NR507 / NR 507 Week 8 Exam Q &amp; A (Latest 2024 / 2025): Advanced Pathophysiology &#8211; Chamberlain

This statement is true. Post-ictal phase of a seizure is characterized by confusion, unresponsiveness and muscle flaccidity.

False

Etiology of Seizures

Which of the following is an etiology of a seizure?

Meningitis.

Psychiatric disorders.

Which of the following is a characteristic of a focal seizure?

Can involve both brain hemispheres.

Usually involves one brain hemisphere.

The symptoms are generalized.

Patient will have both motor and sensory symptoms at the same time.

A focal seizure only involves on brain hemisphere.

This statement is true. Febrile seizures are most common in children ages 6 months to 5 years.

Seizure Development

Which of the following electrolyte abnormality is involved in the initiation and propagation phase of seizure development?

The initiation and propagation phase of seizure development is impacted by hyponatremia.

Epilepsy vs Seizure

Convulsions

Epilepsy is a disorder that is due to one or more chronic conditions in the body. It is characterized by disturbed nerve cell activity in the brain. This leads to recurrent seizures. Seizures may occur due to brain trauma that leads to disturbed and uncontrolled nerve activity in the brain. It is important to differentiate between epilepsy and seizure.

Seizure is a condition that occurs due to excessive and uncontrolled neuronal activity in the brain. The uncontrolled neuron activity can be generalized or localized to one area of the brain. For example, it can be localized just to the area that perceives the touch sensation. Whether it is generalized or localized, the excessive neuronal activity lead to the seizure. The type of seizure will depend on the area of the brain affected.

Mechanisms of Seizure Development

Normally there exists a balance between the excitation and inhibition of neurons in the CNS. Neuronal activity is regulated by acetylcholine (ACH) and gamma-Aminobutyric acid (GABA). Neurons are synchronously active at the same time when they are not supposed to be. The term active denotes neuron firing where they are sending electrical signals from neuron to neuron. A microscope view of a neuron will demonstrate that each electrical signal that passes through it are just ions floating in and out through protein channels (see diagram below). The ion flow is controlled through neurotransmitters. Neurotransmitters bind to the receptors to tell the cell to either open the ion channels to relay the chemical message (excitatory neurotransmitters) or close the ion channels to inhibit the electrical message (inhibitory neurotransmitters).

Phases of seizures

Phases of Seizures
During a seizure, clusters of neurons in the brain become temporarily impaired. Seizures develop in a group of neurons when there is hyperexcitability and usually happens in two phases:
Initiation phase: Some neurons become hyperexcited and start to have excess neuron discharges. One of the most important reasons relates to the body’s sodium level as in the case of hyponatremia.
Propagation phase: Normally the neurons that have neuronal discharges are surround by a zone of inhibitory neurons called the zone of hyperpolarization. This zone prevents the spread of excessive neuron discharges to other parts of the brain. But due to some abnormality in the brain, as in the case of decreased sodium levels, the zone of hyperpolarization gets depolarized that allows the spread of neurons to other parts of the brain.
In the diagram below, the electrical activity in the normal brain is displayed. Seizures can be partial or generalized in terms of the extent of the neuronal discharges. In a partial seizure, a portion of the brain is involved. During a generalized seizure, the neuronal discharge encompasses the entire cerebral cortex.

Seizure Etiology

This seizure is most common in children. It is caused by a genetic abnormality. They are characterized by sudden and brief loss of consciousness without muscle tone and last for only a few seconds. There is no associated post-ictal confusion.

Absent Seizures

This seizure is characterized by unconsciousness and muscle rigidity.

Tonic Seizures

There is wide-spread and uncontrolled neuron activity in the entire cerebral cortex. These occur in 10% of patients who have epilepsy. There is excessive neuronal discharge in the motor nerves through the brain.

Generalized tonic-clonic seizures:

This seizure is characterized by muscle spasms.

Clonic Seizures

Post-Ictal Phase

The post-ictal phase of a seizure can last up to two hours.

An individual having a focal seizure without dyscognitive features will:

Not be able to interact with the environment

Have gradual loss of consciousness

Have no impairment of consciousness.

Lose cognitive ability momentarily

A lack of dyscognitive features will have no impairment of consciousness.

