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1Current > GLM MTB step3 Neurology > Flashcards

GLM MTB step3 Neurology Flashcards

1
Q

How do strokes/TIA present

A

“1) sudden onset of one-sided body weakness.

2) one-sided facial weakness and aphasia
3) partial or total loss of vision (transient)
4) Stoke spares upper third of face (from eyes up)


“

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2
Q

What is the cause of stroke/TIA

A

“decreased or altered cerebral blood flow


“

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3
Q

How are strokes different from TIA

A

“-The difference is based on time

1) Strokes last >24 hrs w/ permanent neuro deficits
2) TIA symptoms last <24 hrs & resolve completely


“

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4
Q

Which part of the face is spared in stroke patients

A

upper third (from eyes up)

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5
Q

Name the different types of strokes

A

“1) 80% ischemic (from emboli or thrombosis)

2) 20% hemorrhagic


“

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6
Q

Which type of stroke presents with more sudden symptoms emboli or thrombosis

A

emboli

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7
Q

What is amaurosis fugax

A

“transient loss of vision in TIA


“

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8
Q

What type of vision loss is seen in TIA

A

transient loss (amaurosis fugax)

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9
Q

What is the cause of amaurosis fugax

A

“decrease blood of branch of the carotid artery (ophthalmic artery)-> decrease in retinal circulation -> causes retinal hypoxia


“

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10
Q

What is the origin of TIA

A

thrombosis or emboli

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11
Q

Can TIA be caused by hemorrhage? Why or why not?

A

No; because hemorrhages don’t resolve within 24 hrs

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12
Q

A 67-year-old man with a history of hypertension and diabetes comes to the emergency department with a sudden onset of weakness in the right arm and leg over the last hour. On exam, he cannot lift the bottom half of the right side of his face. What is the best initial step? a. Head CT with contrast b. Head CT without contrast c. Aspirin d. Thrombolytics e. MRI

A

Answer: The correct answer is B.

Prior to administering thrombolytics or any anticoagulation, you need to *rule out hemorrhagic stroke, which is a contraindication to thrombolytics.*

You cannot even give aspirin without doing a head CT first.

Thrombolytics are indicated within the first *3 hours* of the onset of the symptoms of a stroke.

Remember, 20% of strokes are hemorrhagic.

You do not need contrast to visualize blood, contrast is used to detect cancer or infection, such as an abscess.

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13
Q

What can be visualized with contrast

A

cancer and infections

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14
Q

Symptoms of anterior cerebral artery lesion

A

“1) lower extremity weakness (contralateral in the case of unilateral arterial occlusion)

2) upper extremity weakness (contralateral in the case of unilateral arterial occlusion)
3) Personality changes or psychiatric disturbance
4) Urinary incontinence


“

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15
Q

Symptoms of Middle cerebral artery lesion

A

“1) upper extremity weakness (contralateral in the case of unilateral arterial occlusion)

2) Aphasia
3) Apraxia/neglect
4) The eyes deviate towards the side of the lesion
5) Contralateral homonymous hemianopsia, with macular sparing

Difficulty with A-B-Cs in M-C-A””

A-Apraxia
B-Blindness in corresponding half of the visual field (contralateral homonymous hemianopsia)
C-Contralateral Clumsiness of arm, face. — Leg is somewhat spared.

M-Memorization difficulties
C-Calculation difficulties
A-Aphasia with language-dominant hemispheral involvement


“

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16
Q

What is apraxia/neglect

A

“apraxia-motor disorder caused by damage to the brain, in which someone has difficulty with the motor planning to produce speech

neglect-


“

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17
Q

What is aphasia

A

acquired language disorder caused by damage to the brain.This class of language disorder ranges from having difficulty remembering words to losing the ability to speak, read, or write, but does not affect intelligence

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18
Q

Symptoms of posterior cerebral artery lesion

A

1) Prosopagnosia (inability to recognize faces)

Posterior cerebral artery (PCA) occlusion: P-O-S-T

P-Proximal fling movements
O-Occipital lobe infarction results in contralateral homonymous hemianopsia which may be complete
S-Speech and Spelling maintained, but unable to read fluently
T-Thalamic syndrome

1) Contralateral loss of pain and temperature sensations.
2) Visual field defects (contralateral hemianopia with macular sparing).
3) Prosopagnosia (inability to recognize faces)
4) Superior Alternating Syndrome (Weber’s syndrome)
5) Ipsilateral deficits of oculomotor nerve,
6) Contralateral deficits of facial nerve (only lower face, upper face receives bilateral input), vagus nerve and hypoglossal nerve
7) Horner’s Syndrome:
- ipsilateral partial ptosis
- upside-down ptosis (slight elevation of the lower lid)
- anhidrosis
- miosis

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19
Q

Symptoms of Vertebrobasilar artery lesion

A

“1) Vertigo

2) Nausea and vomiting
3) May be described as a ““drop attack””
4) Vertical nystagmus
5) Dysarthria and dystonia
6) Sensory changes in face and scalp
7) Ataxia
8) Labile blood pressure

vertebral-basilar circulation: 4D

  • Dizziness
  • Diplopia
  • Dysarthria
  • Dysphagia

Vertebro BANDS

  • Vertigo
  • Nausea and vomiting
  • May be described as a ““drop attack,”” LOC
  • Vertical nystagmus
  • Dysarthria and dystonia
  • Sensory changes in face and scalp
  • Ataxia
  • Bilateral findings”
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20
Q

Symptoms of lacunar infarct lesion

A

“P-BASH

1) There must be an absence of cortical deficits.
2) Ataxia
3) Parkinsonian signs
4) Sensory deficits
5) Hemiparesis (most notable in the face)
6) Possible bulbar signs

Lacunar infarct: ““Lacunar”” from the Latin for G-A-P or- D-I-S-P-A-R-I-T-Y

G-deep Gray matter: basal ganglia
A-Atherosclerosis
P-hyPertension

D-Dysarthria and a contralateral clumsy hand or arm due to infarction in the base of the pons or in the genu
of the internal capsule. (20%)
I-Internal Capsule: Lacunae in the posterior limb of the Internal capsule may cause pure motor hemiplegia
involving the face, arm, leg, foot. (60%)
S-Subcortical, capsular, or thalamic lacunae
P-Pontine lesions
A-Ataxic hemiparesis due to an infarct in the base of the pons
R-Rare: Lacunae in the anterior limb of the Internal capsule may cause severe dysarthria with facial weakness.
I-Ipsilateral ataxia (arm/leg) with leg weakness: Pontine lesion (rare)
T-Thalamus: Lacunae in the Thalamus may cause pure sensory stroke (10%)
y-V-Ventrolateral Thalamic lacunae

BASH

Lacunes are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%)

  • There must be an absence of cortical deficits.
  • Ataxia
  • Parkinsonian signs
  • Sensory deficits
  • Hemiparesis (most notable in the face)
  • Possible bulbar signs

Lacunes are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%)”

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21
Q

What is Dysarthria and dystonia

A

“dysarthria-condition in which problems effectively occur with the muscles that help produce speech, often making it very difficult to pronounce words.

dystonia-sustained muscle contractions cause twisting and repetitive movements or abnormal postures. The movements may resemble a tremor.


