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H&D > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

What is ergosterol?

A

A substance similar to cholesterol found in fungal cell walls

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2
Q

What enzyme in the fungal cell wall is responsible for synthesizing ergosterol?

A

14-a-demethylase

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3
Q

What drug classes are used to target 14-a-demethylase in fungal cell walls?

A

Azoles

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4
Q

Do the following descriptors better match a yeast or mold?

A

Yeast

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5
Q

Do the following descriptors better match a yeast or mold?

A

Mold

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6
Q

Does the pictured agar resemble a yeast or a mold?

A

Yeast

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7
Q

Does the pictured agar resemble a yeast or a mold?

A

Mold

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8
Q

A multicellular, filamentous organism would most likely be a yeast or a mold?

A

A mold

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9
Q

In molds, what word is used to describe thread-like filaments?

A

Hyphae

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10
Q

What name is given to hyphae interweaves in molds?

A

Mycelium

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11
Q

What is the makeup of over 90% of the fungal cell wall?

A

Polysaccharides

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12
Q

Are yeasts multicellular?

A
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13
Q

Yeasts grow by budding. What is another name for a bud?

A

A blastoconidia

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14
Q

True hyphae (not pseudohypha) begin as what transient structure from the parent yeast cell?

A

A germ tube

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15
Q

What is an example of a yeast that makes psuedohyphae and true hyphae?

A

Candida albicans

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16
Q

Is candida albicans germ tube + or germ tube -?

A

Germ tube +

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17
Q

What descriptor of pseudohyphae differentiates it from true hyphae?

A

Pseudohyphae resembles sausage-links (septate/non-septate hyphae will resemble branches)

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18
Q

What are the correct names for asexual and sexual sporulation?

A

Asexual state- anamorph
Sexual state- teleomorph

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19
Q

How do yeast reproduce?

A

Budding

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20
Q

How do molds reproduce?

A

Production of conidia (conidiospores, or separation of hyphal elements)

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21
Q

How do yeasts/molds undergo sexual sporulation?

A

Halpoid nuclei of donor and recipient fertile cells/spores fuse

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22
Q

What are the temperature constraints of dimophic fungi?

A

Mold at 25-30 C
Yeast at 35- 37 C

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23
Q

Define endemic fungi:

A

Fungi geographically restricted in the environment

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24
Q

Define opportunistic fungi:

A

Fungi that only cause disease in compromised hosts

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25
Q

Define dermatophytes:

A

Fungi causing superficial skin infections

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26
Q

Define dematiaceous fungi:

A

Dark brown-black pigmented molds

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27
Q

Is Candida albicans dimorphic?

A

Yes, but for the purpose of H&D, think of it as a yeast

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28
Q

What are 2 pros and 2 cons for Direct microscopy lab testing for yeasts/molds (KOH +/- Calcofluor)?

A
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29
Q

What are pros and cons for a culture in testing for yeasts/molds?

A
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30
Q

What are the pros and cons for PCR in testing for yeasts/molds?

A
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31
Q

What laboratory test is the gold standard for invasive disease?

A

Histopathology

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32
Q

What is the moa of terbinafine?

A

Inhibition of squalene epoxidase

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33
Q

What drug class inhibits glucan synthase?

A

Echinocandins

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34
Q

What four criteria are required for fungal pathogens to cause disease?

A

1) Growth at or above 37 C
2) Penetrate host barriers
3) Digest/absorb nutrients
4) Evade immune system

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35
Q

What is a definite host in the context of parasitism?

A

Where sexual maturity & reproduction occur for completion of transmission cycles

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36
Q

What is an intermediate host in context of parasitism?

A

Where asexual or developmental stages occur (larvae, excystation, etc), but not competent for development to final lifecycle stages

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37
Q

What is a reservoir host in context of parasitism?

A

A host which harbours only immature stage; used for further trasmission

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38
Q

What is a dead-end or accidental host in context of parasitism?

A

Various levels of life cycle can occur, but cycle cannot complete and gametes fail to perpetuate or fully mature

39
Q

What are two significant histological features of Plasmodium falciparum?

A
40
Q

Is induction immunosuppression necessary before surgery?

A

Not necessarily, but it is often used to optimize patient outcomes

41
Q

What are the three chief roles of induction immunosuppression therapy?

A

1) Potent acute immunosuppression in peri-operative period
2) Minimize risk of acute rejection in early post- transplant period
3) Allow for delay in initiation of CNI/allows medications to reach therapeutic levels

42
Q

What are the two primary roles of maintenance immunosuppression therapy?

A

1) Prevent chronic organ transplant rejection
2) Minimize drug toxicity

43
Q

What primary immunodeficiency is caused by a loss of the common gamma chain (IL-2R-gamma)?

A

X-linked Severe Combined Immunodeficiency (SCID)

44
Q

What is the status of the T cells, NK cells, B cells, and antibodies of a patient diagnosed with X-linked SCID?

