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POD > POD E3 > Flashcards

POD E3 Flashcards

1
Q

What is in fungi cell wall? cell membrane?

A

cell wall- chitin and glucan

cell membrane- ergosterol

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2
Q

difference in mold and yeast?

A

yeast- unicellular, reproduce by budding

mold- multicellular filamentous; long filaments (hyphae) or a mat (mycelium)

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3
Q

2 types of hyphae

A

coenocytic- non-septated

septate- single cells separated by cross walls

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4
Q

what is dimorphism?

A

fungi exists in two diff forms (typically mold in the cold and yeast in the heat)

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5
Q

what are the different classifications of fungal infections?

A

superficial- outermost layers of skin & hair
cutaneous- extends deeper into epidermis; invasive hair/nail diseases
subcutaneous- dermis, subcutaneous tissues, muscle, & fascia
systemic (deep seated)- originate primarily in lung, may spread to many organs
opportunistic- members of normal flora when host defenses compromised

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6
Q

what lab technique provides digestion and clarity of the tissue so fungi can be observed?

A

KOH mount

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7
Q

what stain detects fungal cell wall chitin by fluorescence?

A

calciflor white stain

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8
Q

what fungal stain stains yeasts and hyphae, reacting with chitin and aldehyde?

A

periodic acid Schiff reagent

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9
Q

what is the best stain for detecting all fungi? stains hyphae and yeast forms black against green background

A

GMS (gomori methanamine silver) stain

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10
Q

can Gram stain be used for fungi?

A

yes, stains most yeasts and hyphal elements; however, fungi not classified as Gram +/-

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11
Q

what organisms are the Giemsa stain useful?

A

Histoplasma capsulatum, Pneumocystis jirovecii; also stains others

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12
Q

what is the most commonly used agar for culturing fungi?

A

Sabouraud’s agar

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13
Q

this fungal species is a dimorphic fungi that produces pseudohyphae & is the fourth most common cause of nosocomial bloodstream infections? part of the normal human flora

A

Candida

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14
Q

which fungus is known for forming germ tubes?

A

Candida albicans

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15
Q

what are virulence factors of C. albicans?

A

adhesins, germtube/hyphal formation, gliotoxin (immunosuppressive toxin)

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16
Q

where is Candida primarily found?

A

GI tract (From mouth to rectum); part of normal flora

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17
Q

infections caused by Candida?

A
  • thrush (white patches on oral mucosa)
  • vaginal candidiasis: thick, white “cottage cheese/curd-like” discharge; itching/burning
  • dermatitis: diaper rash; assoc w/ moisture
  • onychomycosis & paronchia: nail tissue destruction
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18
Q

how is Candida detected/diagnosed?

A
  • KOH w/ calcifluor white stain detected under microscope (can see budding yeast and pseudohyphae)
  • germ tube test- IDs C. albicans
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19
Q

treatment of Candida?

A
  • azoles for mucosal/cutaneous infections

- ampho B (IV) & flucytosine for systemic infection

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20
Q

this fungus exists in mold form, is not dimorphic, and forms septate hyphae? forms acute branching angles and is responsible for allergic manifestations as well as pulmonary effects

A

aspergillus

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21
Q

treatment for aspergillus

A

amphotericin B or 5-flucytosine; surgical removal of infected tissue

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22
Q

this aseptate mold can cause rhinocerebral, pulmonary, and subcutaneous disease; fungi invade blood vessel walls, causing tissue necrosis

A

mucormycosis (Rhizopus, Mucor, & Absidia species)

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23
Q

rhinocerebral mucormycosis penetrates the cribiform plate and invade surrounding tissue, causing necrosis. what patients are at increased risk for this?

A

diabetics, esp those with DKA; as well as severely burnt, and immunocompromised; treatment is amphotericin B and correction of underlying predisposing condition

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24
Q

what is the most common cause of fungal meningitis?

A

Cryptococcus neoformans

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25
Q

which yeast-like fungi has an anti-phagocytic capsule? (only fungi w/ capsule!)

A

Cryptococcus

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26
Q

what stain is used for Cryptococcus? how is it identified

A

India ink– appears as distinguishing “halos”; also capsular polysaccharide antigen test via latex agglutination test

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27
Q

treatment for cryptococcal meningtitis & other forms of cryptococcal infections?

A

amphotericin B plus flucytosine followed by consolidation therapy w/ fluconazole or itraconazole

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28
Q

this “round cup” shaped fungal organism looks like a protozoa and lacks ergosterol

A

Pneumocystis carini (jiroveci)

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29
Q

how is PJP diagnosed, and what is the treatment?

A

microscopy of biopsy or BAL fluid; has “ground glass” appearance on radiograph; use Gomori’s methanamine silver stain– see round cup shaped organism
Tx!: TMP-SMX (trimethoprim-sulfamethoxazole) or pentamidine isothionate in sulfa allergies

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30
Q

what type of macrophages are primarily involved in terminating inflammation and inducing repair?

A

M2 (alternatively activated) type

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31
Q

tissues are able to replace damaged components and return to normal state

A

regeneration

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32
Q

injured tissues are incapable of complete restitution, or supporting structures of tissue are severely damaged; repair occurs by laying down connective tissue; may result in scar; excessive deposition of collagen

A

fibrosis

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33
Q

what are the main components of connective tissue repair?

A

angiogenesis, formation of granulation tissue, and remodeling of CT

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34
Q

what are some factors that affect tissue repair?

A

infection***; diabetes; nutritional status; glucocorticoid use; poor perfusion; mechanical factors; foreign bodies; type/extent of tissue injury & location

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35
Q

what are the first type of cells involved in tissue repair? when are they replaced and by what?

A

neutrophils= 1st cell; replaced by macrophages by day 3; macrophages= main cell for repair

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36
Q

differences in 1st vs. 2nd intention healing

A

2nd intention: large wounds where cell/tissue loss is more extensive; form larger amounts of granulation tissue, inflammation more intense, greater scar tissue mass; involves contraction of myofibroblasts

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37
Q

compare/contrast keloid and hypertrophic scars

A

both due to excessive amounts of collagen, whose formation persists for a longer period of time than normal
keloids often extend beyond site of original injury, rarely regress, will recur if excised; have higher incidence among those with darker pigmented skin

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38
Q

what are the hallmarks of inflammation?

A

heat (calor), redness (rubor), swelling (tumor), pain (dolor); also loss of function (functio laesa)

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39
Q

what are the 5 R’s of inflammation?