“

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22
Q

List Parkinsonian signs

A

“M-BIRTH

1) Tremor at rest
2) Bradykinesis
3) Postural instability
4) rigidity
5) mask-like facies=hypomimia
6) small hand writing=micro???

T - Tremor - Involuntary trembling of the limbs (resting tremor)
R - Rigidity - Stiffness of the muscles
A - Akinesia - Lack of movement or slowness in initiating and maintaining movement
P - Postural instability - Characteristic bending or flexion of the body, associated with difficulty in balance and disturbances in gait


“

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23
Q

What is a bulbar sign

A

“1) Bulbar relates to the *medulla*.

2) Bulbar palsy is the result of diseases affecting the *lower cranial nerves (VII-XII). *
3) A speech deficit occurs due to *paralysis or weakness of the muscles of articulation* which are supplied by these cranial nerves.


“

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24
Q

Symptoms of Posterior inferior cerebellar artery lesion

A

“VICH

1) ipsilateral face
2) contralateral body
3) Vertigo and Horner’s symptoms

Horner’s Syndrome (Oculosympathetic paresis) is a rare neurologic condition whose symptoms and signs include:

Ptosis (drooping eyelid)
Anhidrosis (inability to sweat).
Miosis (pupil constriction)

Horner’s syndrome can be caused by any set of sympathetic nerve fiber injuries. Horner’s syndrome is generally classified into Central and Peripheral.

Central: Sympathetic nerves start in the brain and then travel down to the spinal cord and into the chest.
Peripheral: Sympathetic nerves start from the chest to the neck, arteries, head, and into the eyes.

Another feature of Horner’s syndrome is loss of ciliospinal reflex (pupil dilates when pressure / pain applied to neck or face. Patients with Horner’s syndrome also experience Enophthalmos (posterior displacement of the eyeball). These features can all be remembered by the mnemonic ““SAMPLE””

S: Sympathetic Nerve Fiber Injury
A: Anhidrosis
M: Miosis
P: Ptosis
L: Loss of ciliospinal reflex
E: Enophthalmos


“

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25
Q

Symptoms of ophthalmic artery lesion

A

amaurosis fugax

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26
Q

Best initial test for stroke or TIA

A

head CT w/o contrast

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27
Q

Why is MRI not usually done with stroke or TIA

A

CT is …

1) more widely available
2) less expensive
3) more sensitive to blood

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28
Q

What does MRA most accurately image

A

brainstem

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29
Q

Dx for stroke

A

“1) *Head CT*: Extremely sensitive for blood. Needs 3-5 days to achieve > 95
percent sensitivity in the detection of non-hemorrhagic stroke.

2) *MRI*: Achieves 95 percent sensitivity for a non-hemorrhagic stroke within 24 hours.
3) *Magnetic resonance angiogram (MRA)*: Most accurately images the brainstem.


“

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30
Q

On CCS, what tests to order after a head CT w/o contrast, aspirin, and thrombolytics (i.e. move the clock forward)

A

1) Echo
2) Carotid Dopplers/duplex: Endarterectomy for stenosis > 70%, but not if it is 100%
3) EKG and a Holter monitor
4) PT and aPTT

5) Young patients (< 50) with no PMH (DM, HTN) should also have the following tests:
·· ESR
·· VDRL or RPR
·· ANA, dsDNA
·· Protein C, protein S, factor V Leiden mutation, antiphospholipid syndromes

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31
Q

Absolute contraindications to thrombolytic therapy

A

“Absolute contraindications to thrombolytic therapy:

*things that make pt more likely to bleed*

1) History of hemorrhagic stroke
2) Stroke within 1 year
3) Presence of a bleeding disorder
4) Suspicion of aortic dissection
5) Presence of intracranial neoplasm/mass

6) CPR within 3 weeks that was traumatic (e.g., chest compression)
7) Active bleeding or surgery within 6 weeks
8) Cerebral trauma or brain surgery within 6 months


“

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32
Q

Treatment for non-hemorrhagic (Ischemic) stroke

A

“1) *Thrombolytics (e.g rtPA)*: (<3 hrs of onset; give head CT w/o contrast to r/o hemorrhage stroke first); if *>3 hrs give ASA* (best initial for those too late for thrombolytics)
2) *Antiplatelet med: ASA or clopidogrel or ASA + dipyridamole*

3) *Clopidogrel/Dipyridamole*: if the patient had a stroke while on ASA switch to clopidogrel or add dipyridamole to ASA
4) *Statin*: Add for all non-hemorrhagic stroke.


“

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33
Q

Which patients can receive thrombolytics after 3 hours

A

“Thrombolytics (rtPA) may be administered up to 4.5 hr if no high-risk factors for hemorrhage (age >80yrs, severe stroke, DM with previous CVA and any anticoagulation use)

  • NOT used in TIAs


“

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34
Q

What are the contraindications for thrombolytic use

A

“1) >3 hours if patient has high-risk factors for hemorrhage (age >80yrs, severe stroke, DM with previous CVA and any anticoagulation use)

2) If the pt is UNABLE to report the time of onset and there is NO witness to the onset, rtPA Rx is CONTRAINDICATED!!
3) NO rtPA if SPB >185 mmHg, DBP > 110 mmHg


“

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35
Q

What is the treatment for patients presenting >3 hours after stroke

A

”*Catheter retrieval of clot*: Patients coming after 4.5 hours can have their clot removed with a catheter. This is useful up to *6-8 hours after stroke*, unlike angioplasty. Angioplasty would rupture the vessel, whereas a catheter pulls the clot out like a corkscrew.


“

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36
Q

What is the difference in the treatment of ACA stroke and MCA stroke?

A

ACA stroke and MCA stroke are managed the same way.

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37
Q

Further management of strokes

A

After you have done the head CT and given thrombolytics or aspirin, you should move the clock forward on CCS.

