Exam 4 (Critical neuro, organ transplants, and pituitary/adrenal) Flashcards
TTrue or false
Transient ischemic attacks (TIA) or a reversible ischemic neurologic deficit (RIND) may be warning signs of impending ischemic stroke.
True
TIA vs. RIND
**Both warning signs cause transient focal neurologic dysfunction resulting from a brief interruption in cerebral blood flow from cerebral vasospasm or arterial hypertension.
• A TIA lasts a few minutes to less than 24 hours and RIND lasts longer than 24 hours.
• Both TIAs and RINDs may damage the brain tissue with repeated insults.
True or false
A stroke is caused by a change in the normal blood supply to the brain.
True
True or false
Like that of many health problems, the causes of stroke are likely a combination of genetic and environmental risk factors.
True
Describe an occlusive stroke
In an occlusive stroke, arterial blockage or narrowing cause ischemia in the brain tissue ultimately leading to infarction of neurons in the involved area of the brain.
True or false
Most strokes are ischemic, caused by the occlusion of a cerebral artery by either a thrombus or an embolus.
True
Describe a hemmorhagic stroke
Hemorrhagic stroke involves bleeding within or around the brain.
• Intracerebral hemorrhage describes bleeding into the brain tissue generally resulting from severe hypertension.
True or false
Document the history of the stroke’s onset, as ischemic strokes often occur during sleep, whereas hemorrhagic strokes tend to occur during activity.
True
True or false
For patients having occlusive strokes, the standard of practice is to start two IV lines with nondextrose, isotonic saline.
False,
For patients having ischemic strokes, the standard of practice is to start two IV lines with nondextrose, isotonic saline.
What are two main treatments for patients with an acute ischemic stroke
The two major treatment modalities for patients with acute ischemic stroke include fibrinolytic therapy and endovascular interventions.
What is the most important factor in deciding to give rtPA?
The most important factor in whether or not to give rtPA is the time last seen normal (LSN).
- **The standard window for eligibility is 3 hours from time LSN.
- **In 2009, the American Stroke Association recommended an expanded time interval from 3 to 4.5 hours for patients unless they fall into the categories of age older than 80, anticoagulation with an international normalized ratio less than or equal to 1.7, baseline National Institutes of Health Stroke Scale greater than 25, or history of both stroke and diabetes.
What is an aneurysm?
- An aneurysm is an abnormal ballooning or blister along a normal artery.
- A congenital aneurysm is a defect in the media and elastica of the vessel wall.
- A dissecting aneurysm may occur following trauma or from plaque formation.
Diagnosing a stroke
- Clinical history and presentation usually are sufficient to diagnose a stroke.
- Computed tomography and angiography assist in the differential diagnosis.
True or false
Patients are most at risk for the serious complication of increased ICP resulting from edema during the first 72 hours after onset of the stroke.
True
Traumatic brain injury: open vs closed
- Primary brain damage occurs at the time of injury and results from the physical stress within the brain tissue caused by open or closed trauma.
- Open head injury occurs with a skull fracture or piercing by a penetrating object.
- A closed head injury is the result of blunt trauma, is more serious, and the damage to brain tissue depends on the degree and mechanisms of injury.
What are common signs of a TBI
The most common responses are hypotension, hypoxia, ischemia, and edema.
True or false
Increased ICP is the leading cause of death in patients hospitalized with brain injury.
True
What is cushings triad?
Cushing’s triad, a classic yet late sign of increased ICP, is manifested by severe hypertension with a widened pulse pressure and bradycardia.
What is uncal herniation?
Uncal herniation, shifting of one or both areas of the temporal lobe, is one of the most clinically significant changes because it is life threatening.
Brain abcess
A brain abscess is a purulent infection of the brain in which pus forms in the extradural, subdural, or intracerebral area of the brain most often from bacteria.
• The clinical manifestations of a brain abscess begin slowly and may include headache, fever, and neurologic deficits or nonspecific signs and symptoms.
• Computed tomography scanning determines the presence of cerebritis, hydrocephalus, or a midline shift.
• Magnetic resonance imaging detects the presence of an abscess early in the course.
• An EEG can localize the lesion in most cases, and high-voltage, slow-wave activity or electrocerebral silence may be noted in the area of the abscess.
• The mainstay of management for patients with brain abscess is systemic antibiotic therapy.