Febrile Seizures

Antiseizure medication is the first line treatment for a febrile seizure.

what are the phases of tonic-clonic seizure

False

false

Tonic-clonic phase (lasts 10-20 seconds): Due to the excessive discharge of neurons in the motor nerves that results in:
The muscles of the body become contracted. without any relaxation.
Loss of consciousness.
Ictal cry. This is a typical sound produced by the tonic contractions of the laryngeal muscles and muscles of expiration.
Respiratory impairment that results in cyanosis.
Tonic contraction of the jaw muscles that can cause tongue biting.
Increased sympathetic activity. This will cause increased heart rate and blood pressure

Tension Headache

Which of the following is characteristic of a tension headache?

Is the most common type of headache

Is limited to one side of the face

Can be the worst headache experienced

Has associated symptoms

Tension headache is the most common type of headache.

The symptoms of the aural phase of a migraine headache correspond directly to the movement of the cortico-spreading depression across the cerebral cortex.
True
False

This statement is true. The symptoms of the aural phase of a migraine headache correspond directly to the movement of the cortico-spreading depression across the cerebral cortex.

Pharmacological management of a tension headache involves the use of opioids during acute headache
True
False

Simple analgesics and Non-steroidal anti-inflammatory drugs (NSAIDS) are commonly used for a tension headache.

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Types of primary headaches

migraine, tension type, cluster, sinus

Secondary Headaches

Secondary headaches are a result of serious underlying diseases. Secondary headaches will consist of warning signs and symptoms. These most often occur in individuals >50 years of age. It is often described as being “the worst headache of my life”. It also has the maximum intensity at onset (thunderclap headache). It may also be triggered or worsened by exertion (subarachnoid hemorrhage). Other concerns include decreased level of consciousness, fever, seizure, present concurrently with infection, malignancy, pregnancy, thrombotic therapy or ophthalmological findings (papilledema). You can remember these by the acronym SNOOP:

Primary vs secondary headaches

Cluster headaches are a group of idiopathic headaches that are associated with trigeminal neuralgia
True
False

true

Associated symptoms of a cluster headache include:
Nausea and vomiting
Lateral neck pain
Runny nose, eye redness and tearing
Sensitivity to noise

Runny nose, eye redness and tearing are associated with cluster headaches.

Which of the following interventions are used in the treatment of a migraine headache?
Non-steroidal anti-inflammatory drugs (NSAIDS) or Aspirin
Antiemetic medication
Hydration
All of the above

The facial nerve plays a role in taste sensation in the anterior two-thirds of the tongue.
True
False

This statement is true. The facial nerve plays a role in taste sensation in the anterior two-thirds of the tongue.

Which of the following are signs and symptoms of Bell’s Palsy?
Prominent nasolabial fold
Increased taste sensation on the anterior two-thirds of the tongue
Drooping mouth and eyelid
All of the above

Drooping mouth and eyelid are characteristics signs and symptoms of Bell’s Palsy.

Bell’s Palsy is caused by damage to the trigeminal nerve
True
False

It is caused by damage to the 7th cranial nerve (facial nerve).

The trigeminal nerve (5th cranial nerve) has a motor component and lacks a sensory component
True
False

The trigeminal nerve has both a motor and sensory component.

Bell Palsy

Bell’s palsy involves weakness or paralysis of the muscles on one side of the face that is caused by damage to the 7th cranial nerve (facial nerve). The underlying cause of cranial nerve damage is idiopathic. When there is facial nerve paralysis from a known cause (stroke, tumor, trauma), it is not considered a Bell’s palsy. Peripheral nerves that emerge from the brain and brain stem are called cranial nerves. Their anatomical location is shown in the diagram below:

Symptoms of bell palsy

Absence of a nasolabial fold (runs from the side of the nose to the corner of the mouth)
Drooping eyelid
Drooping mouth
Dryness of the affected eye or mouth
Hypersensitivity to loud noises
Loss of taste sensation on anterior two-thirds of the tongue.

trigeminal neuralgia

inflammation of the fifth cranial nerve characterized by sudden, intense, brief attacks of sharp pain on one side of the face.
The trigeminal nerve is the fifth cranial nerve. It originates from the brain and branches into the ophthalmic branch,maxillary branch, and mandibular branch

Treatment of trigeminal neuralgia involves the use of anticonvulsant medication.
True
False

Bell’s palsy involves an upper motor neuron lesion (False)-
True
False

Bell’s palsy involves a lower motor neuron lesion.