On subsequent screens, the most
important issue is to determine the origin of the stroke to prevent another one.

The following are indicated in all patients with stroke or TIA:

· Echocardiogram: Warfarin for clots, possible surgery for valve vegetations

· Carotid Dopplers/duplex: Endarterectomy for stenosis > 70 percent, but not if it is 100 percent

· EKG and a Holter monitor if the EKG is normal: Warfarin for atrial fibrillation

Young patients (< 50) with no past medical history (diabetes, hypertension)
should also have the following tests:
· Sedimentation rate
· VDRL or RPR
· ANA, double-stranded DNA
· Protein C, protein S, factor V Leiden mutation, antiphospholipid
syndromes

Don’t forget to control hypertension, diabetes, and hyperlipidemia in a
patient who has had a stroke. Hypertensive urgency is a relative contraindication to thrombolytic therapy.

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38
Q

In summary, 2° prevention of Ischemic stroke

A

“1 - antiplatelets: aspirin + dipyridamole (clopidogrel if aspirin contraindicated)
2 - anticoagulation (if AF, Lt atrial thrombus)
3 - carotid endarterectomy: ipsilateral stenosis > 70% if Pt likely to live 5 yrs; consider w/ stenosis 50-70% in male likely to live 5 yrs.
4 - stains in ALL pts REGARDLESS of cholesterol level
5 - HTN <140/90 after an acute event
6 - early stroke rehab


“

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39
Q

1) When is Ticlopidine used 2) What is the MOA of Ticlopidine

A

“1) only for Patients intolerant of ASA and clopidogrel

2)


“

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40
Q

Ticlopidine side effects

A

1) TTP (Thrombotic thrombocytopenic purpura)
2) neutropenia

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41
Q

What is Thrombotic thrombocytopenic purpura

A

“rare blood disorder causing thrombosis to form in the small blood vessels throughout the body. These thrombosis can damage many organs including the kidneys, heart and brain


“

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42
Q

What percentage of stroke patients arrive in time to get thrombolytics

A

<20% (<3 hrs)

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43
Q

When you should you use MRI/MRA

A

brainstem

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44
Q

What is the difference between management of anterior and middle cerebral artery stroke

A

nothing. They are managed the same way

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45
Q

What is a more likely cause of the stroke in a young patient

A

1) vasculitis
2) Hypercoaguable state

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46
Q

What should be done after head CT w/o contrast, thrombolytics and ASA in stroke patients

A

Determine the origin of the stroke

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47
Q

What tests and treatments are indicated in all stroke and TIA patients to determine origin of the stroke/TIA

A

1) Echo: Warfarin for clots, possible surgery for valve vegetations
2) Carotid dopplers/duplex: Endarterectomy for stenosis> 70 percent, but not if it is 100 percent
3) EKG and Holter monitor if the EKG is normal: Warfarin for atrial fibrillation
4) Young patients (< 50) with no past medical history (diabetes, hypertension) should also have the following tests:
- Sedimentation rate
- VDRL or RPR
- ANA, double-stranded DNA
- Protein C, Protein S, factor V Leiden mutation, antiphospholipid syndromes

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48
Q

What is the difference between the management of stroke and TIA

A

only difference is TIA does not get thrombolytics because they help resolve symptoms. TIA symptoms have already resolved

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49
Q

Threshold for initiating anti-HTN Rx in acute ischemic stroke

A

SBP > 220 mmHg
DBP > 120 mmHg or
MAP > 140 mmHg
BP target < 185/110 if thrombolytic Rx is planned

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50
Q

What is status epilepticus

A

epileptic seizure of greater than five minutes or more than one seizure within a five minute period without the person returning to normal between them.

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51
Q

Status epilepticus symptoms

A

nonconvulsive versus convulsive

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52
Q

Status epilepticus treatment

A

1) Benzodiazepines, such as Ativan(lorazepam).
2) If the seizure persists after moving the clock forward 10-20 minutes, then add fosphenytoin.
3) If the seizure persists after moving the clock forward 10-20 minutes, then add phenobarbital
4) If the seizure persists after moving the clock forward 10-20 minutes, then add general anesthesia, such as pentobarbital, thiopental, midazolam or propofol

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53
Q

Test to Diagnosis patient having a seizure

A

1) Head CT urgently
2) Sodium, calcium, magnesium, creatinine, glucose, oxygen levels
3) MRI later if the initial testing shows nothing
4) Urine fox screen
5) Liver and kidney function
6) EEG
7) neurology consult after all initial testing is done

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54
Q

What is the next step if initial diagnostic tests do not reveal the etiology of seizure

A

perform EEG

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55
Q

When is chronic antiepileptic drug therapy indicated

A

not usually after single seizure unless:

  • strong family hx
  • abnormal EEG
  • Status epilepticus that required benzos to stop seizure
  • Non-correctable precipitating cause (brain tumor)
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56
Q

Side effects of many anti-epileptics medications

A

bone loss/osteoporosis

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57
Q

Long-term management of seizures

A

1) First-line therapies:
Valproic acid
carbamazepine
phenytoin
levetiracetam (Keppra)
Lamotrigine (Lamictal)- Stevens-Johnson syndrome and severe skin reactions.
2) Second-line therapies:
Gabapentin
phenobarbital
3) Ethosuximide is best for absence or petit mal seizures.

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58
Q

Side effect of Lamotrigine use

A

Stevens-Johnson Syndrome

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59
Q

What is Steven-Johnson Syndrome

A

life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis

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60
Q

Symptoms of Steven-Johnson Syndrome

A

1) usually begins with fever, sore throat, and fatigue
2) Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips but also in the genital and anal regions.
3) Conjunctivitis of the eyes occurs in about 30% of children who develop SJS.
4) A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp

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61
Q

Which anti-epileptic medication is the dangerous in pregnancy

A

Valproic acid
Carbamazepine is dangerous too

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62
Q

Parkinson’s disease Symptoms

A

“1) tremulous patient with a slow, abnormal”” festinating/shuffling”” gait.

2) orthostasis
3) ““Cogwheel”” rigidity
4) Resting tremor (resolves when patient moves or reaches for something)
5) Hypomimia (a masklike, underreactive face)
6) Micrographia (small writing)
7) Intact cognition and memory”

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63
Q

What does tremulous mean

A

relating to tremor

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64
Q

What is cogwheel rigidity

A

ratchety jerks

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65
Q

Diagnostic Test for Parkinson’s Disease

A

none

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66
Q

Treatment for Parkinson’s Disease

A

1) Mild Symptoms
-Under age 60: Anticholinergic agent
benztropine or hrdroxyzine
-Over age 60: Amantadine (Older pts develop far more adverse effects from anticholinergic agent s, including constipation, glaucoma, and urinary retention.)