What is the first sign of ICP?
Be aware that the first sign of increased ICP is a decrease in level of consciousness.
Functions of the brainstem
The brainstem controls functions such as breathing, blood pressure, body temperature, heart rhythms, hunger and thirst, and sleep patterns. It connects the forebrain and the cerebellum with the spinal cord. All the nerve fibers leaving the brain to go to the limbs and trunk of the body pass through here.
How does the blood leave the brain if it doesn’t have a venous system ?
-Dural sinuses in the brain, blood just drains down through them into the jugular veins and into the rest of the body
Veins in the head are very thin and only can drain small amounts of blood
True or false
When people get a head injury they bleed so easliy because those venous wallls are so thin and the blood drains slower
True
What part of the brain is the primary area for blood flow?
- *Cicrle of willis is the primary area for blood flow ( i.e. like the aorta)
- Most of the aneurysm arrive in the circle of wilis
- Carotid artery disease means circle of wilis isn’t getting enough blood flow
- 750 ml per min of blood (the brain gets)
- The brain gets 750 ml which is 15-20% of the resting cardiac output
Blood brain barrier
Physiological barrier between brain and tissues
**Have tight junctures instead of pores therfore only veryyyyyy small things can get through
Specific filtering process, there has to be active transport for anything to get through
Because of that most drugs cant get through and affect the brain
Size of the particle, Lipid solubility , chemical dissociation, and protein binding are all factors
Drugs that are lipid soluble or undissociated at body pH will rapidly enter the brain and cerebrospinal fluid ( i.e. water, O2, CO2. gases, glucose, lipid soluble)
Anatomy of the meninges
Dura on outside
Arachnoid middle like spider web
Pia on the inside
What is the falx cerebra?
Falx cerebri: double fold of dura that descends into the brain, longitudinally splitting the two hemispheres
Tentorium: tent like thing, double fold of dura covers the upper part of the cerebellum, supports the occipital lobe
Glascow coma scale
KNOW the scale in book on test
Pupillary Response Respiratory Status Respiratory Patterns Blood Gas Alterations Cardiovascular Status Temperature
Opiates for neuro
Opiates for neuro problems: Diluadid, morphine, codeine
-can masks symptoms, like to get a baseline first…could diminsh RR, bradycardia, LOC, nausea
Benzos for neuro
Benzos: Propofol, lorazepam, midolzam, valium
BArbitiates for neuro
Barbiturates: Phentobarbital
Sympathothmimetic for neuro
Sympathothomimetic agents: dopamine, levothed, epinephrine, neo or phenylephrine, rocuronium
Lumbar punctures
Lumbar puncture: how do you position someone, is there ever a time when you would not go along with a lumbar puncture: yes when there is increased intracranial puncutre, why would you not…need to know on test
What is an angiography?
Angiography: need to know where the blockage or hemorrhage is, can dissolve it with clot busting drugs, within 6 hours
What is a PET scan?
Positron emission tomography ( PET scan): to see where the disease has progressed to, monitor stroke, alzehimers diseaese, seizures
MRI for neuro
Can take up to 24 hours for a bleed to show up on a ct scan
MRI can be used for : Lacunar stroke, cerebral tumor, changes in dementia, cerebral edema, dymylenating disease such as MS or ALS
What is a trancranial doppler used for?
Transcranial doppler: used to see if they are still spasming
ICP
The skull is a rigid compartment filled to capacity with essentially non-compressible contents Intracranial contents Brain matter: 80% Blood (intravascular): 10% Cerebrospinal fluid: 10%
14oo ml of brain matter
*150 of blood
*150 of CSF
Head roughly contains 1700 ml of stuff
Normal ICP range
The pressure exerted by the CSF within the ventricles.
A dynamic pressure that fluctuates in response to many factors.
Normal range is 0-15 mmHg.
Ideally the ICP is < 10 mmHg.
What is the Monro-Kellie Hypothesis?
The volume of the three components remains nearly constant.
If any one component increases in volume, another component must decrease, or the intracranial pressure (ICP) will rise.
This applies only to skulls that are fused.
IF brain matter becomes edematous then you have to decrease csf or blood volume or you will get ICP
True or false
Brain starts to atrophy over 40, therefore someone over 40 often has more room for ICP
True
Intracranial compliance
Compliance is a measure if the adaptive ability of the brain to maintain intracranial equilibrium in response to physiological and external challenges to that system
Compliance represents the ratio of change in volume to the resulting change in pressure.