Which of the following are characteristic of trigeminal nerve pain?
Often attacks suddenly and is intermittent
Pain can be incapacitating
Pain is described as sharp and stabbing
All of the above

Which of the following organisms are the most common causes of bacterial meningitis in newborns?
Streptococci pneumoniae
Group B streptococci
Cryptococcus
Varicella zoster

Group B streptococci are the most common bacteria causing bacterial meningitis in newborn.

The ability for the bacteria that causes meningitis to exit the primary infection site to enter the meninges is based on the organism’s virulent factors which include:
Colonization
Immune Evasion
Meningeal invasion
All of the above

All affect the virulence of the bacteria.

The cells responsible for producing cerebrospinal fluid (CSF) in the ventricle cavity are:
Ependymal cells
Synaptic cells
Glial cells
Nerve cells

The epidymal cells are responsible for producing CSF.

The basement membrane of the blood-brain barrier is surrounded by astrocytes (glial cells).
True
False

This statement is true. The basement membrane of the blood-brain barrier is surrounded by astrocytes (glial cells).

Meningitis

Meningitis is inflammation of the meninges. The meninges are the layers that surround and protect the brain. It can be caused by either a bacteria, virus or fungus

Bacterial Meningitis

Newborns: Group B streptococci; E. Coli; Listeria Monocytogenes

Children and Teens: Neisseria Meningitidis; Streptococcus Pneumoniae

Streptococcus Pneumoniae; Listeria Monocytogenes

viral meningitis

More common:Enteroviruses, Herpes simplex, HIV

Less common: Mumps, varicella zoster, lymphocytic choriomeningitis

Fungal meningitis

Affects immunocompromised:

Cryptococcus

Coccidioides genuses

Tubercular Meningitis: Mycobacterium tuberculosis

Parasitic Meningitis:P. Falciparum

Pathophysiology of Meningitis

In bacterial meningitis, the bacteria from the primary source allow it to enter the meninges based on the its virulent factors.:
Colonization: the bacteria’s ability to colonize the area. For example, the bacteria streptococcus pneumoniae can break down the hosts’ antibodies using IgA proteins which breaks down the mucosal antibody IgA. This allows bacteria to colonize the area. Some bacteria also have pili or fimbriae that allows them to attach to the host’s epithelium and invade the area. At this point, the bacteria cause the infection. We can say that this is the primary infection, whether it is pneumonia or sinusitis. Some bacteria have virulent factors or mechanisms that allow them to invade.
Immune evasion: some bacteria have virulent factors or mechanisms that allow them to evade the immune system. For example, the bacteria group B streptococcus and streptococcus pneumoniae have a capsule that allow it to evade macrophages as well as complement factors. The bacteria can enter the blood stream that causes bacteremia allowing it to travel towards the brain. This is known as hematogenous spread. It is important to know that the bacteria can invade the meninges directly from sinusitis, pneumonia or it can go through the cerebrospinal fluid.
Meningeal invasion: Let’s focus on the cerebral spinal fluid (CSF). The CSF is produced in the brain by the lateral ventricle and provides nourishment for the brain tissues. After production, it flows to the third ventricles then to the fourth ventricle. From the fourth ventricle it enters the subarachnoid space. From the subarachnoid space, it will go through arachnoid granulation and enter the venous sinus. The venous sinus are the big veins that transport the blood back to the heart.
The brain is protected by the blood-brain barrier which is a semi-permeable membrane barrier that separates circulation from the brain and prevents substances from getting inside the brain. Blood vessels are composed of endothelial cells. The endothelial cells are surrounded by the basement membrane. The basement membrane is surrounded by astrocytes (glial cells). These are the brain’s supporting cells. This formation only allows certain things to pass through to the brain. The blood brain barrier allows glucose and oxygen to get inside the brain.

Arachnoid Space
Let’s focus even further into the arachnoid space. The dura mater is located below the skull. The arachnoid membrane is located below the dura mater followed by the arachnoid space.

Image: Arachnoid Space
Let's focus even further into the arachnoid space. The dura mater is located below the skull. The arachnoid membrane is located below the dura mater followed by the arachnoid space.