A

recognition; recruitment; removal; regulation; resolution/repair

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40
Q

features of acute vs. chronic inflammation

A

acute: short duration, hours-days; develops w/in minutes-hours; mostly neutrophils; mild & self-limited tissue damage; HALLMARK= increased vascular permeability/leakage; innate immunity
chronic: slow onset (days); longer duration; macrophages main cell; often severe & progressive tissue injury; adaptive immunity

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41
Q

3 main processes at site of (acute) inflammation

A

1) vasodilation (brief initial vasoconstriction followed by vasodilation
2) vascular leakage & edema (increased vascular permeability)
3) leukocyte emigration to extravascular tissues

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42
Q

exudate vs. transudate

A

exudate- extravascular fluid w/ high [protein] & cellular debris; presence implies an increase in permeability of blood vessels
transudate- fluid w/ low protein content (mostly albumin), little/no cellular material, & low specific gravity; result of osmotic or hydrostatic imbalance

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43
Q

what is the hallmark of acute inflammation?

A

increased vascular permeability (vascular leakage)

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44
Q

what are 2 mechanisms for increased vascular permeability?

A 
-retraction of endothelial cells resulting in increased 
interendothelial spaces (most common mechanism); mediated by histamine, bradykinin, leukotrienes; occurs rapidly and is short-lived
-increased transport of fluids & proteins (transcytosis) through the endothelial cell; may involve intracellular channels (stimulated by VEGF)
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45
Q

steps of leukocyte recruitment to sites of inflammation

A
  • margination, rolling (selectins), & adhesion to endothelium (integrins)
  • migration across endothelium & vessel wall (CD31/PECAM)
  • migration in tissues toward chemotactic stimulus (chemotaxis; involves endogenous- IL-8, C5a, LTB4 and exogenous agents- LPS, N-formylmethionine)
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46
Q

3 steps of phagocytosis

A

1) recognition & opsonization of particle to be ingested
2) engulfment, w/ formation of phagocytic vacuole that then fuses w/ lysosomal granule (phagolysosome)
3) killing or degradation of ingested material

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47
Q

describe oxygen-dependent killing of ingested material

A

ROS are produced by assembly/activation of NADPH oxidase; ROS can act on ingested particles w/o damaging host cell; ROS converted to H2O2; H2O2 converted to hypochlorite (active ingredient in bleach) by myeloperoxidase; hypochlorite is a potent antimicrobial that destroys via halogenation or oxidation of proteins & lipids

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48
Q

what factors are involved in oxygen-independent killing of ingested material?

A

lysozyme, lactoferrin, & major basic protein

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49
Q

what is the role of NO in inflammation? what are the 3 types of NO?

A

relaxes vascular smooth muscle & promotes vasodilation; is an inhibitor of cellular component of inflammatory responses; 3 types- endothelial, neuronal, & inducible; eNOS & nNOS are constituitively expressed

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50
Q

describe characteristics of Chediak-Higashi disease

A

autosomal recessive; neutropenia w/ recurrent infections; aberrant granules in neutrophils & WBCs– giant lysosomes; giant melanosomes

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51
Q

describe characteristics of Chronic Granulomatous disease

A

X-linked recessive (mostly); recurrent infections, esp. by catalase + organisms; defect in NADPH oxidase

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52
Q

distinguish between serous & fibrinous inflammation, and ulcer

A

serous- contains low MW proteins (mainly albumin); no cells; clear yellow fluid
fibrinous- contains larger proteins (esp. fibrin); no cells; often coats a surface
ulcer- local defect of surface of organ/tissue produced by necrosis of cells and sloughing/shedding of necrotic and inflammatory tissue

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53
Q

what is a hallmark of chronic inflammation?

A

tissue destruction

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54
Q

differentiate btwn the diff types of exudate

A
  • purulent (suppurative): contain albumin, fibrin & other proteins as well as neuts (pus)
  • eosinophils: eos are prominant; typically in type 1 HSR or parasite infections
  • hemorrhagic: damage to endothelial cells & vessel walls allow RBCs to leak into surrounding tissue
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55
Q

a diffuse area of acute inflammation composed of edema fluid, bacteria, & neuts spread through tissue; typically in skin & sub-cu tissue

A

cellulitis

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56
Q

injury results in necrosis of affected tissue lining a surface; results in formation of a “membrane” composed of fluid, proteins, neuts, RBCs & necrotic tissue

A

pseudomembranous; seen in diptheria, enterocolitis

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57
Q

inflammation in tissue containing abundant mucin-secreting glands, likely to stimulate secretion

A

mucinous

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58
Q

a focus of acute inflammation composed of pyogenic exudate & necrotic tissue; can occur anywhere in body

A

abscess

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59
Q

a subcutaneous abscess

A

furuncle (boil)

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60
Q

coalesced furuncles

A

carbuncle

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61
Q

causes vasodilation, increased vascular permeability (principal mediator)

A

histamine; stored as preformed molecules in mast cells & basophils

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62
Q

what effect do cyclooxygenase inhibitors have?

A

inhibit both COX1 & COX2, inhibiting prostaglandin synthesis–treat pain & fever

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63
Q

what effect do lipoxygenase inhibitors have?

A

inhibit leukotriene production, useful in treating asthma

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64
Q

what effect do corticosteroids have?

A

broad-spectrum antiinflammatory agents; reduce transcription of genes coding for COX2, phospholipase A2, proinflammatory cytokines (TNF & IL1), & iNOS

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65
Q

what are prostaglandins (PGs)?

A

produced via COX1 & COX2; involved in pathogenesis of pain & fever in inflammation; come from mast cells, leukocytes

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66
Q

what are leukotrienes (LTs)?

A

produced by leukocytes & mast cells; involved in vascular & smooth muscle reactions and leukocyte recruitment; generated by lipoxygenase enzyme

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67
Q

what leukotrienes are responsible for vasoconstriction & bronchospasm?

A

LTC4, LTD4, LTE4

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68
Q

what leukotriene is a potent chemotactic agent & activator of neuts?

A

LTB4

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69
Q

what is platelet activating factor (PAF)?

A

phospholipid mediator generated by action of phospholipase A2; stimulates platelets, vasoconstriction, bronchoconstriction, vasodilation, increased vascular permeability; leukocyte activation

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70
Q

what are the functions of various complement proteins in inflammation?

A

C3a, C5a- anaphylatoxins; increase vascular permeability, cause vasodilation by binding mast cells & inducing histamine release
C5a- chemtactant; increases adhesiveness of neuts to endothelium; stimulates synthesis & secretion of AA metabolites
C3b, iC3b- opsonization & phagocytosis

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71
Q

what is Hageman factor?

A

protein synthesized by liver (aka clotting factor 12-inactive form); provides source of vasoactive mediators; activates prokallikrein to kallikrein, which is involved in kinin cascade

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72
Q

what is bradykinin?

A

short-lived vasoactive peptide; vasodilator, increases vascular permeability, bronchial smooth m. contraction, pain

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73
Q

what are the primary cells in acute and chronic inflammation?

A

acute- neutrophils; chronic- macrophages

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74
Q

what cytokine activates macrophages?

A

IFNy

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75
Q

what are the characteristics of granulomatous inflammation?

A

presence of granuloma; presence of macrophage, lymphocytes & epithelioid cells; presence or absence of giant cell; sometimes central necrosis

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76
Q

what are epithelioid cells?