Factors that impact intracranial compliance include:
Factors that impact compliance include:
Amount of volume increase
Time for accommodation
Size of intracranial compartments
Normal compensatory adaptations
- Rise in tissue volume
- Change in blood volume
- Change in CSF volume
What is the first sign of ICp?
Patient will get confused at first because they arent getting good perfusion
Cerebral blood flow
Autoregulation
Cerebral Perfusion Pressure (CPP)
CPP = MAP - ICP
What are the types of cerebral edema?
Vasogenic: increased permeability of the capillary walls (brain tumors, abcesses, cerebral ishemia are common causes)
Cytotoxic: Increase of fluid in the intracellualr space( SIDAH, water intoxication, reyes syndrome)
Interstitial: Movemnet of csf across ventricular wall ( Hydracephalous)
What is the gold standard for measuring ICP?
Intraventricular catheter is golden standard
What has the greatest risk for infection when measuring ICP?
Intraparenchymal fiberoptic catheter has the highest risk for infection
Ventricuostomy drainage system
Ventricuostomy drainage system most be level to the correct space usually the tragus of the ear or the inner/outer canthus of the eye. If its too low too much leaks out and your patient could herniate
Signs and symptoms of increased ICP
Altered level of consciousness (LOC) Alteration in vital signs Cushing’s Triad Alteration in ocular signs Alteration in motor function Posturing Headache Vomiting
What is cushings triad?
- Hypertension (progressively increasing systolic blood pressure)
- Bradycardia
- Widening pulse pressure (an increase in the difference between systolic and diastolic pressure over time)
Other signs of increased ICP
Alterations in ocular signs, motor function and posturing ON TEST!!!
Decaribrate arms out, dicorticate arms to the core across chest ( not good)
Temperature rises when posturing, extreme posturing can fracture bones
True or false
When ICP is increased, the pressure is transmitted to the venous system, resulting in decreased cerebral blood flow
True
MAnaging ICP
If you fill up vascular space patients wont spasm that’s why hypertonic saline is used
Mannitol: usuallyl only used in extreme circumstances/emergencies because mannitol dehydrates brains
Hyperventilation:
NEED TO KNOW BLOOD GASES FOR TEST
Positioning: raise head of bed, keep head in neutral position to help with venous drainage because drainage is passive
Barbituates are fat soluble: was it the barbituares or head injury that made them not breathe
Managing ICP cont..
- Hypertonic Saline
- Mannitol
- Hyperventilation
- Drainage of CSF
- Positioning
- Analgesia, Sedation
- NMB, Barbiturate Coma
- Seizure Management
- Temperature Management
Cerberal perfusion pressure
Normal range of CPP is 70-100 mm Hg.
CPP > 150 results in hyperemia.
CPP < 50 mm Hg results in ischemia.
CPP < 30 mm Hg is incompatible with life.
When the MAP equals the ICP, the CPP is zero. *At this point there is no cerebral blood flow.
Hormones from the anterior pituitary gland
Hormones secreted from the anterior pituitary gland regulate growth, metabolism, and sexual development.
Hormones from the posterior pituitary gland
The posterior pituitary gland secretes vasopressin, known as antidiuretic hormone.
True or false
A person with hypopituitarism has a deficiency of one or more anterior pituitary hormones, resulting in metabolic problems and sexual dysfunction.
True
What is hyperpituaitarism?
Hyperpituitarism is hormone oversecretion occurring with tumors or hyperplasia.
• The most common cause of hyperpituitarism is a pituitary adenoma, a benign tumor classified by size, invasiveness, and the hormone secreted.
Treating hyperpituitarism
Surgical removal of the pituitary gland and tumor, called hypophysectomy, is the most common treatment for hyperpituitarism.
True or false
Disorders of the posterior pituitary gland—the neurohypophysis—are related to a deficiency or excess of the hormone vasopressin.
True
What is DI?
Diabetes insipidus is a water metabolism problem caused by an antidiuretic hormone, ADH, deficiency.
What is SIADH?
The syndrome of inappropriate antidiuretic hormone is a problem in which vasopressin is secreted even when plasma osmolarity is low or normal.