Clinical Manifestations of Meningitis

There is a triad of classic meningitis symptoms:

Headache

Fever

Nuchal rigidity (neck stiffness)

Meningitis Diagnosis

Physical exam: Kernig’s sign Brudzinski’s sign
Lumbar puncture: if meningitis is suspected: Measures pressure Analyze CSF: WBCs, protein, and glucose
Polymerase Chain Reaction (PCR): can be used to identify specific causes of the meningitis (HIV, enteroviruses, HSV, or tuberculosis). If the specific cause is identified, a test for it may be used. For example: The Western Blot for Borrelia Burgdorferi Thin blood smear for malaria

meninigis treatment

Treatment

The treatment of meningitis depends on the underlying cause.

Bacterial: Steroids followed by antibiotics to prevent massive injury the leptomeninges from the inflammation that can be caused as the antibiotics destroy the bacteria.

In general, drug treatments using antivirals, antibiotics, antifungals and antiparasitic drugs are aimed at a specific cause of meningitis

Prevention: a vaccine can be given for some causes such as Neisseria meningitis, mumps and disseminated tuberculosis.

Prophylactic antibiotics: to avoid outbreaks of bacterial meningitis

Kernig’s sign

Kernig’s is performed by having the supine patient, with hips and knees flexed, extend the leg passively. pain upon extension is a positive sign

The Brudzinski’s sign

The Brudzinski’s sign is positive when passive forward flexion of the neck causes the patient to involuntarily raise his knees or hips in flexion.

The meninges are pain sensitive.
True
False

This statement is true. The meninges are pain sensitive.

Polymerase Chain Reaction

Polymerase Chain Reaction (PCR) test is used to differentiate between bacterial and viral meningitis

It is used to establish the cause of the meningitis.

False

Which of the following is one of the layers of the meninges?
Dura mater
Pia
Arachnoid membrane
All of the above

Which of the following are part of the triad of classic symptoms of meningitis?
Hypothermia
Ptosis
Neck flaccidity
Nuchal rigidity

Nuchal rigidity is the only symptom listed that is part of the triad of classic symptoms of meningitis.

Subclavian Steal Syndrome

Subclavian steal syndrome is characterized by:

Hemianopia.

Symptomatic at rest and with activity at the onset of subclavian artery blockage.

Pain in the occipital area.

Asymptomatic until the patient engages in arm movement.

Individuals with subclavian steal syndrome will be asymptomatic until they engage in arm movement.

In atherosclerosis of the vertebral arteries, that patient will report pain in neck or occipital area
True
False

This statement is true. In atherosclerosis of the vertebral arteries, that patient will report pain in neck or occipital area.

Choose the following that are part of the posterior cerebral circulation:
Posterior Inferior cerebellar artery (PICA)
Vertebral arteries
Middle cerebral artery
Posterior cerebral artery
Anterior cerebral artery
Superior cerebellar artery
Basilar artery

Parts of the posterior cerebral circulation include:
Vertebral arteries
Posterior Inferior cerebellar artery (PICA)
Basilar artery
Superior cerebellar artery
Posterior cerebral artery

vessel involvement

Anterior Cerebral Artery

Lower extremities: (leg and foot)

Slight upper extremity involvement

Middle Cerebral Artery

Upper extremities and face

Decrease in conjugate gaze

Homonymous hemianopia (decreased vision on one half of both sides)

Speech (motor): aphasia

Transient Ischemic Attack (TIA)

A transient ischemic attack (TIA) is an episode of neurological dysfunction. If an infarction does not occur, it is a TIA (reversible ischemia). If an infarction does occur, then it is a stroke (irreversible infarct). A TIA increases the risk for a future stroke. It can be associated with sudden onsets of syncope, amnesia or seizures. Risk factors for a TIA include:
Hypertension
Atherosclerosis
Diabetes mellitus
Obesity
Hypercoagulable states
Amyloid angiopathy
Atrial fibrillation
Myocardial infarction
Previous TIA
Valvular disease

TIA pathophysiology

Anterior Circulation: the first artery encountered in the anterior circulation is the internal carotid artery. There is a branch from the internal carotid artery to the ophthalmic artery that innervates the eyeball. Sometimes when there is a TIA involving the ophthalmic artery, the patient may present with ocular blindness. The internal carotid artery continues to the Circle of Willis and branches into the anterior towards the brain between the two hemispheres. It also splits into the middle cerebral artery on the side of the brain

Posterior Circulation: The posterior circulation: starts at the vertebral arteries and continues into the back of the brain.