A

Absent T & NK cells

B cells may be present

No functional antibodies

45
Q

Would a patient diagnosed with X-linked SCID have germinal centers in their lymph nodes/spleen? Why not?

A

No, the absence of Tfh cells prevents naive B cells from being activated

46
Q

What are common symptoms of X-linked SCID?

A

Failure to thrive
Recurrent infections
Chronic diarrhea

47
Q

What is the role of Bruton’s tyrosine kinase in developing B cells?

A

Successful heavy chain rearrangement of developing B cells culminates in an intraceullular signal mediated by Btk promoting cell survival

Failed heavy chain rearrangement culminates in apoptosis of the developing cell

48
Q

85% of X-linked agammaglobulinemia cases are due to a deficiency in what?

A

Bruton’s tyrosine kinase (Btk)

49
Q

Why do patients with X-linked agammaglobulinemia lack the capacity to produce Ig?

A

B cells cannot mature due to lack of Btk -> developing B cells will apoptose

50
Q

What are clinical symptoms of X-linked agammaglobulinemia?

A

Recurrent sinusitis, otitis media, pneumonia starting at least 6mo after birth with chronic enteroviral meningoencephalitis

51
Q

What is a granuloma?

A
52
Q

What is the MoA of Calcineurin inhibitors (Tacrolimus, Cyclosporin)?

A

CNIs bind to immunophilins -> Immunophilin complex binds calcineurin & prevents NFAT activation -> Reduced T-cell activation & proliferation

53
Q

What is the mechanism of X-linked Hyper IgM?

A

A defect in CD40L -> poor AID activity -> defective affinity maturation and isotype switching (i.e. Tfh and Th1 cannot effectively influence B cells)

54
Q

What blood abnormalities are consistant with X-linked hyper IgM?

A

High IgM, with low IgG and IgA, as well as neutropenia

55
Q

What is the clinical presentation of Hyper IgM syndrome?

A

Onset 6 months after birth, with recurrent bacterial and opportunistic infections (Pneumocystis jirovecii pneumonia)

56
Q

What is the mechanism of IgA deficiency?

A

Defect in IgA production, usually associated with autoimmune disease or anaphylatic reaction to blood transfusion
*Can progress to CVID

57
Q

What is the clinical presentation of IgA deficiency?

A

80-90% asymptomatic, but can present with sinopulmonary infections, Giardiasis

58
Q

What is the mechanism of CVID?

A

Mostly unknown etiology, but about 10% if TACI

Defects in antibody production, low IgG and/or IgA and/or IgM

59
Q

What is the clinical presentation of CVID?

A

Usually adult onset (2nd or 3rd decade)

Recurrent sinopulmonary infections (i.e. Giardia)

60
Q

What is the etiology of chronic granulomatous disease? What is the clinical test that can be administered?

A

Defects in NADPH oxidase

CT: Phagocytes fail to reduce nitro blue tetrazolium (NBT)

61
Q

Granulomatous disease poses an extra risk of infection by what type of organisms?

A

Catalase-expressing organism infections (Staph Aureus, Pseudomonas, Candida, etc)

62
Q

What is the etiology of Leukocyte adhesion deficiency (LAD)?

A

Defect in subunit of LFA-1 (CD18)

63
Q

What is the clinical presenation of LAD?

A

-Neutrophilia
-Failed Rebuck test
- Low CD18
-Delayed separation of umbilical cord
-Poor wound healing w/ no pus

64
Q

What two disorders are primarily due to defects in complement?

A

Hereditary angioedema

PNH

65
Q

What is the etiology of Hereditary angioedema?

A

Defect in C1 INH -> increased bradykinin -> vascular permeability leads to diffuse edema

66
Q

When does Hereditary angioedema typically increased in severity?

A

Late childhood or adolescence

67
Q

What is the etiology of PNH? What particlar organism does this condition increase susceptibility to?

A

PIG-A can’t add GPI anchors to cells -> poor surface expression of DAF, CD59 -> sporadic RBC lysis

Neisseria meningitidis

68
Q

What is the etiology of DiGeorge syndrome (complete)?

A

22q11 deletion

Defects in 3rd/4th pharyngeal pouches lead to thymic hypoplasia -> deficient T cell maturation

69
Q

What is the clinical presentation for DiGeorge syndrome?

A

Absent parathyroid, abnormal development and facial abnormalities, as well as small or absent thymus

70
Q

What is the MOA, CU, and TOX for Acetaminophen?

A

MOA: Inhibition of peroxidase in CNS?
CU: Analgesic, antipyretic (NOT anti-inflammatory)
TOX: Hepatotoxicity and liver failure in overdose

71
Q

What is the MOA, CU, and TOX for Aspirin?

A

MOA: Irreversible inhibition of COX 1 & 2

CU: Analgesic, antipyretic, anti-inflammatory, anti-platelet agent

TOX: Tinnitus, nephrotoxicity, GI pain & ulcer risk, prolonged bleeding time, increased risk of MI/stroke w/ long term use

72
Q

Which NSAID has a unique risk of Reye’s syndrome in children?