2) Severe Symptoms
1st line
- Levodopa/Carbidopa
-DA agonists (pramipexole, ropinirole, cabergoline)

2nd Line

  • COMT inhibitors: Tolcapone, entacapone
  • MAO inhibitors: Selegiline, rasagiline
  • Deep brain stimulation
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67
Q

What is considered Severe Parkinson’s symptoms

A

Severe symptoms are defined as the inability to perform activities of daily living, such as cooking, cleaning, personal grooming, and shopping.

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68
Q

What are the advantages and disadvantages for treating Parkinson’s Disease with Levodopa/Carbidopa

A

“advantages: greatest efficacy
disadvantages: ““On-Off”” phenomena with uneven long-term and more adverse effects”

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69
Q

What are the advantages and disadvantages for treating Parkinson’s Disease with Dopamine agonsists

A

advantage: fewer side effects
disadvantages: less efficacy

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70
Q

Types of Dopamine agonists

A

pramipexole, ropinirole, cabergoline

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71
Q

MOA of COMT inhibitors

A

These medications block the metabolism of dopamine and extend the effect of dopamine-based medications. They are not effective by themselves .

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72
Q

Examples of COMT inhibitors

A

Tolcapone, entacapone

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73
Q

Examples of MAOIs used to treat Parkinson’s Disease

A

Selegiline, rasagiline

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74
Q

What should be done when levodopa causes psychosis

A

add quetiapine to control psychosis

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75
Q

Resting Tremor Dx Tx

A

1) Parkinson’s Disease
2) Amantadine

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76
Q

Tremor with intention (action) only Dx Tx

A

1) Cerebellar disorders
2) Tx etiology

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77
Q

Tremor both at rest and with intention Dx Tx

A

1) Essential tremor
2) Propranolol

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78
Q

Multiple sclerosis Symptoms

A

1) optic neuritis
2) motor and sensory problems
3) bladder defects (atonic bladder)
4) fatigue
5) hyperreflexia
6) spasticity
7) depression

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79
Q

What is hyperreflexia

A

overactive or overresponsive reflexes. Examples of this can include twitching or spastic tendencies, which are indicative of upper motor neuron disease as well as the lessening or loss of control ordinarily exerted by higher brain centers of lower neural pathways (disinhibition).

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80
Q

What is spasticity

A

“altered skeletal muscle performance in muscle tone involving hypertonia; it is also referred to as an unusual ““tightness””, stiffness, or ““pull”” of muscles.”

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81
Q

Multiple Sclerosis Dx

A

1) BI & MA: MRI
2) CSF (lumbar tap): oligoclonal bands

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82
Q

Multiple Sclerosis Tx

A

1) Acute exacerbations: Steroids (BI)
2) Disease -modifying therapy:
- Beta interferon
- Glatiramer
- mitoxantrone
- natalizumab
3) Additional medications for other symptoms:
- Fatigue: Amantadine
- Spasticity: Baclofen or tizanadine

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83
Q

Side effect of Natalizumab

A

Progressive multifocal leukoencephalopathy

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84
Q

What is Progressive multifocal leukoencephalopathy

A

fatal viral disease characterized by progressive damage (-pathy) or inflammation of the white matter (leuko-) of the brain (-encephalo-) at multiple locations (multifocal).

It occurs almost exclusively in people with severe immune deficiency, such as transplant patients on immunosuppressive medications,[1] those receiving certain kinds of chemotherapy, receiving natalizumab (Tysabri) for multiple sclerosis,[2] on long-term efalizumab (Raptiva) for psoriasis,[3] brentuximab (Adcetris) for Hodgkin’s Lymphoma,[4] or those with AIDS.

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85
Q

Types of Dementia

A

“1) Alzheimer’s Disease

2) Creutzfeldt-Jakob Disease (CJD)
3) Frontotemporal Dementia (Picks)
4) HUNTINGTON’S DISEASE/CHOREA
5) ““LEWY BODY’’ DEMENTIA
6) NORMAL PRESSURE HYDROCEPHALUS (NPH)”

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86
Q

Alzheimer’s Disease symptoms

A

1) slow loss of memory in older patients (> 65).
2) apathy
3) imprecise speech.
4) No focal deficits

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87
Q

What is apathy

A

lack of feeling, emotion, interest, or concern

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88
Q

Which tests must be ordered in all patients with memory loss/Dementia

A

1) Head CT
2) B12 level
3) Thyroid function testing (T4/TSH)
4) RPR or VDRL

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89
Q

Alzheimer’s Disease Dx

A

1) Dx of exclusion
2) head CT: diffuse, symmetrical atrophy

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90
Q

Alzheimer’s Disease Tx

A

1) Anticholinesterase medications
2) Memantine: modest benefit

91
Q

Types of anticholinesterase medications

A

1) donepezil
2) rivastigmine
3) galantamine)

92
Q

Frontotemporal Dementia is also known as what

A

Pick’s Disease

93
Q

Frontotemporal Dementia Sx

A

1st abnormal personality and behavior then memory is lost

94
Q

Frontotemporal Dementia Dx

A

CT or MRI: focal atrophy of frontal and temporal lobes

95
Q

Frontotemporal Dementia Tx

A

Same as Alzheimer’s Disease

1) Anticholinesterase medications
1) donepezil
2) rivastigmine
3) galantamine)
2) Memantine: modest benefit

96
Q

Cause of Creutzfeldt-Jakob Disease (CJD)

A

prions transmissible protein particles

97
Q

Creutzfeldt-Jakob Disease (CJD) Sx

A

1) rapidly progressive dementia
2) myoclonus

98
Q

What is myoclonus

A

brief, involuntary twitching of a muscle or a group of muscle

99
Q

Creutzfeldt-Jakob Disease (CJD) Dx

A

1) EEG is abnormal
2) MA: brain biopsy
***3) On CCS cases, an MRI should be performed as well
4) CSF shows a 14-3-3 protein: spares the need for brain bx

100
Q

”"”LEWY BODY’’ DEMENTIA Sx”

A

Parkinson’s Disease + dementia

101
Q

NORMAL PRESSURE HYDROCEPHALUS (NPH) Sx

A

WWW: wet, weird, wobbly:
Wet: Urinary incontinence
Weird: Dementia
Wobbly: Wide-based gait/ataxia