Vertebral arteries (two): posterior circulation starts here and continues to the back of the brain

Posterior Inferior cerebellar artery (PICA): it supplies the posterior brain and inferior cerebellum. Blood then circulates to the dura mater and eventually becomes:

Basilar artery: the two vertebral arteries converge to form one basilar artery.

Superior cerebellar artery

Posterior cerebral artery

CVA

Cerebrovascular Accident (CVA)
Ischemic stroke: is due to decreased blood flow to the brain due to an embolus that may originate from:
Cardiogenic: it begins in the heart. The embolus can break and travel into the aorta to the carotid artery and continue moving on into either the anterior cerebral artery or the middle cerebral artery.

Clinical Manifestations of Ischemic Stroke

Anterior circulation:

Internal carotid artery: an atherosclerotic plaque is commonly involved that leads to a decreased blood flow to the area. The patient is typically asymptomatic because the Circle of Willis can compensate for diminished blood flow for the lack of blood flow on one side. To exhibit symptoms, both the carotid arteries would have to exhibit diminished blood flow. However, the patient may present with ocular blindness because of the disruption of blood flow to the ophthalmic artery. Clinically, there will be a high-pitched carotid bruit identified on exam.

anterior cerebral artery

Anterior Cerebral Artery

Lower extremities: (leg and foot)

Slight upper extremity involvement

Abulia: lack of will: due to some frontal lobe involvement

Urinary incontinence

Middle cerebral artery

Upper extremities and face

Decrease in conjugate gaze

Homonymous hemianopia (decreased vision on one half of both sides)

Dominant side symptoms

Speech (motor): aphasia

Non-dominant side symptoms:

Neglect

Anosognosia

Posterior Circulation

The posterior circulation supplies the entire brainstem, cerebellum and spine. There are two vertebral arteries that eventually form the single basilar artery. Before branching out to form the basilar artery it gives branch to the posterior cerebral artery shown in the diagram below. The area of the brain supplied by the posterior cerebral artery is shaded in blue in the second diagram. The anterior inferior cerebellar artery and then splits into the superior cerebellar arteries. This comprises the entire brainstem and is controlled by the posterior circulation.

Vertebral Arteries

Extracranial: Subclavian steal syndrome: as you locate the subclavian artery below note that with this syndrome, there will be a blockage in the subclavian artery. Also note that one of the first branches of the subclavian artery is the vertebral artery that eventually come together to form the basilar artery. When there is a subclavian artery blockage, the patient will be asymptomatic. But when the individual begins to use their arms (e.g. during exercise), there is more blood flow required and instead of traveling up, travels down. The patient will experience dizziness, diplopia due to decreased circulation to the posterior cerebral artery. They may have staggering due to lack of blood flow to the cerebellum. Atherosclerosis of the vertebral arteries: the patient will report pain in the neck or in the occipital area. There may also be some minor complaints of dizziness and hemianopia as the severity increases. A bruit may be heard in the supraclavicular region or the posterior cervical muscles since the vertebral artery goes through the vertebrae.

Lateral Medullary Syndrome (Sensory Symptoms)

Wallenberg syndrome: involves the posterior-inferior cerebellar artery

e.g. if lesion is on the left brain

Symptoms: face symptoms will be ipsilateral to the lesion. In the rest of the body, symptoms will be on the right side (contralateral):

Face symptoms: pain and numbness related to the trigeminal nerve (5th cranial nerve); nystagmus; diplopia; vertigo; nausea and vomiting

Body symptoms: Decreased pain and temperature sensation in the lower extremities due to major effect on spinothalamic area.

Dysphagia*

Hoarseness*

Decreased gag reflex*

*9th and 10th cranial nerves

Medial Medullary Syndrome (Motor Symptoms)

Involves the anterior spinal artery
e.g. If lesion is on the left brain
Symptoms: face symptoms will be ipsilateral to lesion. In the rest of the body, symptoms will be on the right side (contralateral)
Face symptoms: tongue paralysis (12th cranial nerve)
Body symptoms: paralysis of the entire body on affected side and decreased proprioception

Basilar Artery and Midbrain Syndrome

Basilar Artery Syndrome

Affects the pons area of the brain. Locked in syndrome indicates that the patient cannot move or talk, but their sensory functions are intact. The only intact motor movement is eye movement.

