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Symptoms 2 > Headache > Flashcards

Headache Flashcards

1
Q

A 65 yo F presents to the ED with a complaint of headache. The patient is brought in by her husband. The patient states the headache is a 10/10 and started while she was carrying laundry up the stairs. The patient has a history of migraines, but this headache is ‘much worse and feels different’. She has vomited twice since the start of the headache and continues to be nauseated. She also has light and noise sensitivity. The patient also feels lightheaded and like she might ‘pass out’.

A

Most like subarachnoid hemorrhage

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2
Q

You suspect your pt has a subarachnoid hemorrhage, what labs do you order?

A

●Complete blood count

●Basic metabolic panel

●Coagulation studies

●EKG

●CT scan of brain (non-contrast)

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3
Q

Define Subarachnoid hemorrhage. What are they two types?

A

acute extravasation of blood into the space between the arachnoid membrane and the pia mater.

– Spontaneous SAH: rupture of focally weakened artery in the

subarachnoid space: Aneurysm

– Secondary SAH:
• Trauma: Hemorrhage may derive from several sources: trauma, Rupture or dissection of vertebral arteries, Intracerebral hematoma

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4
Q

Saccular (berry) aneurysm

– Not present at birth, but defect in____ is congenital and the aneurysm develops over time

– Increasing risk of rupture as _____
– Occur typically at branch points, 90% in the _____

A

media

size increases

anterior circulation

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5
Q

What are some increased risks for rupture or devo of Berry Aneurysms

A

Increased risk with hypertension, smoking, arteriovenous malformations, polycystic kidney disease, defects in vascular collagen, smooth muscle or elastic tissue (Ehlers- Danlos syndrome)

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6
Q

Aneurysm due to infection (bacteria or fungus)

Fusiform, atherosclerotic aneurysm: usually ______ arteries

A

Mycotic aneurysm:

vertebral basilar

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7
Q

Regarding pharmacologic management of your patient with subarachnoid hemorrhage, what are your goals for managing this patient’s blood pressure?

A

Avoid reducing blood pressure too much or too quickly

●Goal of SBP<150 or DBP <90mmHg or within 5% of baseline

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8
Q

Medications to initially manage subarachnoid hemorrhage

A

–Labetalol (beta blocker)

–Hydralazine (direct vasodilator)

–Nicardipine (Ca channel blocker)

–Esmolol (beta blocker)

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9
Q

Best way to deliver meds to pt with subarachnoid hemorrhage

A

i.v. to allow for titration of blood pressure

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10
Q

Why don’t we want to use nitrate or RAAS for pts with subarachnoid hemorrhage?

What do we need to keep in mind when giving Beta blockers?

A
  • Avoid use of nitrates – increases ICP
  • RAAS Inhibitors – too slow in onset
  • β-Blockers – i.v. with short half-life that can be titrated and do not increase ICP
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11
Q

Role of B-1 receptors

A

– heart, kidney

– stimulation increases HR, contractility, renin release

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12
Q

Role f B-2 receptors

A

– lungs, liver, pancreas, arteriolar smooth muscle

– stimulation causes bronchodilation & vasodilation

– mediate insulin secretion & glycogenolysis

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13
Q

What B blockers are specific for B-1 receptor

A

Metoprolol and Atenolol

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14
Q

What B blockers cover B1 and B2 receptors

A

Propranolol and Labetalol

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15
Q

Understand B blocker mechanism in regards to regulating Blood Pressure

A

Start by blocking renin and decreasing HR

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16
Q

During a subarachnoid hemorrhage neighboring vessels may experience cerebral vasospasm, what can we use to tx this? how does it work?

A

CCB: use a Dihydropyridine, specifically Nimodipine

Nimodipine has selectivity for cerebral vascular smooth muscle cell Ca2+ channels

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17
Q

nifedipine, amlodipine, nimodipine are what kind of drugs

A

Dihydropyridine CCBs

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18
Q

Non-dihydropyridine CCBs

A

Diltiazem and Verapamil

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19
Q

You suspect your pt had a subarachnoid hemorrhage but the CT scan was negative, what would your next test be and why? Describe the findings on this test that would confirm a subarachnoid hemorrhage.

A

Lumbar puncture: we would expect to see xanthochromia

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20
Q

A 5 yo M presents via EMS after falling from a tree house in his neighbor’s backyard. The child is awake at this time, but was reported to be unresponsive immediately after the fall. He is in full c-spine and backboard precautions. He is crying and is trying to get up off of the backboard. He is noticed to have a laceration and hematoma to the right side of his head, bleeding is controlled. His parents are with him and are having a hard time consoling him. The patient has vomited twice en route to the hospital.

