Week 8 roop Flashcards

1
Q

double vision

A

dipoplia

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2
Q

slurred speech

A

dysarthria

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3
Q

difficulty swallowing

A

dysphagia

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4
Q

nerve conduction and muscle conduction. It can diagnose motor neuron diseases.

A

EMG

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5
Q

____: muscle strengthener and it rules out Myasthenia gravis
-it is acetylcholinesterase inhibitors

A

edrophonium

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6
Q

why do you need to keep atropine on hand when you use edrophonium?

A

decreases heart rate and constricts airways

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7
Q

if your muscle strength improves after use of edrophonium you have _____, if your muscle strength does not improve ______

A
  1. myasthenia gravis
  2. muscle weakness is due to other reasons
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8
Q

____is gram positive, spore-forming, anaerobic bacillus
-produces neurotoxin, botulinum
-people still die from this today from home canning

A

clostridum Botulinum

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9
Q

in botulinum neurotoxin, what happens at a motor neuron when action potential arrives at presynaptic terminal?

A

-calcium influx
-botulinum destroys SNARE proteins, vesicles cant fuse, no ach release cant bind to receptors, FLACCID PARALYSIS

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10
Q

____help vesicles fuse to presynaptic membranes

A

snare proteins

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11
Q

the SNAP SNARE proteins allow docking of the vesicles with the cell membrane, fusion and then ____of the ACh into the synaptic cleft

A

exocytosis

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12
Q

Flaccid paralysis occurs first in cranial muscles and is ______
-it will spread to other proximal muscles and then to distal muscles

A

symmetrical

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13
Q

what are the muscles paralyzed that result in droopy eyelids _____

A

levator palpebrae superioris muscle

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14
Q

what are the muscles that result in dysphagia _____

A

upper esophageal sphincter muscle

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15
Q

what muscles are effected causing double vision ____

A

any optic muscles

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16
Q

what is the time for symptoms to appear after ingestion of food-borne toxin?

A

begin 18-36 hours on average

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17
Q

what is the treatment for botulinum toxin?

A

-doctors treat with antitoxin, this prevents the toxin from causing any more harm
-antitoxin does not heal damage the toxin has already done

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18
Q

what will happen if patient is not treated for botulinum toxin?

A

-the disease may progress and symptoms may worsen to cause full paralysis of some muscles, including those used in breathing and those in the arms, legs and trunk (part of body from neck to pelvis area, called torso)
-will affect diaphragm muscles so patient is unable to breathe give ventilator

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19
Q

how long would patient have to remain in hospital? what are you trying to achieve physiologically?

A

-weeks to months, until symptoms disappear
-restoration of snare proteins

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20
Q

botulinum neurotoxin is considered the _____

A

deadliest toxin

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21
Q

____: breakdown of heme
-happens in the spleen
-goes to the liver
-makes it into bile

A

bilirubin

22
Q

____: all of the extra bilirubin, too much breakdown of RBC

A

hemolytic anemia

23
Q

____: influx of neutrophils and lymphocytes
-still see fundate glands
-epithelium shedding

A

Non-atrophic gastritis

24
Q

___: clenching of teeth

A

bruxism

25
Q

patients gums displayed burtons lines which indicates ____

A

lead poisoning

26
Q

-burtons line is a blue purplish line on the gums seen in lead poisoning
-it is caused by a reaction between circulating lead with ____ions released by oral bacterial activity, which deposits lead sulfide at the junction of the teeth and gums

A

sulphur

27
Q

_____of RBCs indicative of heavy metal poisoning

A

basophilic stippling

28
Q

what is the treatment for lead poisoning?

A

chelating agent

29
Q

for lead poisoning: succimer and penicillamine are given ____

A

orally

30
Q

for lead poisoning: dimeroeaprol and edetate, calcium disodium (CaNa2EDTA) are given ____

A

parenterally

31
Q

lead can block what enzymes and this can block heme?

A

aminolevulinate dehydratase and ferrochelatase

32
Q

basophilic stippling is due to lead inhibiting enzyme ____which clears clumps of degraded RNA

A

5 prime nucleotidases

33
Q

lead also attaches to RBCs membrane making ____ much easier hence the increase in bilirubin levels

A

hemolysis

34
Q

lead can cross BBB, leading to edema: ____

A

increase in ICP leads to encephalopathy

35
Q

lead can cross BBB and can block enzymes in heme synthesis pathway leading to ___

A

anemia

36
Q

____: RNA left back in RBC, not cleared because enzyme is inhibited

A

basophilic stippling

37
Q

what are the two major components of hemostasis

A
  1. platelet plug
  2. clotting cascade
38
Q

patients blood results indicate something is wrong with ____

A

clotting cascade

39
Q

pathophysiology: bleeding of the oral mucus membrane could also indicate internal bleeding, indicated by ___

A

stool sample

40
Q

platelets are also known as ____

A

thrombocytes

41
Q

platelets are derived from ____

A

megakaryocytes

42
Q

what is the life span of platelets?

A

7-10 days

43
Q

platlet formation is regulated by the hormone ____

A

thrombopoietin

44
Q

what are the three types of granules?

A

alpha, dense, lysosomes

45
Q

what granule?
____ comprise the bulk of platelet secretome, hemostatic factors (Factor V, VWF, fibrinogen); angiogenic factors (angiogenin, PF4); growth (PDGF, BFGF, SDF1alpha); proteases (MMP2, MMP9)

A

alpha

46
Q

what granule?
__serotonin, ATP, ADP, histamine, coagulants

A

dense

47
Q

what is the mechanism of action of warfarin?
-inhibits ___-clotting factors
-clotting factor II= ____
-thrombin converts fibronogen to fibrin warfarin—inhibits vitamin K clotting factor II —prothrombin

A
  1. vitamin K
  2. prothrombin
48
Q

warfarin inhibts the effective synthesis of biologically active forms of the vitamin K dependent clotting factors: ____ as well as the regulatory factors _____

A
  1. II, VII, IX and X
  2. protein C, protein S, and protein Z
49
Q

____inhibits platelet adhesion

A

garlic

50
Q

___increases activity of warfarin (potentiates), vasodilator (peripheral vascular disease), side effects: MASSIVE HEADACHE

A

ginkgo biloba