Image: Basilar Artery and Midbrain Syndrome

Midbrain syndrome (Weber’s syndrome)

Affects 3rd cranial nerve, the ocular motor nerve (ptosis); eye is also down and out as shown in the individual’s right eye below:

Treatment of TIA and Ischemic Stroke

Management of the patient will occur in the acute care setting. Perform stabilizing measures if necessary: Check airway, breathing and circulation Check vital signs Obtain blood glucose level Arterial blood gas
Obtain CT scan without contrast to rule out hemorrhagic stroke
If hemorrhagic stroke is ruled out, the individual would receive thrombolytic therapy or thrombectomy
To identify the cause of the stroke: Duplex ultrasound and doppler of cerebral arteries MRI-to visual smaller cerebral arteries Cardiac evaluation to identify valve disorders, thrombus ECG and holter monitor (to identify A-fib)
Our next focus is on the hemorrhagic stroke which requires a different type of management from that of the ischemic stroke.

Hemorrhagic Stroke

Hemorrhagic stroke is caused by a rupture of a blood vessel that leads to a hemorrhage. It accounts for approximately 10-15% of all strokes. Cause can be related to long-standing hypertension or venous malformation. The location of the hemorrhage may be inside the brain parenchyma (intracerebral) or in the subarachnoid or subdural spaces.

Etiology

Primary hypertensive hemorrhage: Uncontrolled hypertension weakens the arterial wall. The most common site is the basal ganglia. There will be dilation of the arterial wall

Secondary to ruptured arteriovenous malformation (AVM) or aneurysm

Subdural hematoma due to trauma

Pathophysiology

A hemorrhage involves a mass of formed blood. Brain tissue that is adjacent to the hemorrhage becomes compressed which leads to ischemia, edema (due to neutrophil activity in the area) and increased intracranial pressure. The hemorrhage will typically resolve through reabsorption. The macrophages and astrocytes play a role in clearing the blood from the area followed by formation of a cavity surrounded by a thick glial scar. A massive hemorrhage may be fatal.

Clinical Manifestations of Hemorrhagic Stroke

The clinical manifestations are like an ischemic stroke and depend on the location and size of the bleed. An individual with an intracranial hemorrhage due to a leaking or ruptured aneurysm may present with one of the three sets of symptoms below:
“Worst headache of my life”-excruciating generalized headache with onset of immediate unresponsive state
Onset of headache with no loss of consciousness
Sudden onset of unconsciousness
Typically, there may be no local signs if the hemorrhage is confined to the subarachnoid space. If it is not confined, bleeding spreads into the brain tissue to cause hemiparesis/paralysis, aphasia or homonymous hemianopsia.
The role of the NP may involve recognizing the warning signs of an impending rupture of the aneurysm which include transient unilateral weakness, numbness and tingling. There may also be transient aphasia. Prompt referral to the emergency department and a neurologist is indicated. The NP should also be aware that the American Heart Association/American Stroke Association provided clinical guidelines for the management of intracerebral hemorrhage.

Diagnosis of Hemorrhagic Stroke

The following factors will guide the diagnosis of a hemorrhagic stroke:
Health history
Clinical presentation
Laboratory tests
Neurological imaging procedures CT and MRI
First, treatment must be initiated within 3-4 hours of the onset of symptoms in order to reverse brain ischemia. This further underscores the need for the NP to perform a thorough health history and symptom analysis. If signs point to a hemorrhagic stroke, then again, prompt referral is necessary.

Treatment of Hemorrhagic Stroke

Reduction or cessation of the bleeding
Controlling cerebral edema to prevent increased intracranial pressure
Prevention of the development of a future bleed
Prevention of vasospasm
Prevention and/or control of seizures

A hemorrhagic stroke confined to the subarachnoid space will present with no local signs.
True
False

This statement is true. A hemorrhagic stroke confined to the subarachnoid space will present with no local signs.

Which of the following relate to medial medullary syndrome?
Facial symptoms ipsilateral to the lesion
Body symptoms contralateral to the lesion
Decreased proprioception
All of the above

The onset of hemiparesis, aphasia or homonymous hemianopsia in a hemorrhagic stroke indicates that the bleed is not confined to the subarachnoid space.
True
False

This statement is true. The onset of hemiparesis, aphasia or homonymous hemianopsia in a hemorrhagic stroke indicates that the bleed is not confined to the subarachnoid space.

