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Test reviews DEDICATED > Wed jul 29 > Flashcards

Wed jul 29 Flashcards

1
Q

what is a cavernous hemangioma?

A

vascular malformation most commonly in the brain parenchyma - consists of dilated thin walled capillaries

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2
Q

presentation of a cavernous hemangioma?

A

may have seizures and neurologic symptoms due to mass effect. May also result in a bleed

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3
Q

where would the hemorhage from a cavernous hemangioma be?

A

intraCEREBRAL area

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4
Q

do the melanocytes in a junctional nevus go into the dermis?

A

no

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5
Q

presentation of junctional nevus?

A

flat, pigmented macule

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6
Q

do the melanocytes of a compound nevus extend into the dermis?

A

yes

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7
Q

presentatino of compound nevus?

A

raised papule, pigmented

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8
Q

presention of intradermal nevi?

A

raised, skin to tan coloured, dome shaped moles

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9
Q

where does the maxillary branch of CN V exits the skull?

A

infraorbital foramen

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10
Q

where does the opthalmic branch of CN V exits the skull?

A

supraorbital foramen

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11
Q

how is neurocysticercosis spread?

A

ingestion of eggs from stool of carriers (can be from eating pork)

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12
Q

where is HIV-2 found?

A

west africa

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13
Q

waht is the asymptomatic period of HIV2?

A

10-25 years

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14
Q

HIV2 is intrinsically resistance to which drugs?

A

NNRTIs and fusion inhibitors

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15
Q

what is modafinil?

A

stimulant used to treat narcolepsy

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16
Q

what happens to pyruvate under hypoxic conditions?

A

instead of being converted to acetylcoa for TCA cycle, it is converted to lactate by lactate dehydrogenase leading to lactic acidosis

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17
Q

what substances inhibits pyruvate dehydrogenase under hypoxic conditions?

A

NADH

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18
Q

phenylalanine is converetd into what, by phenylalanine hydroxylase?

A

tyrosine

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19
Q

what is the precursor substance to DOPA?

A

tyrosine

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20
Q

what will be seen grossly in the brain of someone with PKU?

A

hypopigmentation of catecholaminergic nuclei

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21
Q

I cell disease has a lack of what?

A

mannose-6-phosphate

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22
Q

The lack of mannose-6-phosphate in I cell disease results in what?

A

lysosomal enzymes secreted extracellularly instead of being delivered to lysosomes

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23
Q

pathophys of I cell disease?

A

lysosomal enzymes secreted extracellularly -> enzymes in blood can lead to tissue damage, and the substances that would have been broken down in lysosomes accumulate intracellularly

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24
Q

clinical manifestations of i cell disease?

A

claw hand deformity, joint stiffness, kyphoscoliosis, clouded cornea, coarse facies, gingival hyperplasia

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25
Q

enterobius vermicularis AKA

A

pinworm

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26
Q

enterobius vermicularis presentation

A

itchy anus at night time

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27
Q

where are eggs found in enterobius vermicularis ?

A

eggs are laid around anus

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28
Q

transmission of enterobius vermicularis ?

A

fecal oral route

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29
Q

who is typically affected by enterobius vermicularis ?

A

children

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30
Q

diagnosis of enterobius vermicularis ?

A

scotch tape test- will see eggs

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31
Q

treatment of enterobius vermicularis

A

pyrantal pamoate OR albendozale

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32
Q

ancyclostoma duodenale and necator americanus are what type of worms?

A

hookworms

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33
Q

where are ancyclostoma duodenale and necator americanus found?

A

southern USA

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34
Q

transmission of ancyclostoma duodenale and necator americanus?

A

penetrate skin, move to lungs, get coughed up and get into intestine

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35
Q

ancyclostoma duodenale and necator americanus may lead to what complication?

A

iron deficiency anemia

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36
Q

diagnosis of ancyclostoma duodenale and necator americanus?

A

eggs in stool, high eosinophil count

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37
Q

treatment of ancyclostoma duodenale and necator americanus?

A

pyrantel pamoate or albendazole and WEAR SHOES

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38
Q

transmission of ascaris lumbricoides?

A

eating eggs in contaminated food/water, then eggs hatch in intestine and largva crawl through wall into blood, go to lungs, swallowed and go back down into intestine and repeat

39
Q

what type of worm is ascaris lumbricoides?

A

giant roundworm

40
Q

presentation of ascaris lumbricoides?

A

asymptomatic, or may present with respiratory symptoms or malnutrition, or intestinal obstruction at ileocecal valve

41
Q

diagnosis of ascaris lumbricoides?

A

eggs in feces and eosinophilia

42
Q

treatment of ascaris lumbricoides?

A

albendazole

43
Q

strongyloides stercoralis tranmission?

A
  • penetrate skin and travel in blood to lungs, gets swallowed and mature in GI tract
  • may autoinfect its host by laying eggs in intestine wall
44
Q

diagnosis of strongyloides stercoralis

A

NO EGGS IN stool. Will find LARVAE in stool

45
Q

what will be found in the stool of an infection with strongyloides stercoralis?