102
Q

NORMAL PRESSURE HYDROCEPHALUS (NPH) Dx

A

1) head CT
2) lumbar puncture (LP): normal pressure
**should be done on CCS

103
Q

NORMAL PRESSURE HYDROCEPHALUS (NPH) Tx

A

Shunt

104
Q

HUNTINGTON’S DISEASE/CHOREA Sx

A

1) young patient (30s) with family hx
2) Psychiatric disturbance with personality changes
3) Chorea /movement disorder

105
Q

HUNTINGTON’S DISEASE/CHOREA Dx

A

1) genetic testing: AD inheritance

106
Q

HUNTINGTON’S DISEASE/CHOREA Tx

A

No treatment available

107
Q

Types of headaches

A

Cluster HA
Migraine
Pseudotumor cerebri
Temporal arteritis

108
Q

Things that trigger Migraine

A

1) Cheese
2) Caffeine
3) Menstruation
4) Oral contraceptive

109
Q

What percentage of migraines are unilateral, bilateral

A

unilateral: 60%
bilateral: 40%

110
Q

Migraine Sx

A

headache is preceded by
Aura of bright lights
Scotomata
Abnormal smells

111
Q

What is a scotomata

A

area of partial alteration in the field of vision consisting of a partially diminished or entirely degenerated visual acuity that is surrounded by a field of normal - or relatively well-preserved - vision

112
Q

Migraine Dx

A

Head CT or MRI should be done when the headache has any of the following characteristics:

Sudden and/or severe
On set after age 40
Associated with focal neurological findings

113
Q

Migraine Tx

A

1) BI abortive therapy: Sumatriptan or ergotamine
2) Prophylactic therapy:
>4 HA/mth: Propranolol
Alt prophylactic medications: CCB, TCA or SSRIs.

114
Q

How long does it take for prophylactic Migraine therapy to become effective

A

several weeks

115
Q

Which gender gets more cluster headaches

A

10 times more in men than women

116
Q

Cluster headache Sx

A

1) unilateral
2) redness and tearing of eyes
3) rhinorrhea
4) No aura

117
Q

Cluster headache treatment

A

1) BI abortive therapy:
Sumatriptan
100 percent oxygen
steroids
2) Prophylactic therapy:
CCB (verapamil) but verapamil does not prevent cluster headaches

118
Q

Temporal arteritis Sx

A

1) Tenderness of the temporal area
2) Jaw claudication

119
Q

Temporal arteritis

A

1) Sedimentation rate (ESR)
2) Most accurate test: Temporal artery biopsy

120
Q

Temporal arteritis Tx

A

Give steroids first and fast (delay may result in permanent vision loss)

121
Q

Pseudotumor cerebri Sx

A

1) obese young women
2) Headache
3) double vision
4) papilledema
5) normal CT/MRI

122
Q

Pseudotumor cerebri Dx

A

1) MA: lumbar puncture with opening pressure measurement: elevated pressure

123
Q

Pseudotumor cerebri Tx

A

1) Weight loss
2) Acetazolamide
3) Surgery: VP shunt, optic nerve fenestration

124
Q

What is the cause of Pseudotumor cerebri

A

vitamin A use

125
Q

Symptoms of ALL patients with vertigo

A

1) room spinning sensation
2) N/V
3) nystagmus

126
Q

What test should be done on anyone with vertigo

A

MRI of the internal auditory canal

127
Q

Types of Dizziness/Vertigo

A

Acoutstic neuromaBenign Positional Vertigo (BPV)
Labyrinthitis
Meniere’s Disease
Perilymph fistula
Vestibular neuritis
Wernicke-Korsakoff Syndrome

128
Q

Benign Positional Vertigo (BPV) Sx

A

1) Vertigo only
2) no hearing loss
3) no tinnitus
4) no ataxia

129
Q

Benign Positional Vertigo (BPV) Dx

A

Dix-Hallpike maneuver

patient sitting upright with the legs extended. The patient’s head is then rotated by approximately 45 degrees. The clinician helps the patient to lie down backwards quickly with the head held in approximately 20. The patient’s eyes are then observed for about 45 seconds as there is a characteristic 5-10 second period of latency prior to the onset of nystagmus. If rotational nystagmus occurs then the test is considered positive for benign positional vertigo. During a positive test, the fast phase of the rotatory nystagmus is toward the affected ear, which is the ear closest to the ground. The direction of the fast phase is defined by the rotation of the top of the eye, either clockwise or counter-clockwise.

130
Q

Benign Positional Vertigo (BPV) Tx

A

Meclizine (Antivert)

131
Q

What is Vestibular neuritis

A

This is an idiopathic inflammation of the vestibular portion of the VIII (8th) cranial nerve.

Viral cause

132
Q

Vestibular neuritis Sx

A

1) vertigo and dizziness not related to position
2) no hearing loss
3) no tinnitus

133
Q

Vestibular neuritis Tx

A

meclizine

134
Q

What is Labyrinthitis

A

inflammation of t he cochlear portion of the inner ear.

135
Q

Labyrinthitis Sx

A

1) vertigo
2) hearing loss
3) tinnitus

136
Q

Labyrinthitis Tx

A

1) self-limiting
2) meclizine

137
Q

Meniere’s Disease Sx

A

Just like Labyrinthitis except its chronic with remitting & relapsing episodes

1) vertigo
2) hearing loss
3) tinnitus

138
Q

Meniere’s Disease Tx

A

1) salt restriction + diuretics

139
Q

What is Acoustic neuroma

A

8th cranial nerve tumor related to neurofibromatosis and Von Recklinghausen’s disease

140
Q

Acoustic neuroma Sx

A

1) vertigo
2) hearing loss
3) tinnitus
***4) ataxia

141
Q

Acoustic neuroma Dx

A

MRI of internal auditory canal

142
Q

Acoustic neuroma Tx

A

Surgical resection

143
Q

What is the cause of Perilymph fistula

A

Head trauma or any form of barotrauma to the ear may rupture the tympanic membrane and lead to a perilymph fistula.

144
Q

What is barotrauma

A

Barotrauma is physical damage to body tissues caused by a difference in pressure between a gas space inside, or in contact with the body, and the surrounding fluid.