A

activated macrophages w/ abundant cytoplasm that begin to resemble epithelial cells

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77
Q

what are giant cells?

A

fusion of activated macrophages; multinucleate cells

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78
Q

difference in foreign body giant cells & immune granulomas

A

foreign body giant cell- absence of T-cell mediated immune response; foreign material can be identified in center of granuloma
immune granuloma- caused by variety of agents capable of inducing persistent T-cell mediated immune response; produces granulomas when inciting agent is difficult to eradicate

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79
Q

difference btwn caseating & noncaseating granuloma

A
  • caseous: coagulative + liquefactive center; TB & fungal infections; granular, cheesy appearance, necrosis in center; activated macrophages have pink granular cytoplasm w/ indistinct boundaries
  • non-caseating: reaction to foreign material; talc, suture, Crohn’s disease, cat scratch disease; non-necrotic centers
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80
Q

what are major cytokines released by macrophages?

A

IL12, IL6, IL23

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81
Q

what are some non-specific indicators of inflammation?

A

“left shift” of neuts, ESR, CRP

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82
Q

when the number/percentage of immature neutrophils (bands) is increased in certain infections (esp. bacterial)

A

left-shift; a leukemoid reaction is when you have a very high WBC w/ pronounced left-shift

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83
Q

the rate at which RBCs settle to bottom of a tube; determined by amount of protein in blood, esp. fibrinogen

A

erythrocyte sedimentation rate (ESR); increased in pts undergoing inflammatory response

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84
Q

glycoprotein synthesized by liver; non-specifically elevated in pts undergoing an inflammatory response

A

C-reactive protein (CRP)

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85
Q

substances that induce fever; what are exogenous & endogenous example?

A

pyrogens; exo- LPS; endo- IL1 & TNF

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86
Q

what is the role of prostaglandins in fever?

A

COX enzymes convert AA into PGs; in the hypothalamus, PGs (esp. PGE2) stimulate production of NTs that reset the temp set point at a higher level; NSAIDs reduce fever by inhibiting PG synthesis

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87
Q

what role does IL12 have in chronic inflammation?

A

increases production of IFNy; released from macrophages and dendritic cells

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88
Q

what chemokines are involved in pain?

A

bradykinin & prostaglandins

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89
Q

which drugs can be used to treat & prevent Influenza A? MOA= prevents virus from entering host cell

A

amantadine & rimantadine

amantadine has more pronounced CNS ADR, rimantidine more likely to be safe in elderly

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90
Q

which drugs can be used to treat & prevent Influenza A AND B? MOA= inhibits neuroaminidase, which is required for release of virus from infected cell

A

osteltamivir (Tamiflu) & zanamivir; zanamir is a dry powder that must be inhaled, can cause bronchospasm

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91
Q

which viral Tx! is topical only and can be used for HSV cold sores?

A

penciclovir; MOA similar to acyclovir

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92
Q

this drug is phosphorylated to monophosphate form via HZV or VZV thymidine kinase

A

acyclovir; valacyclovir is a prodrug that converts to acyclovir via intestinal & hepatic metabolism (must be given orally); ADR= nephrotoxicity (crystal deposition in kidneys)

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93
Q

what is the DOC for viral encephalitis due to HSV?

A

IV acyclovir; can switch over to valacyclovir w/ improvement

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94
Q

what are some topical antiviral agents?

A

docosanol (Abreva), imiquimod, podofilox, podophyllin

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95
Q

what is Tx! for CMV?

A

ganciclovir & valganciclovir (prodrug); MOA similar to acyclovir; ADR= neutropenia, N/V, CNS effects; use for CMV retinitis prophylaxis & treatment

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96
Q

drug Tx! for AIDS pts w/ CMV retinitis?

A

valaganciclovir

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97
Q

prodrug used for HS/HZV infection w/ high oral bioavailability

A

famciclovir; MOA similar to acyclovir; best if started w/in 72 hours; renally excreted

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98
Q

2nd line Tx! for CMV; interacts w/ DNA pol as competitive inhibitor or alternate substrate

A

cidofovir; ADR: highly nephrotoxic–administer w/ normal saline to decrease ADR; must be administered w/ probenecid

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99
Q

2nd tier drug that competes for pyrophosphate in viral DNA pol; can be used for CMV or HSV in immunocompromised

A

foscarnet; ADR: electrolyte imbalance; seizures, EKG changes

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100
Q

topical Tx! for warts; induces local immuno-response (IFNs, TNF) to decrease viral load

A

imiquimod

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101
Q

what is Tx! for EBV?

A

rest, supportive care; no drug shortens symptoms; avoid strain if splenomegaly present

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102
Q

these drugs are CCNS; bind to guanine in DNA forming intrastrand crosslinks

A

platinum drugs (-platin ending); nephrotoxicity major ADR

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103
Q

drugs that bind tightly btwn base pairs in DNA; block activity of topoisomerase 2, & inhibit DNA repair; CCNS; can produce ROS

A

doxorubicin, daunorubicin, & related anthracyclines; unique ADR: cardiotoxicity

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104
Q

binds to DNA like doxorubicin; does not produce free radicals; lower cardiotoxicity risk

A

mitoxantrone

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105
Q

CCS drug that forms ternary complex w/ DNA topo2; kills in S & G2 phases

A

epipodophyllotoxins- etoposide & tenopside

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106
Q

CCS (S phase) inhibitors of topoisomerase 1

A

camptothecin, topotecan, & irinotecan (prodrug activated by tissue carboxyesterases)

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107
Q

drug mostly active in G2 phase; produces free radicals & breaks in DNA strand; unique toxicity of pulmonary fibrosis & pneumonitis

A

abx: bleomycins

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108
Q

CCNS drug that intercalates btwn DNA strands, preventing DNA transcription

A

dactinomycin (actinomycin D); most potent anti-tumor agent known; ADR- oral & GI ulceration, stomatitis

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109
Q

CCS (S phase) drugs that are folic acid analogs, inhibit dihydrofolate reductase

A

methotrexate, trimetrexate, pemetrexed; ADR- oral & GI ulcer, hepatotox, pulmonary tox

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110
Q

this drug is administered after MTX to minimize toxic effects of folate depletion in normal cells

A

leucovorin (citrovorum, folinic acid)

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111
Q

a pyrimidine antimetabolite that inhibits thymidylate synthase & decreases DNA synthesis; CCS at G1 & S

A

5-fluorouracil (5-FU)

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112
Q

pyrimidine antimetabolite that inhibits DNA pol alpha; CCS (S phase)

A

cytarabine

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113
Q

pyrimidine antimetabolite that inhibits DNA synthesis; CCNS

A

gemcitabine

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114
Q

purine antimetabolite that inhibits synthesis of A & G; CCS (S phase)

A

mercaptopurine (6-MP); inhibited by gout drug allopurinol

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115
Q

purine antimetabolite that inhibits synthesis of A & G; CCS (S phase)

A

thioguanine (6-TG)

