-2 expands the pool of activated CD8 cells and _____ their cytotoxic killing with granzymes and perforins.

A

CD8 cells: IL-2 expands the pool of activated CD8 cells and increases their cytotoxic killing with granzymes and perforins.

69
Q

NK cells: IL-2 triggers proliferation of NK cells and dramatically ______ their cytotoxic activity; most of the antitumor effect of IL-2 therapy comes from increased NK cell activity.

A

NK cells: IL-2 triggers proliferation of NK cells and dramatically increases their cytotoxic activity; most of the antitumor effect of IL-2 therapy comes from increased NK cell activity.

70
Q

Although patients with advanced renal cell carcinoma who undergo ___ therapy may enter long-lasting remission, high-dose IL-2 treatment is nonspecific and causes significant adverse effects due to excessive cytokine production (eg, capillary leak syndrome). Therefore, most patients are now treated with newer immunotherapy agents such as ___ inhibitors (eg, ipilimumab) or PD-1 protein inhibitors (eg, nivolumab) that deliver more targeted therapy and are better tolerated.

A

Although patients with advanced renal cell carcinoma who undergo IL-2 therapy may enter long-lasting remission, high-dose IL-2 treatment is nonspecific and causes significant adverse effects due to excessive cytokine production (eg, capillary leak syndrome). Therefore, most patients are now treated with newer immunotherapy agents such as CTLA-4 inhibitors (eg, ipilimumab) or PD-1 protein inhibitors (eg, nivolumab) that deliver more targeted therapy and are better tolerated.

71
Q

Tumor hypoxia and lactic acid production increase release of _____, which promotes angiogenesis required for tumor growth. Therefore, anti-VEGF immunotherapy (eg, bevacizumab) can induce a potent antitumor response; it is often used for lung and colorectal cancer.

A

vascular endothelial growth factor (VEGF)

72
Q

Although CD8 and NK cells induce cell death via ____, this effect is not mediated by direct binding of IL-2 to the tumor cell. Certain chemotherapy drugs (eg, etoposide, vincristine, cyclophosphamide) directly induce apoptosis by damaging tumor cell DNA, the cytoskeleton, or mitochondria.

A
73
Q

Monoclonal antibodies that target specific cell ____ molecules on the tumor can induce tumor cell death via _____-dependent cellular cytotoxicity. An example of this type of immunotherapy is alemtuzumab, a drug for chronic lymphocytic leukemia that targets a cell surface receptor (CD52) found primarily on mature lymphocytes. However, IL-2 does not directly interact with the Fc receptor on cytotoxic cells.

A

Monoclonal antibodies that target specific cell surface molecules on the tumor can induce tumor cell death via antibody-dependent cellular cytotoxicity. An example of this type of immunotherapy is alemtuzumab, a drug for chronic lymphocytic leukemia that targets a cell surface receptor (CD52) found primarily on mature lymphocytes. However, IL-2 does not directly interact with the Fc receptor on cytotoxic cells.

74
Q

Although IL-2 triggers CD8 cells to ____ expression of the inhibitory receptor PD-1 (programmed cell death protein 1), engagement of this receptor leads to T-cell _____, not increased antitumor activity.

A

Although IL-2 triggers CD8 cells to increase expression of the inhibitory receptor PD-1 (programmed cell death protein 1), engagement of this receptor leads to T-cell exhaustion, not increased antitumor activity.

75
Q

_____ is paralysis of one side of the body.

A

hemiplagia

76
Q

Aphasia is ____

A

loss of ability to understand or express speech, caused by brain damage.

77
Q

_____ necrosis: Etiology (cause)

-Severe bacterial infections (eg, gangrene)
-CNS infarcts

A

Liquefactive necrosis:

78
Q

Liquefactive necrosis: Morphology

Necrotic tissue is digested by _____ enzymes into a viscous fluid:
-Infected abscess fluid is creamy yellow due to dead ____ (pus)
-Brain infarcts resolve into CSF-filled spaces

A

Liquefactive necrosis:

Necrotic tissue is digested by hydrolytic enzymes into a viscous fluid:
-Infected abscess fluid is creamy yellow due to dead leukocytes (pus)
-Brain infarcts resolve into CSF-filled spaces

79
Q

_____ necrosis: (cause)
-Hypertension
-Vasculitis

A

Fibrinoid

80
Q

Fibrinoid Necrosis: Morphology

-Damaged vessels leak ___/____ complexes
-____philic layer of proteinaceous material in vessel walls

A

Fibrinoid Necrosis: Morphology

-Damaged vessels leak fibrin/immune complexes
-Eosinophilic layer of proteinaceous material in vessel walls

81
Q

___ necrosis: (cause)

-Acute pancreatitis
-Trauma (subcutaneous adipose tissue)

A

Fat

82
Q

Fat necrosis: Morphology

-___ fatty acids released by active enzymes (eg, lipases) or mechanical damage
-Fatty acids combine with ___, forming chalky-white deposits (saponification)

A

Fat necrosis: Morphology

-Free fatty acids released by active enzymes (eg, lipases) or mechanical damage
-Fatty acids combine with calcium, forming chalky-white deposits (saponification)

83
Q

____ necrosis: (cause)

-Mycobacterial infections -Fungal infections (eg, Histoplasma, Cryptococcus, Coccidioides)

A

Caseous

84
Q

Caseous necrosis: Morphology

-Friable, cheeselike material composed of cell fragments & amorphous ____ debris

-Surrounded by ___ macrophages & giant cells (____)

A

Caseous necrosis: Morphology

-Friable, cheeselike material composed of cell fragments & amorphous proteinaceous debris

-Surrounded by epithelioid macrophages & giant cells (granuloma)

85
Q

____ necrosis (cause)

-Irreversible ischemic injury outside CNS

A

Coagulative

86
Q

Coagulative necrosis (morphology)

Tissue architecture is preserved due to denaturation of ___ enzymes:
-Cells are anucleate with ____philic cytoplasm
-Leukocytes eventually infiltrate & ___ necrotic tissue

A

Coagulative necrosis (morphology)

Tissue architecture is preserved due to denaturation of lytic enzymes:
-Cells are anucleate with eosinophilic cytoplasm
-Leukocytes eventually infiltrate & digest necrotic tissue

87
Q

____ necrosis is a pattern of injury that results in accumulation of fibrin-like material in the walls of blood vessels affected by vasculitis syndromes (eg, polyarteritis nodosa) or malignant hypertension. Although fibrinoid necrosis in cerebral arteries can predispose a patient to hemorrhagic stroke, this change would not be an expected complication of acute ischemic stroke.

A

Fibrinoid

88
Q

__ ____ infection can occur in the CNS and cause granulomas with caseous necrosis (epithelioid macrophages around a necrotic focus) within the affected parenchyma. However, the onset of neurologic symptoms in patients with tuberculous brain abscesses tends to be more chronic and progressive than this patient’s acute presentation.

A

Focal tuberculous

89
Q

____ necrosis occurs following hypoxic cell death in all tissues except the CNS. It results in the acute denaturation of structural and enzymatic cellular proteins. Cell nuclei disappear, but the basic architecture of the affected tissue is preserved because intracellular proteolytic enzymes are inactivated during the injury process.

A

Coagulative

STEP 1: UWORLD (3 decks)

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