145
Q

Wernicke-Korsakoff Syndrome Sx

A

1) History of chronic heavy alcohol use
2) Confusion with confabulation
3) Ataxia
4) Memory loss
5) Gaze palsy/ophthalmoplegia
6) Nystagmus

146
Q

Wernicke-Korsakoff Syndrome Dx

A

1) Head CT
2) Bl2 level
3) Thyroid function (T4/TSH)
4) RPR or VDRL

147
Q

Wernicke-Korsakoff Syndrome Tx

A

1) thiamine first: Acutely, give IV dose; then switch to oral.
2) then, glucose

148
Q

Types of CNS infections

A

…

149
Q

When a CNS infection is suspected when should a head CT be performed before a lumbar puncture

A

1) hx of CNS disease
2) Focal neuro deficits
3) Papilledema
4) Seizures
5) Altered mental status
6)

150
Q

Initial work-up for CNS infection

A

blood cultures
Start empirical therapy
Head CT

151
Q

“A 45- year old man comes to the emergency department with fever, headache, photapho• b/a, and o stiff neck. What is the next best step in the management of tllis potient”“l a. Lumbar puncture b. Head CT scan c. Ceftrloxone and vancomycin d. Penicillir! e. Movement of patient to /CU”

A

Answer: The correct answer is A. When you suspect bacterial meningitis, adminiHer anti biotics quickly. Further, do blood cultures stat simultonenously with o lumbar puncture or immediately prior. Penicillin con never be used as empiric therapy for meningitis; it is not sufficiently brood in coverage to be effective empiric therapy. In this case, perform the LP;
answer A is the best choiCe.

152
Q

Bacterial meningitis Dx

A

1) Best initial: Cell count
2) Most accurate: culture
3) CSF analysis

153
Q

Gram positive diplococcic gram stain indicates

A

Pneumococcus

154
Q

Gram negative diplococcic gram stain indicates

A

Neisseria

155
Q

Gram negative pleomorphic, coccobacillary gram stain indicates

A

Haemophilus

156
Q

Gram positive bacilli gram stain indicates

A

Listeria

157
Q

What is the best initial test for Dx of meningitis

A

cell count

158
Q

Bacterial meningitis treatment

A

If thousands of neutrophils are present in CSF
start with IV ceftriaxone, vancomycin, steroids

159
Q

Cryptococcus presentation

A

an HIV positive patient with < 100 CD4 cells

160
Q

Meningeal signs

A

neck stiffness, photophobia, and high fever, all at the same time.

161
Q

Cryptococcus Dx

A
  • Best initial test: Ind ia ink
  • Most accurate test: Cryptococcal antigen
162
Q

Cryptococcus Tx

A

• Best initial therapy: Amphoter icin
Amphotericin is followed with oral fluconazo le.
If the patient’s CD4 cells do not rise, fluconazole must be continued indefinitely.
• If the CD4 count rises above 100, the fluconazole can be stopped.

163
Q

Lyme disease presentation

A

Look for a patient who has recently been on a camping or hiking trip. Tick exposure is remembered only by 20 percent of patients.

164
Q

Lyme disease Dx

A

There are no characteristic CSF findi ngs to confirm a diagnosis of CNS Lyme. Specific serologic or western blot testing on the CSF is the most accurate test. Look for a patient with a history of joint pain, VII (7t h) cranial nerve palsy, or a rash with central dearing (target lesion).

165
Q

Lyme Disease Tx

A

). Treat with IV ceftriaxone or penicillin

166
Q

Rocky Mountain Spotted Fever presentation

A

Look for a camper or h iker with a rash that starts on the wrists and an kles and moves centripetally towards the center. Fever, headache, and malaise precede the rash. Only 60 percent at most will rem e mber a tick bite.

167
Q

Rocky Mountain Spotted Fever Dx

A

D i agnose with specific serology.

168
Q

Rocky Mountain Spotted Fever Tx

A

Doxycycline

169
Q

TB meningitis presentation

A

. Look for a n immi grant wit h a h i story of lung tuberculosi s. The presen tation is 'Cry slow over weeks to mont hs; i f the case desc ribes fever, heada che, and neck st iffness over hours then it is not TB.

170
Q

TB meningitis Dx

A

TB me n ingitis has a very high CSF protein level. Acid fast (mycobac terial) stain of the CSH is positive i n 10 percent or less of pat ients. For acid•fast cu i • t u re, you need three high•volume taps that are centrifuged.

171
Q

TB meningitis Tx

A

Treat wit h r i fampin , isonizaid, py rizi namide , and ethambuto l (R IPE) as you would for pulmon ary TB. The only difference i s that you should add steroids and extend the length of therapy for m eningitis when compa red with pu l mo• na ry disease.

172
Q

VIRAL MENINGITIS Dx

A

Viral meningitis is, in genera l , a diagnosis of exclusion. There is a lymphocytic pleocytosis in t he CSF. and none of the ot her findings is present.

173
Q

Viral meningitis Tx

A

The only difference i s that you should add steroids and extend the length of therapy for m eningitis when compa red with pu l mo• na ry disease.

174
Q

An elderly man comes to the emergency dtportmen! with fever, heodocht, o iliff neck, and photophobia. He is HIV po1Wve with< 50 CD4 cells and a history of pneumocystis pneumonia. His htad CT is normal. CSF .shows 1.500 white cells that ore all ntutrophi/5: gram stoln is normal. What is thf’ best initial theropy? a. Ctftrlaxone and metronidazole b. Cefoxi!in and mefloquint c. Ceftriaxon . ampicillin. and vancomycin d. Fluconazole e. Amphotericin

A

Amwer; The correct answer is C. Listeria monocytogenes is a cause of meningitis that is not adequately treated by any form of cephalosporin. Ampicillm is added to the usual regimen of ceftriaxone and vancomycin to cover Listeria. This cannot be fungal meningitis, because the CSF is character ized exclusively by a high number of neutraphils; neutrophils are not consistent with fungal meningitis

175
Q

A 17-y or-o/d malt is brought to tht tmtrgt>ncy department with feYer, headache, Iliff neck, and photophobia. Ht ho1 a pd«.h/o/ rash. CSF shows 2,499 nl’utrophiii Ceftriaxone and vancomycin art ltarled. What should be done neAt! a. Test for HIV b. Wait for rnulb of culture c. Add ampicillin d. Enforu rtlpiratory Isolation r. Enforce respiratory i.mlation and preJcribe rifampin for close contacts

A

Amwer: The correct answer is E. When an adolescent presents with a petechial ra5h and increased neutrophils on CSF, it is suggestive of Neisseria meningitides. These patients should be placed on respiratory isolation, and close contacts should receive prophylaxis

176
Q

Listeria presentation

A

Look for elderly, neona t al, and HIV-positive patients and those with who have no spleen, are on steroids, or are immunocompromised with leukemia or lymphoma.