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116
Q

adenosine deaminase inhibitors; decreases DNA synthesis; used in hairy cell leukemia, as well as other leukemias & lymphomas

A

pentostatin, cladribine**, & fludarabine

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117
Q

bind to soluble tubulin (key protein component of MTs), blocking polymerization & arrest cellular mitosis in metaphase (CCS- M phase)

A

vincristine, vinblastine, vinorelbine (think vines– like tubules); ADR- peripheral neuropathy, alopecia, nephrogenic SIADH secretion

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118
Q

prevent MT depolymerization by binding & stabilizing tubulin; cells arrested in late G2 or M phase (CCS- M phase)

A

paclitaxel (Taxol) & Docetaxel (Taxotere); ADR- peripheral neuropathy

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119
Q

CCNS drug that blocks hormone production by adrenal gland

A

mitotane; ADR- fatigue, nausea; also destroys healthy adrenal tissue

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120
Q

CCNS drug that inhibits tumors by regulating host immune system; also have direct activity against cancer cells

A

IFN-alpha

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121
Q

used in estrogen receptor positive breast cancer; have weak estrogen activity

A

tamoxifen, toremefine

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122
Q

part of MOPP regimen; has anti-inflammatory properties & alters immune response; cause apoptosis in certain leukemic cells

A

prednisone

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123
Q

MOA of anti-androgens & the drug names

A

bicalutamide, flutamide, nilutamide; block androgen induced growth; combined w/ leuprolide or other LH releasing hormone; combo of anti-androgen w/ leuprolide facilitates total androgen ablation

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124
Q

CTLA4 inhibitors

A

ipilimumab, tremelimumab

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125
Q

PD1 inhibitors

A

nivolumab, pembrolizumab; ADR- fatigue, skin rash

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126
Q

blocks Bcr-Abl kinase

A

imatinib

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127
Q

drug that binds & inhibits Bcl-2 (an anti-apoptotic protein)

A

venetoclax

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128
Q

HDAC inhibitors

A

vorinostat & romidepsin

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129
Q

PARP-1 inhibitor (targets DNA repair process)

A

olaparib

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130
Q

most abundant & important precursor of eicosanoids; synthesized in liver from linoleic acid

A

arachidonic acid; phospholipases release AA from membrane

131
Q

this enzyme produces prostanoids as their product from AA

A

cyclooxygenase; COX1= constitutive form, COX2= inducible form (inflammation & immune)

132
Q

this molecule is a powerful vasodilator; inhibits platelet aggregation; inhibits gastric acid secretion & increases mucus secretion; & induces pain

A

PGI2

133
Q

this molecule induces pain & fever; can contract & relax uterine smooth muscle

A

PGE2

134
Q

this molecule is a major product of COX1; stimulates platelet aggregation; amplifies signal of thrombin & ADP

A

TXA2

135
Q

this molecule is a vasoconstrictor; can terminate pregnancy; **decreases intraocular pressure–used for glaucoma

A

PGF2alpha

136
Q

drug used to reduce ulcer formation; inhibits gastric acid secretion; contraindicated in pregnancy

A

misoprostol (PGE1 analog)

137
Q

drug used for open angle glaucoma to reduce intraocular pressure

A

latanoprost (PGF2alpha analog)

138
Q

temporarily maintains patent ductus arteriosus; can be used for ED

A

alprostadil (PGE1)

139
Q

AA is converted by lipoxygenase enzyme to what molecules?

A

leukotrienes

140
Q

what is the intermediate from AA to leukotrienes?

A

5-HPETE

141
Q

what lipoxygenase products are chemotactic agents for leukocytes, eos, & monocytes?

A

5-HPETE & LTB4

142
Q

these lipoxygenase products are potent bronchoconstrictors & can increase vascular permeability

A

LTC4, LTD4, LTE4

143
Q

what drug is a 5-lipoxygenase inhibitor?

A

zileuton; prophylaxis for asthma; affect CYPs (drug-drug interactions); contraindicated in liver disease

144
Q

what drugs are competitive LTD4 receptor antagonists?

A

zafirlukast & montelukast; inhibit LT effects of bronchoconstriction & vascular permeability; used for prophylactic asthma Tx!, allergic rhinitis

145
Q

which is better, zafirlukast or montelukast, why?

A

montelukast- given once daily (instead of 2x); has less ADR & no drug-drug interactions; does not have to be taken on empty stomach; can be used in children

146
Q

drugs that inhibit cycloxygenases; are antipyretics, analgesics & anti-inflammatory

A

aspirin & tNSAIDs (propionic acid, acetic acid)

147
Q

this drugs are selective COX2 inhibitors

A

celecoxib, valdecoxib, rofecoxib

148
Q

ADRs of aspirin & tNSAIDs

A

increased risk of GI ulcers & pain; increased risk of bleeding (inhibit platelet aggregation); fluid retention (inhibit PG effects in kidney); hypersensitivity w/ aspirin; drug-drug interactions w/ ACE inhibitors, glucocorticoids & warfarin

149
Q

irreversible inhibitor of COX; acetylates serine residue on enzyme; used for antipyretic, anti-inflammatory & analgesic; prevents platelet aggregation (prolongs bleed time)

A

aspirin (acetyl salicylate); ADR- GI pain, bleeding, ulcers

150
Q

fatal, fulminating hepatitis w/ cerebral edema in children

A

Reye’s syndrome; do not use aspirin in children w/ viral infection

151
Q

characterized by tinnitis, high frequency hearing loss, HA, N, & dimness of vision; reversible

A

salicylism; mild intoxication w/ aspirin, salicylates

152
Q

competitive, reversible active site inhibitors of COX1/2; analgesic, antipyretic, anti-inflammatory; less GI problems

A

ibuprofen, naproxen

153
Q

topical opthalmic preparation used for seasonal allergy & recovery from cataract Sx!; ADR of bleeding, hepatic effects

A

ketorolac; must stop before Sx!; cannot use w/ h/o peptic ulcer or GI bleeding; do not use w/ aspirin/other NSAIDs or w/ probenecid (gout drug)

154
Q

most commonly used tNSAID in Europe; COX2 selectivity; contraindicated in pregnancy; metabolized by CYP2C9

A

diclofenac

155
Q

specific for COX1; used to close patent ductus arteriosus–decreases PGE levels; use for arthritis, tendinitis, AS

A

indomethacin; ADR= renal toxicity, must monitor levels; displaces bilirubin from albumin

156
Q

selective COX2 inhibitor; has increased risk for stroke & MI; used in arthritis, AS, primary dysmenorrhea; metabolized by CYP2C9

A

celecoxib; ADR- GI pain, nausea

157
Q

risk of using of NSAIDs during pregnancy?

A

bleeding during delivery (if used in last trimester); premature closure of PDA; inhibit uterine motility

158
Q

effect of PGs in kidney?