A

Aspirin

73
Q

What is the MOA, CU, and TOX of ibuprofen and naproxen?

A

MOA: Inhibition of COX 1 & 2

CU: Analgesic, antipyretic, anti-inflammatory

TOX: Acute interstitial nephritis, nephrotoxicity, GI pain & ulcer risk, prolonged bleeding time, increased risk of MI/stroke w/ long term use

74
Q

Which NSAIDs have a unique risk of Stevens-Johnson syndrome?

A

Ibuprofen and naproxen

75
Q

What are the MOA, CU, and TOX for celecoxib & meloxicam?

A

MOA: COX 2 inhibition

CU: analgesic, antpyretic, anti-inflammatory

TOX: CV risk similar to ibuprofen or naproven, may increase in risk with dose

76
Q

What are the MOA, CU, and TOX for corticosteroids (prednisone, hydrocortisone, dexamethasome)?

A

MOA: Inhibition of phospholipase A2, cyclooxygenase, and cytokines

CU: Immune suppression, pain management (reduction of inflammation)

TOX:
acute- mood changes, hyperkalemia, hyperglycemia
chronic- HPA-axis suppression, muscle wasting, cushingnoid cataract, glioma

77
Q

What are the broad MOA, CU, and TOX for calcineurin inhibitors (CNIs)?

A

MOA: Binds to immunophilin -> immunophilin complex binds calcineurin to block NFAT activation -> decreased T-cell activation and proliferation

CU: Maintenance immunosuppression

TOX: Nephrotoxicity (caution with NSAID & ACEI use) and CYP3A4 and PgP substrate interactions

78
Q

What are the two most pertinent CNIs?

A

Cyclosporin and tacrolimus

79
Q

What is the specific MOA and TOX for cyclosporin?

A

MOA: Binds cyclophilin
TOX: Hypertension, hyperlipidemia

80
Q

What is the specific MOA and TOX for tacrolimus?

A

MOA: Binds FK binding protein (FKBP-12)
TOX: Neurotoxicity, hyperglycemia

81
Q

What are the two most pertinent TOR inhibitors?

A

Sirolimus and Everolimus

82
Q

What are the MOA, CU, and TOX for TOR inhibitors?

A

MOA: Binds to FKBP-12 and inhibits MTOR -> bloackage of IL2 -> cell cycle arrest in G1-S phase -> suppression of T and B cell proliferation

CU: Used during CNI minimization or withdrawal, adjunct immunosuppressive therapy, CAV, CLAD, or cancer

TOX: Proteinuria, hyperlipidemia, edema, oral ulcers
BBW (lung): impaired wound healing
BBW (kidney and liver): thrombosis
BBW (heart): increased mortality

83
Q

What are the two most pertinent proliferation/metabolic inhibitors?

A

Azathioprine and mycophenolate mofetil

84
Q

What is the general MOA of proliferation/metabolic inhibitors?

A

6-MP and MPA inhibit purine nucleotide synthesis -> impaired DNA synthesis -> inhibition of T and B cell proliferation

85
Q

What are the specific MOA, CU, and TOX of azathioprine?

A

MOA: Prodrug of 6-mercaptopurine (6-MP)

CU: Immunosuppressive therapy

TOX: Hemolytic anemia, pancreatitis, drug interactions
BBW: malignancy

86
Q

What are the specific MOA, CU, and TOX of mycophenolate mofetil?

A

MOA: Converted to mycophenolic acid

CU: Decreased organ rejection rates compaired to azathioprine

TOX: BM suppression, N/D, drug interactions w/ magnesium containing products & antacids, teratogen

87
Q

What are pros and cons of using azathioprine for immunosuppression vs. mycophenolate mofetil?

A

Pros:
-1x daily dosing
- less GI SE than mycophenolate mofetil
Cons:
-worse rejection rates in kidney, liver, and heart transplant pts

88
Q

What are the most common causes of infectious esophagitis?

A

Candida spp.
HSV
CMV

89
Q

What are the most common causes of infectious gastritis?

A

H. pylori
CMV
Others (Candida, mucor, histoplasma, mycobacteria, giardia, strongyloides)

90
Q

What are the most common causes of infective ileitis?

A

Mycobacterium tuberculosis
Yersinia enterocolitica
Salmonella spp.
C. diff
MAC
Histoplasma

91
Q

What are the most common causes of infective colitis?

A

Diarrheal pathogens
CMV
adenovirus
C. diff
MAC
Entamoeba histolytica

92
Q

What are common symptoms of diverticulitis?

A

LLQ pain, fever, N/V, leukocytosis

93
Q

What are common symptoms of peritonitis?

A

Abodminal pain, fever, encephalopathy

94
Q

What are the most common infectious causes of peritonitis?

A

E. coli
Klebsiella spp.
Streptococcus spp.

H&D (10 decks)

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