177
Q

Listeria Tx

A

There will be elevated neutrophils in the CSF.

178
Q

Listeria Dx

A

Ampicillin

179
Q

NEISSERIA MENINGITIDES presentation

A

Look for patients who are adolescent, in the military, or asplenic or who have terminal complement deficiency.

180
Q

NEISSERIA MENINGITIDES Tx

A

Treal as follows:

Patient: Begin respiratory isolation.
Close contacts: Start proph ylaxis with rifampin or ciprofloxacin for close contacts, such as household members and those who share utensi l s, cups, or kisses.
Rout ine contacts : Routine school a n d work co n tacts do not need to receive prophylaxis.

181
Q

Which individuals need prophylaxis with Neisseria

A

kissing and other saliva type contact

182
Q

Encephalitis = ???

A

Encephalitis = fever + confusion

183
Q

Encephalitis presentation

A

Look for a patient with fever and altered mental status over a few hours. If the patient also has photophobia and a stiff neck, you will not be able to diagnose encephalitis. Almost all encephalitis in the Un ited States is from herpes. The patient does not have to reca ll a herpes infection in the past for the condition to be herpes encephalitis.

184
Q

Encephalitis Dx

A
  • Best initial test: Head CT scan
  • Most accurate test: PCR of the CSF
185
Q

Encephalitis Tx

A

Best i nitial the rapy: Acyclovir
• For acyclovir-resis tant pat ients: Foscarnet

186
Q

What is shown in the following picture

A

pic Brain abscess

187
Q

Brain abscess presentation

A

A brain abscess presents with fever, h eadache, and focal neurological deficits.

188
Q

Brain abscess Mgmt

A

”. A CT sca n finds a ““r i ng,”” or contrast-enhancing, lesion. Contrast (““rin g””) e n hancement basically mean s either cancer or i nfection.

Consider HIV status in the context of a brain abscess as follows:

  • HIV-negative: Brain biopsy is t he next be st step.
  • HJV-positive: Treat for toxoplasmosis with pyrim ethamine and sulfadiazine for two weeks and repeat t h e head CT.”
189
Q

Progressive Multifocal Leukoencephalopathy (PML) Dx and Tx

A

These brain lesions in HIV-posit ive pat ients are not associ ated w ith ri n g enhancement or mass effect.
There is no specific t herapy. Treat t h e HIV and raise t he CD4. Whe n the HJ V is improved, the lesions will disappear .

190
Q

NEUROCYSTICERCOSIS presentation

A

Look for a pat ient from Mexico wit h a seizu re.

191
Q

NEUROCYSTICERCOSIS Dx

A

Head CT shows multip le 1 em cyst ic lesions . Over time, the lesions calcify. Confirm diagnosis wit h serology.

192
Q

NEUROCYSTICERCOSIS Tx

A

When still act ive and uncalcifie d , t he lesions are treated with a lbend azole. Use steroids to preven t a reac t ion to dy i ng parasites.

193
Q

Types of head trauma and intracranial hemorrhages

A

…

194
Q

Loss of consciousness=

A

LOC= CT scan

195
Q

Any head trauma resulting in LOC or altered mental status should receive what

A

Any head trau m a resu lting in a loss of consciousness (LOC) or altered mental stat u s should lead to aCT scan of t he head wit h out cont rast.

196
Q

Types of head trauma that can lead to loss of consciousness

A

pic

197
Q

What is shown in this picture?

A

pic cerebral contusion

198
Q

What is shown in this picture?

A

pic subdural hematoma

199
Q

What is shown in this picture?

A

pic epidural hematoma

200
Q

Head trauma Tx

A

Concussion: none
Contussion: Admit, but vast majority get no tx
Subdural and epidural: Large ones are drained; small ones are left alone to reabsorb on their own
Large intracranial hemorrhage w/ mass effect
-intubation/hyperventilation to decr intracranial pressure. Decr pCO2 to 25-30, which will constrict cerebral blood vessels
-administer mannitol as an osmotic diuretic to decrease intracranial pressure
-perform surgical evacuation

201
Q

Which patients should receive proton pump inhibitors as prophylaxis against stress ulcers

A

Head trauma
Burns
Endotracheal intubation w/ mechanical ventilation

202
Q

What is Amyotrophic Lateral Sclerosis

A

This is an idiopathic disorder of both upper and lower motor neu rons. It is treat ed with riluzo le, a unique agent that blocks the accumulation of glutamate.

203
Q

Upper motor neuron signs seen in ALS

A

hyperreflexia
upgoing toes on plantar reflex
spasticity
weakness

204
Q

Lower motor neuron signs in ALS

A

wasting
fasciculations
weakness

205
Q

Types of peripheral neuropathies

A

…

206
Q

What is the most common cause of peripheral neuropathy

A

Diabetes

207
Q

Diabetic neuropathy Tx

A

Gabapentin or pregabalin

208
Q

Carpal tunnel presentation

A

Look for pain and weak n ess of the fi rst three digits of the hand. Symptoms may wor sen wit h repetitive use.

209
Q

Carpal tunnel Tx

A

I nit ial management is a splint. i n CSS, inject steroids w hen you move the clock
forward if symptoms persist or worsen.

210
Q

radial nerve palsy presentation

A

“Also known as ““Saturday n ight pa lsy,”” this results from fa ll ing asleep or passing out wit h pressu re on the anns u n dern eath t h e body or outstretched, perhaps draped over the back of a cha i r. Radial nerve palsy results in a wrist drop.”

211
Q

Peroneal nerve palsy presentation

A

“Th is results from high boots pressing at the back of the knee. It results in fooj
drop and the inability to evert the fooL May see ““high boots”” in the case.”

212
Q

Peroneal nerve palsy Tx

A

There is no therapy. Peroneal nerve palsy resolves on its own.

213
Q

VII (7TH) CRANIAL NERVE (BELL’S PALSY) presentation

A

“Bel l’s palsy resu lts in hemifacia l paralysis of bot h the upper a n d lower halves of the face. There i s a lso loss of taste on the anterior two thirds of the ton gue, hype raccusis, and the i nability to dose the eye at night. Hyper accu sis results in the i n ability to cont rol the stapedius muscle of t he middle ear, wh ich acts as a k ind of”“shock absor ber “” for sounds. Bell’s palsy is bel ieved to result from a viral infect ion.”