Dx?

A

Trauma: likely an epidural hematoma

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21
Q

Range of normals for pediatric vital signs

A

Note patterns, do not memorize

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22
Q

What is key for initial management of pt you suspect has an epidural hematoma

A

Airway, Breathing, Circulation, Disability, Examine, Fahrenheit, Get vials, Head-to-toe assessment, Intervention

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23
Q

Epidural hematomas are most often in the temporal region because:

A

– Bone is relatively thin in this area & more susceptible to fracture – Middle meningeal artery courses in this region & so is torn

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24
Q

Mechanism of epidural hematoma

A

Mechanism: dura is firmly adherent to inner table of skull

• May take time (minutes to hours) for the dura to come free from the

skull as hematoma grows (explains lucid interval)

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25
Q

What is the Cushing Reflex (triad)

A

– Increased Blood Pressure
• Sympathetic nervous system - vasoconstriction

– Decreased Heart Rate

• Parasympathetic nervous system – reflex bradycardia

– Irregular Breathing
• Compression of brain stem

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26
Q

How do you treat and manage increased intracranial pressure?

A

• Osmotic agents – mannitol does not cross blood brain barrier

– Dramatic decrease ICP 50% within 30 minutes

• Loop Diuretics – furosemide – Decrease ICP

27
Q

Mannitol:

  1. _____ filtered
  2. Not reabsorbed
  3. Metabolically____
A

Freely

inert

28
Q

What is the mechanism of mannitol?

A

Given intravenously only

Act in tubular lumen as non-reabsorbable solute

Urine volume and sodium excretion are proportional to the osmotic load

Increases the urinary excretion of sodium, potassium, chloride, water and mannitol

29
Q

Uses of mannitol

A

Edema
Glaucoma-reduces intraocular pressure

Acute renal failure

30
Q

Loops:

Orally and intravenously active

High efficacy (____of filtered sodium load excreted)

____in onset

____ duration of action

A

20-30%

rapid onset

short duration of action

31
Q

MOA of Loop diuretics

A

Filtered and secreted by the OAT

Inhibits Na-K-2Cl symporter

Acts on the cortical and medullarymsegments of the ascending limb of the loop of Henle

Increase the excretion of sodium, potassium, chloride and water

32
Q

What are my three loop diuretics

A

furosemide, Bumetanide, Ethacrynic acid

33
Q

Subfalcine herniation:

what’s herniating and what structures are at risk of damage?

A

Cingulate gyrus herniates under the falx

Caused by asymmetric expanding hemispheric lesions

May cause in compression of ant. cerebral art. resulting in infarction

34
Q

Medial temporal lobe displaced through the tentorial opening because of asymmetric expanding lesion

A

Uncal hernaition

35
Q

4 complications of Uncal herniation

A

Ipsilateral 3rd nerve compression + pupillary dialation

Compression of brainstem (midbrain peduncle containing corticospinal tracts) against the tentorial edge opposite the direction of herniation (can lead to false localization of motor deficit- ipsilateral hemiparesis) (Kernohan’s notch)

Posterior cerebral artery compression (ipsi- or bilateral)

Duret hemorrhage

36
Q

Why do you experience ipsilateral 3rd nerve compresion in uncal hernation?

A

the tentorium is firmly attached to the skull and taut. When the midbrain is pushed down from above it is pushed against the tentorium compressing the 3rd nerve.

37
Q

Why is there pupillary dialtion in uncal herniation?

A

Pupillary constrictor fibers are located on surface of 3rd nerve

38
Q

What is Kernohans notch (seen in uncal hernation)

A

With compression of the midbrain due to herniation from above the opposite cerebral penduncle is pushed against the opposite free edge of the tentorium

Causes weakness and a Babinski sign ipsilateral to the cerebral hemispheric lesion (because of crossing of corticospinal tracts in distal medulla)

39
Q

Fatal brainstem hemorrhage

Secondary to progression of uncal herniation and resultant tearing of vessels in midbrain/pons

A

Duret hemorrhage

40
Q

– Symmetric expansion of supratentorial contents into posterior fossa or

– Expanding mass lesion in posterior fossa

A

Cerebellar tonsillar herniation

Caudal cerebellar structures (“tonsils”) attempt to escape through the foramen magnum

41
Q

Consequence of cerebellar tonsilar herniation

A

Medullary compression results in cardiorespiratory arrest

42
Q

An 19 yo F presents to the ER with complaint of fever and headache. Her family is with her. She is home on Spring Break vacation from college, but the family feels that she is not acting like herself. She was feeling sick since she got home yesterday with headache, fever, chills, nausea and vomiting. Her mom has given her Tylenol for pain and her fever with only mild improvement in her symptoms. The patient is fully clothed in winter attire, but is shaking and complaining of feeling ‘cold’.

