Wed jul 29 Flashcards

(94 cards)

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
enterobius vermicularis AKA
pinworm
26
enterobius vermicularis presentation
itchy anus at night time
27
where are eggs found in enterobius vermicularis ?
eggs are laid around anus
28
transmission of enterobius vermicularis ?
fecal oral route
29
who is typically affected by enterobius vermicularis ?
children
30
diagnosis of enterobius vermicularis ?
scotch tape test- will see eggs
31
treatment of enterobius vermicularis
pyrantal pamoate OR albendozale
32
ancyclostoma duodenale and necator americanus are what type of worms?
hookworms
33
where are ancyclostoma duodenale and necator americanus found?
southern USA
34
transmission of ancyclostoma duodenale and necator americanus?
penetrate skin, move to lungs, get coughed up and get into intestine
35
ancyclostoma duodenale and necator americanus may lead to what complication?
iron deficiency anemia
36
diagnosis of ancyclostoma duodenale and necator americanus?
eggs in stool, high eosinophil count
37
treatment of ancyclostoma duodenale and necator americanus?
pyrantel pamoate or albendazole and WEAR SHOES
38
transmission of ascaris lumbricoides?
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
what type of worm is ascaris lumbricoides?
giant roundworm
40
presentation of ascaris lumbricoides?
asymptomatic, or may present with respiratory symptoms or malnutrition, or intestinal obstruction at ileocecal valve
41
diagnosis of ascaris lumbricoides?
eggs in feces and eosinophilia
42
treatment of ascaris lumbricoides?
albendazole
43
strongyloides stercoralis tranmission?
- 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
diagnosis of strongyloides stercoralis
NO EGGS IN stool. Will find LARVAE in stool
45
what will be found in the stool of an infection with strongyloides stercoralis?
larvae
46
treatment of strongyloides stercoralis
ivermectan or albendazole
47
trichinella spiralis presentation?
fever, vomiting, periorbital edema, myalgia
48
transmission of trichinella spiralis?
undercooked meat such as pork or bear
49
what type of worm is trichinella spiralis?
nematode
50
trichinella spiralis leads to inflammation where?
striated muscle
51
dracula medinensis transmission?
water contanimated with copepods containing larvae
52
presenation of dracula medinensis?
adult female migrates to skin and forms painful skin ulcer
53
treatment of dracula medinensis?
slowly pull worm out
54
onchocerca volvulus transmission?
black fly bites host, and large go into skin and mature and the microfliaria migrate throughout body
55
presentation of onchocerca volvulus
hyper or hypopigmentated spots on skin. may go into eye and cause blindness - liver blindness
56
dx of onchocerca volvulus
microfilariea seen on skin biopsy
57
treatment of onchocerca volvulus
ivermectan
58
wucheraria bancrofti presentation?
elephantiasis and cough
59
intermediate host of wucheraria bancrofti
mosquito
60
dx of wucheraria bancrofti ?
thick blood smear
61
treatment of wucheraria bancrofti
diethylcarbamozine
62
toxicara canis complication?
blindness
63
treatment of toxicara canis?
albendozale
64
loa loa presentation?
transient angioedema, calibar swellings, and worm across eye
65
loa loa transmission?
deer fly
66
loa loa treatment?
diethylcarbamazine or albendazole
67
ecg findings of wolf parkinson white?
shortened PR interval, early upslope of QRS (delta wave), widened QRS
68
filtration fraction formula
GFR/RPF
69
presentation of IPEX
immunodeficiency with recurrent infections, autoimmune enteropathy, endocrinopathy and dermatitis
70
MHC II structure?
alpha and beta polypeptide chains
71
what drugs are class IB antiarythmics?
Lidocaine, mexiletine
72
what drugs are class IC antiarythmics?
flecainide, propafenone
73
what drugs are class IA antiarythmics?
procainamide, quinidine, disopyramide
74
what subtype of class I antiarthymics has the greatest Na binding affinity?
IC
75
what subtype of class I antiarthymics has the lowest Na binding affinity?
IB
76
what subtype of class I antiarthymics has has an intermediate Na binding affinity?
IA
77
chronic granulomatous disease has what deficiency?
NADPH oxidase
78
function of NADPH oxidase?
uses oxygen to make superoxide free radicals to kill pathogens in respiratory burst
79
patients with CPG are susceptible to which type of organism?
catalase positive
80
staph aureus, e coli, b cepacia and aspergillos are cat + or -?
+
81
what happens when someone with CGD is infected wiht a catalase + organism?
the organism uses catalase to break down ROS before the host immune system can use it --they can survive and cause severe infections
82
most common infection in CGD?
staph aureus
83
inheritance of CGD?
x linked recessive
84
what is a dihydrorhodamine test?
- 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
what is the nitroblue tetrazoleum test?
-nitroblue turns from yellow to blue in the presence of ROS. In CGD, it stays yellow
86
inheritance of IPEX?
x linked
87
mutation in IPEX?
loss of function of FOXP3, resulting in impaired development and function of regulatory t cells
88
presentation of IPEX
immunodeficiency with recurrent infections, autoimmune enteropathy, endocrinopathy and dermatitis
89
common skin findings of IPEX
eczema
90
GI presentation of IPEX?
autoimmune damage to enterocytes leads to chronic diarrhea
91
common endocrine pathologies of IPEX?
diabetes and thyroiditis
92
wiskott-aldrich syndrome inheritance?
x linked
93
wiskott-aldrich syndrome - which gene is mutated?
WAS - leads to problems with cytoskeleton - defective t cell signalling and interactions with APCs - impairs chemotaxis and phagocytosis
94
presentation of wiskott-aldrich syndrome?
recurrent pyogenic infections, eczema, thrombocytopenia