Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
83 Cards in this Set
- Front
- Back
cns hamartomas
|
tuberous sclerosis (adenumsabacum, seizures, MR and cardiac rhabdomyomas)
|
|
rhabdomyomas generaaly produce
|
stenosis
|
|
a dominant cardiaxc effect of catch22
|
tetrology of fallot
|
|
initial loss of proprioception then cardiac hypertrophy
|
friedrichs ataxia
|
|
ostium primum ASD
|
DOwns
|
|
the superior thyroid artery vein and what nerve course together
|
the superior laryngeal nerve which innervates only one muscle the Cricothyroid
|
|
the superior laryngeal nerve innervates only one muscle and is at risk to be cut during a thyroidectomy because it courses with the superior thyroid artery and vein what is the only muscle it innervates
|
cricothyroid
|
|
sensory innervation to the larynx and all the muscles of the larynx other than cricothyroid
|
recurrent laryngeal nerve
|
|
sesnsorry above the vocal folds
|
sln, below rln
|
|
ruptured LV typically occurs within how many days after an infarct
|
3-7
|
|
ruptured LV typically occurs within how many days after an infarct
|
3-7
|
|
ruptured LV typically occurs within how many days after an infarct
|
3-7
|
|
ruptured LV typically occurs within how many days after an infarct
|
3-7
|
|
ruptured LV typically occurs within how many days after an infarct
|
3-7
|
|
how would one present if they had a ruptured ventricle 3-7 days post infarct
|
muffled heart sounds, JVP elevatoion and profound hypotension
|
|
high levels of aflatoxin cause by specific aspergllus cause what mutations resulting in liver cancer
|
p53
|
|
glucagon PTH and TSH have what inn common
|
they stimulate Gs AC cAMP proteins
|
|
PKA phosphorylates what
|
threonine and serine residues
|
|
hemoglobin Barts
|
found in alpha thal homos it has only gamma chains which normally with alpha from HbF but without form BArt Hb Bart has such a high effinity for 02 that it dont release it to the tissues
|
|
inherited def. of alpha galactosidase A
|
fabries increased ceramide trihexoside
acroparesthesia - episodic burning neuropathic pain angiokeratomas - punctate, dark red, nonblacnhing papules between the umbilicus and the knees progressive renal insuff. |
|
inherited def. of alpha galactosidase A
|
fabries increased ceramide trihexoside
acroparesthesia - episodic burning neuropathic pain angiokeratomas - punctate, dark red, nonblacnhing papules between the umbilicus and the knees progressive renal insuff. |
|
inherited def. of alpha galactosidase A
|
fabries increased ceramide trihexoside
acroparesthesia - episodic burning neuropathic pain angiokeratomas - punctate, dark red, nonblacnhing papules between the umbilicus and the knees progressive renal insuff. |
|
inherited def. of alpha galactosidase A
|
fabries increased ceramide trihexoside
acroparesthesia - episodic burning neuropathic pain angiokeratomas - punctate, dark red, nonblacnhing papules between the umbilicus and the knees progressive renal insuff. |
|
inherited def. of alpha galactosidase A
|
fabries increased ceramide trihexoside
acroparesthesia - episodic burning neuropathic pain angiokeratomas - punctate, dark red, nonblacnhing papules between the umbilicus and the knees progressive renal insuff. |
|
hypohidrosis too
|
fbries
|
|
hypohidrosis too
|
fbries
|
|
class 3 agents (sotolol is one too) are notorious for
|
prolonging the qt
|
|
class 3 agents (sotolol is one too) are notorious for
|
prolonging the qt
|
|
class 3 agents (sotolol is one too) are notorious for
|
prolonging the qt
|
|
class 3 agents (sotolol is one too) are notorious for
|
prolonging the qt
|
|
class 3 agents (sotolol is one too) are notorious for
|
prolonging the qt
|
|
slow AV nodal conduction as well as phase 4
|
beta B
|
|
slow AV nodal conduction as well as phase 4
|
beta B
|
|
slow AV nodal conduction as well as phase 4
|
beta B
|
|
slow AV nodal conduction as well as phase 4
|
beta B
|
|
slow AV nodal conduction as well as phase 4
|
beta B
|
|
beta B
|
slow AV nodal conduction as well as phase 4
|
|
beta B
|
slow AV nodal conduction as well as phase 4
|
|
beta B
|
slow AV nodal conduction as well as phase 4
|
|
beta B
|
slow AV nodal conduction as well as phase 4
|
|
beta B
|
slow AV nodal conduction as well as phase 4
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
as calcium channel blockers these meds will
|
slow the phase zero depolarization of cardiac pacemaker cells and phase 2 of the myocyte action potential neither of which will change the QT interval
|
|
when someon is diagnosed with Small cell carcinoma
|
he probably has distant mets at the time of diagnosis
|
|
vimentin is an intermediate filament found within cells of mesenchymal orgin used in the diagnois of
|
sarcomas
|
|
patients with adult type coarctation of the aorta commonly die of
|