Lives with her roommate in a dorm at UW Madison ; Vitals: BP 95/60, HR 120, RR 24, Temp 102.4, Pulse Ox 99% room air , has Neck (Brudzinki and Kernig)

A

looks like meningitis

43
Q

What is the Brudzinski sign?

the Kernig sign?

A

Brudzinski: when you flex pts neck, they bring knees to chest

Kernigs: can’t extend pts leg at the knee when thigh is flexed dt stiffness of the hamstrings

44
Q

Cause of hyperacte meningitis

A

– Sparse inflammation, numerous organisms, congestion

– Meningococcalmeningitis

45
Q

Cause of Acute (2-7 days) menintigits - most common infection in CNS

A

often bacterial with hematogenous spread

46
Q

Cause of Subacute/chronic (> 1 week) meningitis

A

– Tuberculosis, syphilis (often brain parenchyma also affected)

– Lymphocytes, plasma cells, macrophages appear in exudate

47
Q

Cause of “Aseptic” meningits

A

(usually viral) - much less fulminant than bacterial meningitis & less severe symptoms
– Summer&early fall
– Lymphocytic infiltrate in meninges

48
Q

Characteristics of Neisseria

A

Gram negative diplococcus, aerobic

– Capsular polysaccharide biochemical structure determinesserogroup

• Six (of 13) capsular subgroups: cause almost all invasive meningococcal disease

49
Q

What are the virulence factors in Neisseria

A

capsule and endotoxin structures

50
Q

Trasnsmission of Neisseria

A

– 1-5% of exposed persons develop disease

– Transmission: direct contact with respiratory secretions or inhalation of respiratory droplets

  • Crowding/closecontactincreasetransmission
  • Disease occurs within 1 to 14 days of exposure and transmission
51
Q

What is the progression for Neisseria Meningitis

A

– Meningitis: 40-65%
– Meningococcemia with shock (20-30%)

• Progression from initial symptoms to death may be hours

52
Q

What is Meningococcemia

A

– Shock is dominant clinical picture

– Acute sudden-onset fever, malaise, weakness, cold extremities, pallor, leukocytosis or leukopenia, rash, headache, drowsiness, hypotension

• Rash: 40-80% cases

53
Q

What causes the rash seen with Neisseria Meningitidits

A

bacteria in capillaries invade through walls and incite inflammation and bleeding resulting in petechiae that may progress to ecchymoses and eventually ischemic necrosis

54
Q

What is Waterhouse-Friderichsen syndrome

A

massive bilateral hemorrhage into adrenal glands

55
Q

Dx for Meningitis

A

isolation of bacteria or of antigen/DNA in blood, CSF or other body fluid

56
Q

Disease seen in Neisseria Meningitidis

A

– Sudden-onset headache, fever, vomiting, myalgias, photophobia, irritability, agitation, drowsiness, meningeal signs (neck stiffness, Kernig’s or Brudzinski’s sign)

– With or without rash

– High concentration of organisms & inflammatory mediators in CSF.

57
Q

What do we see in the subarachnoid space in bacterial meningitidis

A

Exudate present, numerous polymorphonuclear leukocytes, in subarachnoid space

58
Q

Most common cause of Bacterial meningitidis in <3 months old

What do you tx with?

A

Strep agalactia, E. Coli, Listeria, S.Aureus

Ampicillin + Ceftriaxone OR cefotaxime

59
Q

Most common cause of Meningiditis 3mo-18 yrs

what do you tx it with?

A

Neisseria, S. PNeumonaie, S. Aureus, H.flu

Cefotaxime OR ceftriaxone PLUS Vancomyocin

60
Q

Most common cause of meningitis 18 yrs- 50 yrs

tx?

A

S. Pneumo, Neisseria, S. Aureus

Tx:

Ceftriaxone or Cefotaxime PLUS Vancomyocin

61
Q

Tx for meningitis over age 50

A

S. pneunomiae, Listeria, S. aureus, Gram negatives

Ceftriaxtone PLUS Ampicillin PLUC Vancomyocin

62
Q

Key points on transimission and prophylaxsis of Neisseria meningitidis

A

N. Meningiditis transmitted by exchange of respiratory and throat secretions (kissing, living in close quarters, exposed to patient secretions)

●Those caring for patients with suspected meningitis should wear mask with shield and gloves

●Exposed family/friends, health care workers at high risk should receive antibiotic prophylaxis

63
Q

Prophylaxsis recommendations in those exposed to N.Men

A

see table

Symptoms 2 (11 decks)

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