An individual with an intracranial hemorrhage due to a leaking or ruptured aneurysm may present with:
Worst headache of their life
Onset of headache with no loss of consciousness
Sudden onset of unconsciousness
All of the above

Which of the following microbes plays a role in the development of rosacea?
Demodex mites
H. pylori
Staphylococcal organisms
All of the above

All play a role in the development of rosacea.

Rosacea is characterized by an itchy facial rash that:
Is alleviated with the use of topical creams
Is typically related to starting a new medication
Is contagious
Stings and burns

Rosacea is characterized by stinging and burning facial rash. None of the other choices are true of rosacea.

Factors that can trigger rosacea include:

Exposure to extreme temperatures
Strenuous exercise
Severe sunburn
Stress and anxiety
Cold wind
Hot and spicy foods
Alcohol ingestion
Foods and beverages that contain caffeine
Other triggering factors include:
Medications
H. pylori
Demodex mites
Presence of cathelicidin

Erythematotelangiectatic rosacea is characterized by persistent central/facial erythema and telangiectasias.
True or False

This statement is true. Erythematotelangiectatic rosacea is characterized by persistent central/facial erythema and telangiectasias.

Pathophysiology of Rosacea

Although the exact cause of rosacea is unknown, there are several theories that may help to explain its underlying causes:
Aberrant innate immune system: Activation of the innate immune system causes the release of cytokines and antimicrobial molecules such as peptide cathelicidin. They also envelope viruses and fungi. In rosacea, the peptide cathelicidin is unregulated and therefore, leads to an over response of the innate immune system.
Ultraviolet radiation: this is thought to trigger angiogenesis and increase production of reactive oxygen species that leads to upregulation of matrix metalloproteinases (MMPs) that result is damage to the blood vessels and dermal matrix. MMPs are a group of enzymes responsible for the breakdown of most extracellular proteins during organogenesis, growth and normal tissue turnover.
Vascular changes: there is increased blood flow in skin with associated flushing with rosacea that may be the result of an elevated expression of vascular endothelial growth factor (VEGF) and lymphatic endothelial markers that suggests stimulation of blood vascular and lymphatic endothelial cells.
Epidermal barrier dysfunction: there is increased epidermal water loss which allows for the skin to become irritated easily
Neurogenic inflammation: the sensory nerves release mediators at the site of inflammation that results in vasodilation and loss of plasma proteins. Inflammatory cells are also recruited to the area. This mechanism is not well-understood.
Microbes: Demodex mites: part of normal skin but are found in abundance in patients with rosacea. Infestation is associated with infiltration of CD4+ helper cells H. pylori Staphylococcal organisms: is thought to play a role in the development of rosacea but not exactly clear about how.

Ultraviolet radiation contributes to the development of rosacea because:
Causes the production of peptide cathelicidin
Increases the production of matrix metalloproteinases (MMPs)
It stops the effects of angiogenesis
Causes sensory nerves to release chemical mediators at the site of inflammation

Increases the production of matrix metalloproteinases (MMPs)

Which of the following is part of the pathogenesis of acne vulgaris?
Infection with staph. Aureus
Excess sebum production
Follicular hypoproliferation
All of the above

Excess sebum production is part of the pathogenesis of acne vulgaris.

Which of factors below can worsen acne?
Increased androgen levels
Stress
Family history
All of the above

All

An example of a closed comedone lesion is a blackhead
True
False

(False)- it is an example of a whitehead.

What drugs can exacerbate acne?

corticosteriods, anticunvulsants, barbituates, androgenic steroids.

The skin lesions of acne may be classified as non-inflammatory lesions and inflammatory lesions.
True
False

This statement is true. The skin lesions of acne may be classified as non-inflammatory lesions and inflammatory lesions.

Acne pathophysiology

Pathophysiology

There are several components in the pathogenesis of acne vulgaris: Infection with propionibacterium acnes: Gram-positive bacteria

Is also known as cutibacterium acnes

Follicular hyperproliferation

Excess sebum production: sebum is skin oil

Inflammation

Drugs that exacerbate acne

Some drugs may also exacerbate acne:
Phenytoin
Isoniazid
Lithium
Glucocorticoids
Cyclosporin
Disulfiram
Azothioprine
EGFR inhibitors

Associated conditions that can cause acne include polycystic ovary syndrome and tumors of the adrenal glands and ovaries.
True
False

Blackheads are open pores that contain oxidized lipids.
True
False