A

PGI2 & PGE2 increase GFR & RBF; PGE2 inhibits Cl- reabsorption in thick ascending LOH; NSAIDs lower renal PGI2 & PGE2– result in decreased RBF & GFR, increased tubular reabsorption of water

159
Q

what kidney hormones are effected by PGs?

A

PGE2 inhibits ADH effect; PGI2 & PGE2 stimulate renin release; NSAIDs lower PG levels– result in enhanced ADH effect (water retention), decreased renin lowers aldosterone and leads to decreased K+ secretion (hyperkalemia- most likely in elderly, diabetics, or other diminshed renal function)

160
Q

alternate drug in aspirin sensitive pts; not a NSAID; antipyretic & analgesic but weak anti-inflammatory; weak inhibitor of COX1/2; does not alter platelet function or uric acid levels

A

acetaminophen; ADR: #1 cause of drug induced liver failure in US; renal toxicity

161
Q

what are DMARDs?

A

disease modifying anti-rheumatic drugs; immune modulators that restore normal immune environment w/in joint synovium; slow-acting; little analgesic or anti-inflammatory effect (not COX inhibitors); slow course of disease, prevent joint damage, preserve S&F of joints; used for active RA

162
Q

what is the MOA of resistance to chloroquine?

A

polymorphisms in pfcrt gene codes for transport protein in acidic digestive vacuole membrane; resistant parasites actively transport chloroquine out of vacuole

163
Q

what is the only drug available for treating exoerythrocytic hypnozoite forms of P vivax & P ovale in the liver

A

primaquine

164
Q

what condition is primaquine contraindicated in?

A

G6PD deficiency–causes hemolysis

165
Q

quinine has this ADR

A

cinchonism- dose related, reversible; tinnitus, dec hearing, HA, N/V, visual disturbances

166
Q

this malarial drug causes vivid dreams & neuropsych symptoms; can be used for prophylaxis & Tx!

A

mefloquine

167
Q

DOC for parenteral therapy in chloroquine resistant P. falciparum where quinine not available; can cause EKG changes & hypotension

A

quinidine

168
Q

this malarial drug’s MOA is to bind & reversibly inhibit dihydrofolate reductase; which can lead to anemia due to decreased folic acid (give leucovorin)

A

pyrimethamine +/- sulfadoxazine

169
Q

this combo drug has minimal toxicity and is used for malaria chemoprophylaxis & Tx! of uncomplicated P. falciparum

A

atovaquone-proguanil (malarone)

170
Q

this malarial drug may produce toxic heme adducts & oxidant stress; not used for chemoprophylaxis; derived from plant

A

artemisinin & derivatives

171
Q

what is the most prevalent enteric parasite in the US?

A

giardia; Tx! metronidazole (most common), tinidazole or nitazoxanide

172
Q

this amebicidic agent can cause a disulfiram-like effect and should not be taken with alcohol

A

metronidazole

173
Q

what is the DOC for strongyloidiasis? what is its MOA?

A

ivermectin; GABA receptor agonist

174
Q

what drug is most commonly used for strongyloidiasis but is not DOC?

A

thiabendazole

175
Q

drug used to treat all forms of schistosomiasis

A

praziquantel

176
Q

what differences btwn fungi & mammals are exploited in creating anti-fungal drugs

A

fungi cell wall contains chitin (gives strength) & ergosterol (instead of cholesterol)

177
Q

MOA & ADR of amphotericin B

A
  • binds to ergosterol of fungal plasma membrane, forms pores; broad spectrum
  • ADR: nephrotoxicity!! (80% of people receiving drug); anemia; can cause infusion-related effect
178
Q

what is flucytosine converted to & how?

A

deaminated to 5-FU by fungus specific enzyme, cytosine deaminase; acts as antimetabolite competing w/ uracil; co-administered w/ ampho B (resistance can be problem when used alone); ADR- bone marrow hypoplasia, elevated hepatic enzymes

179
Q

MOA of azoles

A

interfere w/ fungal cyt P450 dependent enzyme used for demethylation of lanosterol & conversion to ergosterol

180
Q

what anti-fungal drug can be used in treating Cushings? why?

A

ketoconazole; azoles depress serum testosterone & adrenocorticotropic hormone (ACTH) hormones

181
Q

what is DOC for coccidioidomycosis, meningitis?

A

fluconazole due to great CSF penetration & less morbidity than intrathecal ampho B

182
Q

this anti-fungal is an echinocandin that blocks cell wall synthesis- inhibits glucan synthesis; can increased LFTs & SrCr

A

caspofungin acetate

183
Q

this anti-fungal disrupts cell mitotic spindle structure & arrests cell division in metaphase; administered orally

A

griseofulvin

184
Q

this drug inhibits squalene epoxidase

A

terbinafine

185
Q

which drug has an ADR of onychomycosis?

A

terbinafine

186
Q

what drugs are used to treat oral candidiasis (thrush)?

A

nystatin oral (swish & swallow); clotrimazole troches; ampho B suspension

187
Q

where does viral varicella zoster DNA reside?

A

dorsal root ganglia; majority are thoracic

188
Q

characteristic of varicella chickenpox lesions

A

asynchronous development of lesions (successive crops of lesions)

189
Q

what are characteristics of the varicella vaccine?

A

live attenuated (CMI & humoral immunity); must have TWO doses

190
Q

is there a zoster vaccine?

A

yes; zostavax given to 60 yo & up, one dose; shingrix-recombinant (recommended) given in 2 doses

191
Q

what syndrome can arise if pts w/ chickenpox are given aspirin?

A

Reyes syndrome; hepatic failure, encephalopathy

192
Q

what type of virus is CMV?

A

dsDNA, icosahedral capsid, enveloped; beta genus of herpetoviridae

193
Q

what is seen on microscopy that is diagnostic of CMV?

A

large “owl eye” inclusions in nucleus; enlargement of cell

194
Q

what is unique about CMV genome?

A

has dsDNA genome PLUS viral messenger RNA

195
Q

what is the most common virus caused congenital infection?

A

CMV; infects fetus in utero, mother is carrier

196
Q

what defines CMV mononucleosis?

A

heterophile negative

197
Q

how can CMV be transferred?

A

blood, breast milk, bodily secretions, sex, transfusions/transplants

198
Q

how long can one have CMV infection before CPE becomes a prominent feature?

A

four-six weeks

199
Q

what is the infectious process of CMV?