HTN asociated complications, including LVF, ruptured dissecting aortic aneurysm, and intracranial hemorrhage, these patients are at an increased risk for ruptured intracranial aneurysms because of the increased incidence of congenitalberry aneurysms
|
|
patients with adult type coarctation of the aorta commonly die of
|
HTN asociated complications, including LVF, ruptured dissecting aortic aneurysm, and intracranial hemorrhage, these patients are at an increased risk for ruptured intracranial aneurysms because of the increased incidence of congenitalberry aneurysms
|
|
patients with adult type coarctation of the aorta commonly die of
|
HTN asociated complications, including LVF, ruptured dissecting aortic aneurysm, and intracranial hemorrhage, these patients are at an increased risk for ruptured intracranial aneurysms because of the increased incidence of congenitalberry aneurysms
|
|
patients with adult type coarctation of the aorta commonly die of
|
HTN asociated complications, including LVF, ruptured dissecting aortic aneurysm, and intracranial hemorrhage, these patients are at an increased risk for ruptured intracranial aneurysms because of the increased incidence of congenitalberry aneurysms
|
|
patients with adult type coarctation of the aorta commonly die of
|
HTN asociated complications, including LVF, ruptured dissecting aortic aneurysm, and intracranial hemorrhage, these patients are at an increased risk for ruptured intracranial aneurysms because of the increased incidence of congenitalberry aneurysms
|
|
patients with adult type coarctation of the aorta commonly die of
|
HTN asociated complications, including LVF, ruptured dissecting aortic aneurysm, and intracranial hemorrhage, these patients are at an increased risk for ruptured intracranial aneurysms because of the increased incidence of congenitalberry aneurysms
|
|
acyclovir has decreased activity against
|
ebv and cmv because they do not produce the same thymidine kinase that HSV and VZV do to phosphorylatee this guanosine analog
|
|
the edema of urticaria is located where?
|
the dermis
|
|
aconthosis is thickening of the epidermis seen in psoriasis seen specifically in what
|
spongiosa
|
|
aconthosis is thickening of the epidermis seen in psoriasis seen specifically in what
|
spongiosa
|
|
aconthosis is thickening of the epidermis seen in psoriasis seen specifically in what
|
spongiosa
|
|
aconthosis is thickening of the epidermis seen in psoriasis seen specifically in what
|
spongiosa
|
|
aconthosis is thickening of the epidermis seen in psoriasis seen specifically in what
|
spongiosa
|
|
aconthosis is thickening of the epidermis seen in psoriasis seen specifically in what
|
spongiosa
|
|
atherosclerotic plaques develop predomintly in
|
large elastic arteries
in humans it is most prevalent in the abdominal aorta around the ostia of major arterial branches |
|
atherosclerotic plaques develop predomintly in
|
large elastic arteries
in humans it is most prevalent in the abdominal aorta around the ostia of major arterial branches |
|
atherosclerotic plaques develop predomintly in
|
large elastic arteries
in humans it is most prevalent in the abdominal aorta around the ostia of major arterial branches |
|
atherosclerotic plaques develop predomintly in
|
large elastic arteries
in humans it is most prevalent in the abdominal aorta around the ostia of major arterial branches |
|
atherosclerotic plaques develop predomintly in
|
large elastic arteries
in humans it is most prevalent in the abdominal aorta around the ostia of major arterial branches |
|
tuberculoid leprosy
|
strong CMI
|
|
foscarnet does not have to be activated intracellularly ad can actually inhibit
|
HIV rt, and DNA polymerase of HSV
|
|
blocks the M2 ion channel protein of Flu A preventing uncoating after host cell endocytosis
|
amantadine
|
|
blocks the M2 ion channel protein of Flu A preventing uncoating after host cell endocytosis
|
amantadine
|
|
blocks the M2 ion channel protein of Flu A preventing uncoating after host cell endocytosis
|
amantadine
|
|
blocks the M2 ion channel protein of Flu A preventing uncoating after host cell endocytosis
|
amantadine
|
|
blocks the M2 ion channel protein of Flu A preventing uncoating after host cell endocytosis
|
amantadine
|
|
silaic acid analog inhibitor of influenza A B neuraminidase so it cant get out
|
oseltamazir
|
|
silaic acid analog inhibitor of influenza A B neuraminidase so it cant get out
|
oseltamazir
|
|
silaic acid analog inhibitor of influenza A B neuraminidase so it cant get out
|
oseltamazir
|
|
silaic acid analog inhibitor of influenza A B neuraminidase so it cant get out
|
oseltamazir
|
|
silaic acid analog inhibitor of influenza A B neuraminidase so it cant get out
|
oseltamazir
|
|
silaic acid analog inhibitor of influenza A B neuraminidase so it cant get out
|
oseltamazir
|