A

larvae

46
Q

treatment of strongyloides stercoralis

A

ivermectan or albendazole

47
Q

trichinella spiralis presentation?

A

fever, vomiting, periorbital edema, myalgia

48
Q

transmission of trichinella spiralis?

A

undercooked meat such as pork or bear

49
Q

what type of worm is trichinella spiralis?

A

nematode

50
Q

trichinella spiralis leads to inflammation where?

A

striated muscle

51
Q

dracula medinensis transmission?

A

water contanimated with copepods containing larvae

52
Q

presenation of dracula medinensis?

A

adult female migrates to skin and forms painful skin ulcer

53
Q

treatment of dracula medinensis?

A

slowly pull worm out

54
Q

onchocerca volvulus transmission?

A

black fly bites host, and large go into skin and mature and the microfliaria migrate throughout body

55
Q

presentation of onchocerca volvulus

A

hyper or hypopigmentated spots on skin. may go into eye and cause blindness - liver blindness

56
Q

dx of onchocerca volvulus

A

microfilariea seen on skin biopsy

57
Q

treatment of onchocerca volvulus

A

ivermectan

58
Q

wucheraria bancrofti presentation?

A

elephantiasis and cough

59
Q

intermediate host of wucheraria bancrofti

A

mosquito

60
Q

dx of wucheraria bancrofti ?

A

thick blood smear

61
Q

treatment of wucheraria bancrofti

A

diethylcarbamozine

62
Q

toxicara canis complication?

A

blindness

63
Q

treatment of toxicara canis?

A

albendozale

64
Q

loa loa presentation?

A

transient angioedema, calibar swellings, and worm across eye

65
Q

loa loa transmission?

A

deer fly

66
Q

loa loa treatment?

A

diethylcarbamazine or albendazole

67
Q

ecg findings of wolf parkinson white?

A

shortened PR interval, early upslope of QRS (delta wave), widened QRS

68
Q

filtration fraction formula

A

GFR/RPF

69
Q

presentation of IPEX

A

immunodeficiency with recurrent infections, autoimmune enteropathy, endocrinopathy and dermatitis

70
Q

MHC II structure?

A

alpha and beta polypeptide chains

71
Q

what drugs are class IB antiarythmics?

A

Lidocaine, mexiletine

72
Q

what drugs are class IC antiarythmics?

A

flecainide, propafenone

73
Q

what drugs are class IA antiarythmics?

A

procainamide, quinidine, disopyramide

74
Q

what subtype of class I antiarthymics has the greatest Na binding affinity?

A

IC

75
Q

what subtype of class I antiarthymics has the lowest Na binding affinity?

A

IB

76
Q

what subtype of class I antiarthymics has has an intermediate Na binding affinity?

A

IA

77
Q

chronic granulomatous disease has what deficiency?

A

NADPH oxidase

78
Q

function of NADPH oxidase?

A

uses oxygen to make superoxide free radicals to kill pathogens in respiratory burst

79
Q

patients with CPG are susceptible to which type of organism?

A

catalase positive

80
Q

staph aureus, e coli, b cepacia and aspergillos are cat + or -?

A

+

81
Q

what happens when someone with CGD is infected wiht a catalase + organism?

A

the organism uses catalase to break down ROS before the host immune system can use it –they can survive and cause severe infections

82
Q

most common infection in CGD?

A

staph aureus

83
Q

inheritance of CGD?

A

x linked recessive

84
Q

what is a dihydrorhodamine test?

A
  • used to diagnose CGD
  • there will be no flurescence due to decreased superoxide and hydrogen peroxide which would oxidize a substance to be fluorescent
85
Q

what is the nitroblue tetrazoleum test?

A

-nitroblue turns from yellow to blue in the presence of ROS. In CGD, it stays yellow

86
Q

inheritance of IPEX?

A

x linked

87
Q

mutation in IPEX?

A

loss of function of FOXP3, resulting in impaired development and function of regulatory t cells

88
Q

presentation of IPEX

A

immunodeficiency with recurrent infections, autoimmune enteropathy, endocrinopathy and dermatitis

89
Q

common skin findings of IPEX

A

eczema

90
Q

GI presentation of IPEX?

A

autoimmune damage to enterocytes leads to chronic diarrhea

91
Q

common endocrine pathologies of IPEX?

A

diabetes and thyroiditis

92
Q

wiskott-aldrich syndrome inheritance?

A

x linked

93
Q

wiskott-aldrich syndrome - which gene is mutated?

A

WAS - leads to problems with cytoskeleton - defective t cell signalling and interactions with APCs - impairs chemotaxis and phagocytosis

94
Q

presentation of wiskott-aldrich syndrome?

A

recurrent pyogenic infections, eczema, thrombocytopenia

Test reviews DEDICATED (70 decks)

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