A

biological fluids are introduced into oral cavity (aerosol); an upper respiratory infection; infected lymphocytes & monocytes spread virus to secondary sites

200
Q

characteristics of picornaviridae

A

ssRNA, icosahedral, NOT enveloped; positive stranded RNA

201
Q

describe attachment & uncoating in picornavirus

A
  • attachment: lose VP4 from capsid; penetrate via endocytosis (no envelope–cannot fuse)
  • uncoating in cytoplasm (where replication occurs); remove VP1, 2, &3 to release genome
202
Q

this structure is essential for picornavirus mRNA translation

A

internal ribosome entry site (IRES)

203
Q

translation of picornavirus

A

+RNA w/o VPg (gets removed) translated to polyprotein P123, a precursor protein that is proteolytically cleaved to structural polypeptides & enzymes; cleavage products include: P1 [becomes VP1, VP3, VPo–> VP2, VP4], P2 (–> proteases), and P3 (–> VPg & 3D–RNA dependent polymerase + Hf)

204
Q

replication of picornavirus

A

+RNA w/ VPg; occurs in cytoplasm; replicative intermediate (RI) formed due to +RNA being converted to many -RNAs

205
Q

characteristics of orthomyxoviridae

A

includes influenza type A, B, C; ssRNA, negative polarity; helical nucleocapsid (must have envelope); RNA dependent RNA pol is part of nucleocapsid

206
Q

what proteins are influenza strain-specific AgS?

A

hemagglutinin & neuraminidase

207
Q

where does orthomyxoviridae replication occur?

A

nucleus

208
Q

influenza replication

A

H protein binds sialic acid containing receptors; penetrates cell via endocytic process & is enclosed in acidic vacuole, which facilitates fusion of virus envelope & vacuole membrane, releasing genome into cytoplasm; viral RNA, RNA pol complex, & assessor proteins travel to nucleus; each -RNA copied to + strand

viral RNA pol (PB1) mediated in nucleus!; - strand RNA copied into full size + RNA through formation of replicative intermediate; + RNA strand serves as template for - RNA synthesis

209
Q

influenza transcription/translation

A

viral mRNA transcribed from - strand RNA template in nucleus; viral mRNA has 3’ poly A tail added & capped RNA at 5’ end (capped RNA primer donated by cell mRNA); each mRNA leaves nucleus & is translated in assoc w/ ER or free in the cytoplasm

210
Q

what virus forms an extracellular virus via budding?

A

influenza; facilitated by H & N proteins

211
Q

____ is the major antigen for immunity in influenza

A

H (hemagglutinin); additive effect if N also changes

212
Q

antigenic ____ refers to H&N varies antigenically due to point mutations; can lead to what?

A

antigenic DRIFT; epidemics

213
Q

antigenic ____ refers to H&N varies antigenically due to gene reassortment btwn human & animal influenza virus; can lead to what?

A

antigenic SHIFT (presentation of entirely new antigens to population w/ no immunity); pandemics

214
Q

______ refers to the propensity of the body’s immune system to preferentially utilize immunological memory based on a previous infection when a second slightly different version of that foreign entity (e.g. influenza A) is encountered

A

antigenic sin

215
Q

characteristics of retroviridae

A 
complex structure (helical nucleocapsid + icosahedral, or cylindrical); 2 identical ssRNA strands joined by tRNAs-- "diploid genome"; RNA dependent- DNA pol (reverse transcriptase); enveloped
subfamilies: oncovirinae, lentivirinae, & spumavirinae
216
Q

RNA genes of retroviridae

A

GAG- Pol- Env- ONC (+/-)

217
Q

2 categories of cancers caused by retroviridae

A

chronic leukemia- lack ONC; no SRC gene
acute leukemia/sarcoma- usually lack Env (requires helper virus–supplies envelope), but have ONC; SRC or other oncogene present; exception- Rous Sarcoma has all genes

218
Q

replication of retrovirus

A
  • provirus formation takes place in cytoplasm, then transported to nucleus for integration in chromosomal DNA (mediated by integrase)
  • conversion of genomic RNA to proviral DNA produces long terminal repeats- regulate expression
219
Q

what viruses can transform cells AND produce progeny virus?

A

retroviruses; DNA tumor viruses can only do one or the other

220
Q

modes of protooncogene activation

A

normally repressed & inactive in cell DNA, must be activated….
chemical carcinogens; insertion of provirus near protooncogene (regulatory LTR); translocation of protooncogene; oncogene (provirus) in cell DNA overdose cell w/ oncogene protein

221
Q

what process changes activity of many proteins in viral cancer?

A

phosphorylation

222
Q

what is RB gene & its function?

A

tumor suppressor gene; repress proto-oncogene; requires loss of both copies; normally phosphorylated-dephosphorylated during cell cycle; DNA tumor virus products can bind Rb & alter its control of cell cycle

223
Q

passive vs. active immunotherapy

A

passive- does not rely on body to attack disease, employs immune system components created outside body; ex- administering antibodies
active- stimulates body’s own immune system to fight tumor; ex- therapeutic vaccines

224
Q

3 E phases of cancer immuno-editing

A

elimination- whether or not eliminated by host protective actions of immunity (immune system prevails)
equilibrium- maintained in dormant or equilibrium state (coexistence)
escape- escapes extrinsic tumor suppressor actions of immunity (tumor prevails, –> host death)

225
Q

from greatest to least potential for immunogenicity, rank the types of monoclonal antibodies

A

-omab (fully mouse), -ximab, -zumab, -umab (fully human)

226
Q

cytokines (IL2) promote differentiation of NK cells to what cell type capable of killing transformed & malignant cells?

A

lymphokine activated killer (LAK) cells

227
Q

what should be done in order to increase effectiveness of TIL (tumor infiltrating lymphocytes) therapy?

A

depletion of lymphocytes prior to TIL infusion

228
Q

what are two molecules that you can transfect a tumor cell with so they present antigens?

A

B7 (can activate TRA specific CD8 T cells w/ costimulatory signal), GMCSF (recruits DCs, which can present tumor antigens to T cells)

229
Q

how does anti-CTLA4 antibody work as immunotherapy?

A

CTLA4 shuts off the immune response; is present on T cell & preferentially binds B7 on APC; by blocking CTLA4, does not shutoff immune response

230
Q

what drug is anti-CTLA4 antibody?

A

ipilimumab

231
Q

what CD marker does CAR T cell therapy utilize?

A

genetically modified CD19-targeted T cell (anti-CD19 CAR T cells)

232
Q

what are ADR of CAR T cell therapy?

A

neurotoxicity, cytokine storm (monitor by IL6 levels); hypotension, hypoxia, & high-grade fevers

233
Q

difference in tumor-specific & tumor-associated antigens

A
  • tumor specific: only on tumor cells; mutated normal cellular proteins, oncogenic viral Ag
  • tumor associated: found on both tumor & normal cells; re-expressed embryonic Ags or over-expressed low abundance self-protein
234
Q

what cells are pro vs. anti-tumorigenic/cancer?

A

pro: M2 macrophages, Tregs, TH17, MDSCs
anti: DCs, M1 macrophages, CD4 & CD8 T cells

235
Q

what type of cells prevent final assembly of MAC?

A

CD59

236
Q

what 2 things do tumors rely on for success?

A

neovascularization (angiogenesis–involves VEGF) & immune evasion strategies (down-regulate MHC1 Ags, downregulate tumor assoc Ags, & release or induce release of suppressive factors–TGF beta & IL10)

237
Q

what do MDSCs in cancer secrete?