214
Q

VII (7TH) CRANIAL NERVE (BELL’S PALSY) Tx

A

Treat with steroids and acyclovi r. It is not clear t hat acyclovir wor ks, but vala cycolvir is often prescr ibed on a trial basis

215
Q

REFLEX SYMPATHETIC DYSTROPHY (CHRONIC REGIONAL PAIN SYNDROME) presentation

A

“This happens in a patient wit h previous injury to the extremity. Light touch, such as from a sheet touching t h e foot, results in extreme pain that is ““burn ing”” in quality.”

216
Q

REFLEX SYMPATHETIC DYSTROPHY (CHRONIC REGIONAL PAIN SYNDROME) Tx

A

Treat with NSA!Ds, gabapentin, and occasionally nerve block. Surgical sym pathectomy may be necessary.

217
Q

Restless Leg syndrome presentation

A

This often comes to the health care provider’s attention when the bed partner comes in complain ing of pa in and bruises in the legs. The patient experiences an uncomfortable feeling in the legs, which is relieved by m ovement.

218
Q

Restless Leg syndrome Tx

A

Treat with prami pexole or ropinerole.

219
Q

A man comes to the emergency deportment with weakness In his legs that hal been get• ting markedly worse aver the last few days. He has weoknen and loss of deep tendon reflexes In the legs . He recalls an upper respiratory illness about 2 4 weeks prior that resolved . What il the most urgent step? a. Steroids b. Intravenous Immunoglobulins c. Peak inspiratory prrssurr d . Intubation e. Lumbar puncture

A

Amwer : The correct answer is C. This case is Guillain Barre. Ascending weakness with loss of deep tendon reflexes is characteristic. Peak inspiratory pressure is the correct answer. The peak inspiratory pressure dimmishes as the diaphragm is weakened. Peak inspiratory pressure predicts who will have respiratory failure before it happens. It is more importan! than to start therapy with either intravenous immunoglobulins (IVIG) or plasmapheresis. Combinations of these medications ore not effective. Steroids ore not effective. LumOOr puncture will show an elevated protein level with no cells.

220
Q

MYASTHENIA GRAVIS presentation

A

Myasthenia gravis presents with weakness of the muscles of mastication, making it hard to finish meals. Blurry vision from diplopia results from the inability to focus the eyes on a single target. The case may classically report drooping of the eyelids as the day progresses.

  1. diplopia
  2. ptosis
  3. dysphagia
221
Q

MYASTHENIA GRAVIS Dx

A

“1) Best initial test: Anti-acetylcholine receptor antibodies (ACHR)
2) Most accurate test: Clinical presentation and ACHR are more sensitive and specific than an edrophonium or ““tensilon”” stimulation test”

222
Q

MYASTHENIA GRAVIS Tx

A

1) Best initial therapy: Pyridostigmine or neostigmine
2) Thymectomy: If pyridostigmine or neostigmine do not work, patients< 60 should undergo thymectomy.
3) Prednisone: If thymectomy does not work, or if there simply is no response to pyridostigmine or neostigmine, then prednisone should be started.
4) Azathioprine and cyclosporine are used to try to keep the patient off of longterm steroids.
5) Acute exacerbation: IVIG or plasmapheresis

223
Q

What are thrombolytics

A

Thrombolytics break up clots by activating fibrinolysis and converting plasminogen to plasmin which lyses the clot. This allows blood and oxygen to reperfuse the area, limiting tissue damage. Thrombolytics are more effective if initiated as soon as possible after the event (such as a heart attack, stroke, or PE) but can be given within three hours of symptom onset for a stroke, or within 12-24 hours of symptom onset for a heart attack

224
Q

Thrombolytic agents What are thrombolytic agents? Thrombolytic agents break down the thrombus or clot itself. This means, that when a thrombolytic agent encounters a clot, it starts its breakdown by directly acting on the clot. This results in breakdown of thrombus. Thrombolytics example Example includes Heparin (natural thrombolytic). When heparin is administered into the blood vessel, for example, it clears and breaks down any clot that comes along its way. Hence working as a thrombolytic agent. Note: theoretically heparin is only anticoagulant, however it works as an indirect thrombolytic agent too.

A

Thrombolytic vs Fibrinolytic vs Anticoagulant agents

There is sometimes confusion among medical students that what’s the difference between the thrombolytic agents, fibrinolytic agents and the anticoagulants. In this article we’ll study the difference between them and also learn which drugs or agents perform each of these actions.

Lets check out what are these blood thinners and what’s the difference between each blood thinner.

Thrombolytic agents

What are thrombolytic agents?

Thrombolytic agents break down the thrombus or clot itself.

This means, that when a thrombolytic agent encounters a clot, it starts its breakdown by directly acting on the clot. This results in breakdown of thrombus.

Thrombolytics example

Example includes Heparin (natural thrombolytic).

When heparin is administered into the blood vessel, for example, it clears and breaks down any clot that comes along its way. Hence working as a thrombolytic agent.

Note: theoretically heparin is only anticoagulant, however it works as an indirect thrombolytic agent too.

thrombolytic vs fibrinolytic vs anticoagulant agents
Fibrinolytic agents

What are fibrinolytic agents?

Fibrinolytic agents are the one which breakdown the fibrin inside the clot but not the thrombus itself.

This means that fibrinolytic drugs given for fibrinolytic therapy and fibrinolytic agents act on the fibrin only. The other contents of thrombus remain acting.

Fibrinolytics example

Example includes Plasminogen (natural fibrinolytic).

Firbrinolytic drugs examples:

Remember not to use any drug on your own without consulting a doctor, these are highly potential drugs and can lead to death even if misused.

Fibrinolytic drugs have mainly three major classes:

tPA - tissue plasminogen activator
SK - streptokinase
UK - urokinase
The drugs included in these three classes have the ability to resolve a blood clot. However their detailed mechanisms of actions vary and thus their choice varies based on the exact condition and patients requirements.

Anticoagulant agents

What are anticoagulant agents?

Anticoagulants work is before the clot is formed. I.e, they prevent the clot from getting formed in first place.

Once the thrombus is formed anticoagulants can’t break it down. Instead, thrombolytic agents are used instead for the breakdown of the clot.

Thrombolytic vs Fibrinolytic vs Anticoagulant agents

Each of them have their own role in normal homeostasis as well as a therapeutic role in specific conditions. It’s important to understand the role of each of them so that the correct one can be used when needed without any confusion.

Hope it clarifies the concept of each of these. If you have any query related to thrombolytics, fibrinolytics or anticoagulants please let me know.

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