A

arginase

238
Q

what is the most common cancer in men by incidence and death?

A

incidence- prostate; death- lung & bronchus

239
Q

what is the most common cancer in women by incidence and death?

A

incidence- breast; death- lung & bronchus

240
Q

the greatest decline recently in cancer mortality has been seen in what demographic?

A

African Americans- better availability of care

241
Q

what are the hallmarks of cancer?

A

avoid apoptosis; sustain proliferative signaling; evade growth suppressors; induce angiogenesis; enable replicative immortality; activate invasion & metastasis

242
Q

what are some non-hereditary predisposing conditions to cancer?

A

chronic inflammation; immunodeficient/suppressed; age (old or really young); geography & environment; obesity

243
Q

what are the top reasons for childhood mortality?

A

1- accidents; #2- cancer

244
Q

what are the effects of radiation on cancer?

A
  • UV: UVB forms pyrimidine dimers, can overwhelm nucleotide excision repair (NER); UVC carcinogenic but filtered by ozone; increased risk of melanoma & nonmelanoma skin carcinoma
  • Ionizing Radiation: directly fracture double helix (double strand breaks), can have chromosome translocations; most sensitive tissue- hematopoietic (leukemia), breast, lung, salivary gland, thyroid (in young)
245
Q

what are some chemical carcinogens?

A

direct acting- do not require metabolic conversion (alkylating & acylating agents); indirect acting- require metabolic conversion (fossil fuels, cigarette smoke, nitrites); aflatoxin B1 from Aspergillus (mold grows on grains & nuts)

246
Q

a false, but apparent, improvement in survival caused by earlier detection of the same inexorable disease is known as what?

A

lead time bias

247
Q

what are some primary prevention strategies to cancer?

A

decrease alcohol/tobacco use; dec carcinogen exposure; dec radiation & sunlight exposure; safe sex; access to clean water & healthy food, avoid obesity; immunization & Tx! of infections

248
Q

what is an example of secondary prevention to cancer?

A

mass population & selective cancer screening

249
Q

what is the warburg effect?

A

cancer cells preferentially switch to aerobic glycolysis; generates less ATP, uses more glucose- basis for imaging scans

250
Q

what are some lab diagnoses of cancer?

A

histology (biopsy/excision, frozen section)
cytology (fine needle aspirate, pap smear, body fluids; immunohistochemistry (stain specific antigens in a cell); electron microscopy;
flow cytometry (count individual cells & characterize); tumor markers (sample blood for byproducts of cancer; better used for monitoring Tx! effect);
molecular diagnostic tests (can detect characteristic translocations & mutations);
microarrays (molecular bio w/ microchip manufacture; can detect methylation & other DNA epigenetic modifications);
genetic (susceptibility) markers of cancer- identify specific genes/loci

251
Q

proliferation of cells w/in organ/tissue

A

hyperplasia

252
Q

substitution of one type of adult tissue for another when under stress

A

metaplasia

253
Q

abnormality in cell size, appearance, w/ or w/o disorganized growth pattern

A

dysplasia

254
Q

benign or malignant tumor growth; disease of cells characterized by alteration of normal growth regulatory mechanisms

A

neoplasia

255
Q

general types of benign tumors

A

adenoma- epithelial; lipoma- mesenchymal

256
Q

general types of malignant tumors

A

carcinoma- epithelial; sarcoma- mesenchymal; lymphoma/leukemia- neoplasm of lymphoid cells

257
Q

types of DNA repair systems that can be defective in some cancer types

A

mismatch repair (HNPCC); nucleotide excision (XP); recombination repair (AT, bloom syndrome, Fanconi anemia)

258
Q

growth-promoting genes that result in gain of function in protein product

A

oncogenes; work via overactivity mutation

259
Q

growth inhibiting genes which result in loss of function

A

tumor suppressor genes; genes involved in apoptosis & DNA repair; ex- p53; work via underactivity mutation

260
Q

normal human gene that can become an oncogene due to mutations or increased expression

A

proto-oncogene

261
Q

what is the two-hit hypothesis?

A

normal cells have 2 undamaged chromosomes; it takes 2 hits in the same cell to cause cancer; people w/ hereditary susceptibility to cancer inherit a damaged chromosome, w/ the 1st hit at conception

262
Q

explain RAS as an oncogene

A

normal cells- RAS protein regulated by GAP; RAS mutations reduce GTPase activity on RAS, allowing it to remain active all the time, stimulating cell growth continuously

263
Q

what is the Bcr-Abl translocation?

A

“Philadelphia chromosome;” chrom 9 & 22 translocate, creating fusion gene that encodes active tyrosine kinase that is continuously active & results in unregulated cell division

264
Q

what “Guardian” tumor suppressor gene that is a transcription factor is mutated in over 50% of human tumors?

A

p53

265
Q

what anti-apoptotic protein is overexpressed in some cancers?

A

Bcl-2

266
Q

cancers may have unlimited replicative potential do to upregulation of what enzyme?

A

telomerase

267
Q

pro-angiongenic cytokines ____ & ____ promote angiogenesis

A

VEGF & bFGF

268
Q

what hallmarks of cancer are universal & specific to solid tumors?

A

universal: uncontrolled proliferation; immortalization; protection from antiproliferative signaling; protection from apoptosis
solid tumors: angiogenesis; invasion & metastasis; occurs in later stage tumors

269
Q

true or false- a tumor has a single-cell origin & thus the entire tumor always consists of a single type of isozyme for gene

A

true

270
Q

what leads to proto-oncogene conversion to oncogene

A

mostly gain of function; increased expression, or loss of protein regulation w/ increased activity

271
Q

compare/contrast familial vs sporadic retinoblastoma

A

familial- autosomal dom Mendelian transmission through germline; multiple tumors, often bilateral, early onset
sporadic- 60% of cases; not transmitted to progeny; single tumor; unilateral; later onset

272
Q

what is the major determining factor of cancers?

A

how many times the stem cell divides

273
Q

what are the various forms of hereditary colorectal syndromes?

A
  • familial adenomatous polyposis (FAP)- germline mutation in APC, most common form; autosomal dom
  • juvenile polyposis (JP)- autosomal dom; usually asymptomatic until puberty; less numerous polyps
  • HNPCC- gene mutation in tumor suppressors in DNA mismatch repair; hereditary nonpolyposis
274
Q

what are causes of chromosomal instability?

A

telomere attrition, aneuploidy, hypomethylation, double strand breaks, cellular stress (hypoxia, pH, high osmolarity), VDJ errors;
-mutations in genes for DNA replication, chromosome segregation, cell cycle check pts, & nucleotide metabolism

275
Q

explain role of methylation in cancer

A

hypermethylation of tumor suppressors silences gene; oncogenes activated by hypomethylation; strongest risk factor for hypomethylation is age

276
Q

etiology of glioblastoma

A

most common brain malignancy, one of most aggressive human cancers;
primary- manifests rapidly de novo w/o recognizable precursor lesions, more common (80%); rapid progression; more so in elderly; short survival time
-secondary: evolves from lower-grade gliomas, typically in younger pts

277
Q

what is the basis for personalized medicine?

A

people respond differently to Tx! based on environment (exposure to carcinogens) & genetics (such as ability to deal w/ carcinogens)

278
Q

Mendelian monogenic disorders vs. polygenic

A

monogenic- result from variation in single genes; phenotype driven by single genetic mutation; most individuals who possess mutant gene will exhibit the disease
complex- arise from interactions of several diff genes; each mutation contributes to risk of acquiring disease phenotype; % of risk due to any gene varies

279
Q

parasites assoc w/ Loeffler’s syndrome

A

Ascaris, hookworm, strongyloides (threadworm)

280
Q

parasite assoc w/ autoinfection

A

pinworm, strongyloides

281
Q

parasite assoc w/ anemia; can cause cutaneous larva migrans

A

hookworm

282
Q

parasite assoc w/ hyperinfection w/ immunosuppression (gram negative sepsis)

A

strongyloides

283
Q

parasite assoc w/ rectal prolapse

A

Trichuris trichiura (whipworm)

284
Q

parasite assoc w/ eosinophilic meningitis

A

raccoon ascarid (roundworm); angiostrongylus cantonensis

285
Q

parasite assoc w/ humans as aberrant/accidental host

A

CLM-cutaneous larva migrans, VLM-visceral larva migrans (toxocariasis), angiostrongyliasis

286
Q

parasite assoc w/ skin eruption

A

CLM (slow), larva currens/strongyloides (fast)

287
Q

parasite assoc w/ wild animal consumption

A

trichinella (esp pork consumption); has intestinal & muscle stage

288
Q

most common helminth infection

A

Ascaris lumbricoides (roundworm); largest intestinal helminth

289
Q

what helminth can have aberrant migration to appendix, bile duct, or pancreatic duct due to high fever or anesthesia?

A

ascaris lumbricoides

290
Q

larva currens is a pathognomonnic rash around buttocks/groin caused by what organism?

A

strongyloides

291
Q

what helminth can cause blindness, asthma-like attacks, urticarial rashes, N/V, etc.

A

toxocariasis; Toxocara canis or cati

292
Q

this roundworm found in raccoons can cause ocular, visceral, or neural larva migrans; also can cause deadly eosinophilic meningitis

A

Baylisacaris procyonis

293
Q

the Scotch tape test is used to diagnose this worm; causes intense anal itching, esp @ night

A

Enterobius vermicularis (pinworm)

294
Q

nematode only found in Phillipines; can cause severe diarrhea, protein loss, & death from heart failure

A

Capillariasis phillippinensis

295
Q

what are the stages of trichinella?

A

1) intestinal (1-7 days) 2) muscle invasion (1-8 wks) 3) myocardial involvement (1-2 mos)

296
Q

most common cause of human eosinophilic meningitis

A

Angiostrongylus cantonensis (rat lungworm)

297
Q

transmitted by direct skin-skin contact, fabrics, or sexual contact; caused by mite; severe form in immunocompromised

A

Scabies; severe form- Scabies Crustosa; do not treat w/o diagnosis; treat whole family

298
Q

cause itchy scalp; can be visualized

A

head louse (Pediculus humanus)

299
Q

vector of louse-borne typhus, trench fever, & relapsing fever; more common in colder regions, overcrowding, wars, famine, natural disasters

A

body louse (Pediculus humanus corporis)

300
Q

sexually transmitted; “moving freckles”; directly visualize

A

crab louse (Phthirus pubis)

301
Q

treatment for louse

A

permethrin, malathion

302
Q

nocturnal creatures; can transmit disease; difficult to control infestations

A

bed bugs (Cimex lectularius)

303
Q

cause of tungiasis (inflammatory skin condition); native to central/south america

A

jigger fleas

304
Q

what is an infection by larva of “higher flies?”

A

myiasis; tumbu & mango fly only in Africa; human botfly in Latin America

305
Q

unwarranted belief that pt is infested w/ live organisms or that inanimate objects are coming from their skin

A

delusional parasitosis; a diagnosis of exclusion–must rule out other diseases

306
Q

cause of Chaga’s disease; buzzword= CHF in Central/Latin American; can be transmitted congenitally

A

American Trypanosomiasis; vector= reduviid “kissing” bug

307
Q

disease w/ characteristic Romana’s sign & chagoma

A

Chagas

308
Q

Tx! for Chagas

A

benznidazole; nifurtimox

309
Q

cause of African sleeping sickness

A

African Trypanosomiasis; vector= tsetse fly; T. brucei gambiense (chronic) & T. b. rhodesiense (rapidly fatal, can cross BBB);

310
Q

invasion of lymph nodes (Winterbottom sign) classic sign for what disease?

A

African trypanosomiasis

311
Q

disease whose vector is sand fly; has 3 types of disease

A

leishmaniasis

312
Q

describe 3 types of leishmaniasis

A

cutaneous- painless ulcer formation; diagnosis= travel history, amastigotes in smear or biopsy
mucocutaneous- “espundia”; untreated primary skin lesions can progress over years
visceral- can cause Kala-azar (black fever); hepatosplenomegaly, anemia (greying of skin); post-kala azar dermatitis (rash)

313
Q

rapidly fatal, pts w/ freshwater exposure; causes primary amebic meningoencephalitis (PAM)

A

Naegleria fowleri

314
Q

causes granulomatous amebic encephalitis; inhaled cysts or direct skin contact; brain abscesses, skin & nasal lesions, fever, HA/N/V

A

Balamuthia mandrillaris

315
Q

inhibited by temps greater than 35C; also causes granulomatous amebic encephalitis; can cause keratitis due to corneal trauma/exposure

A

Acanthamoeba

316
Q

found worldwide in soil/animal feces; causes encephalitis, sinusitis

A

Sappinia

317
Q

intracellular parasite; vector is Ixodes tick; cause flu like symptoms; may develop hemolytic anemia

A

Babesiosis (Babesia macroti)

318
Q

what are the 2 plasmodium hosts?

A

humans & female anopheles mosquito

319
Q

what is plasmodium life cycle?

A

sporozoite- from mosquito, infects liver cells –> schizont- asymptomatic, ruptures & releases–> merozoites- infects RBCs, symptomatic–> ring stage trophozoite- asexual reproduction, release more merozoites or gametocytes–> gametocytes- sexual erythrocytic stage, taken up my mosquito

320
Q

this is dormant in liver in P vivax & ovale for weeks to months after primary infections

A

hypnozoite

321
Q

characterized by HA, chills, cyclical fever, travel history, anemia

A

malaria

322
Q

what is the cause of cerebral malaria?

A

P. falciparum; poor prognosis; crosses BBB; obstructs brain vessels

323
Q

protective factors against malaria

A

sickle cell trait; duffy antigen-negative blood type; immunity (repeat infections)

POD (2 decks)

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