Early manifestations of SIADH
The early manifestations of SIADH are related to water retention or GI disturbances.
Treating SIADH
Medical interventions for SIADH focus on restricting fluid intake, promoting the excretion of water, replacing lost sodium, and interfering with the action of ADH.
True or false
Acute adrenal insufficiency, or Addisonian crisis, is a life-threatening event in which the need for cortisol and aldosterone is greater than the available supply.
True
Acute adrenal insufficiency
Adrenal insufficiency, Addison’s disease, is classified as primary or secondary.
• Anorexia, nausea, vomiting, diarrhea, abdominal pain, and weight loss occur.
• Laboratory findings include low serum cortisol, low fasting blood glucose, low sodium, elevated potassium, and increased serum blood urea nitrogen levels.
What is cushings disease
Hypersecretion by the adrenal cortex results in hypercortisolism, called Cushing’s disease, hyperaldosteronism, or excessive androgen production.
Cushing’s disease causes problems with exaggerated actions of glucocorticoids which affect metabolism and all body systems to some degree.
What is the most common cause of bushings disease?
The most common cause of Cushing’s disease is a pituitary adenoma.
Anterior Pituitary
- Regulate growth
- GH
- Metabolic activity
- TSH
- ACTH
- Sexual development
- LH
- FSH
- Other
- MSH
- PRL
POsterior pituitary
Fluid & Electrolyte balance
Vasopressin (ADH)
What causes hypopituarism
Deficient anterior pituitary hormones
Primary vs secondary hypopituraism
Primary hypopituitarism – caused by pituitary gland dysfunction Pituitary tumors Hypophysectomy Brain irradiation Infection Metastatic cancer Trauma Secondary hypopituitarism – hypothalamus etiology Infection Trauma Brain tumor
Causes of hypopituitarism
Benign or malignant tumors Anorexia nervosa Shock or severe hypotension Head trauma Brain tumors or infection Sheehan’s syndrome postpartum hemorrhage
Intervnetions for hypopituarism
Interventions Hormone replacement therapy GH injection IM or transdermal androgens Estrogen and progesterone
What causes hyperpituitarism
- Hormone oversecretion
- Tumors or hyperplasia
- Neurologic symptoms
- Genetic considerations
Growth Hormone Gigantism Acromegaly PRL Galactorrhea Amenorrhea Infertility ACTH Cushing’s disease
PRL-secreting tumors most common in hyperpituitarism
True
Clinical manifestations of hyperpituitarism
Clinical manifestations ↑ GH Facial features Prognathism (lip, nose,brow ridge,lower jaw) Arthralgias (joint pain) Organomegaly (heart, lungs, liver) Hypertension Hyperglycemia Deepening voice
GH blocks the action of insulin, so hyperglycemia is common
Clinical manifestations of acromegaly
Clinical manifestations ↑ PRL Galactorrhea Amenorrhea ↓ libido Impotence Dyspareunia ↑ ACTH Cushingoid features
Interventions for acromegaly
Surgery Hypophysectomy ↓ hormone levels Relieve headache pain from tumor pressure Reverse changes in sexual function
Hypophysectomy: Postoperative Care
Neuro checks Elevate HOB Avoid coughing Nasal packing, “mustache dressing” Observe for nasal drainage Avoid activities that ↑ ICP Hormone replacement and glucocorticoids as needed.
Posterior Pituitary Disorders
Diabetes insipidus
- ADH deficiency
- Polyuria
- Dehydration
SIADH
- ADH excess
- Dilutional hyponatremia
- Hypervolemia
Symptoms of diabetes insidious
Dilute urine ↑urine output Polydipsia Hypotension Tachycardia Dehydration Hemoconcentration Dry mucous membranes
Symptoms of SIADH
Decreased urine o/p ↑ urine Na+ Hyponatremia serum Weight gain Non-pitting edema GI disturbances Neuro changes (confusion, seizures)
Treatment goals for diabetes insipidus
Control symptoms with drug therapy
Maintain adequate hydration
Treatment goals for SIADH
Restrict fluid intake Promote H2O excretion Replace sodium losses Prevent action of ADH Prevent injury
Interventions for diabetes inspidus
Chlorpropramid (Novo-
Propamide, Diabinese)
Intranasal or oral DDAVP (Desmopressin acetate--synthetic vasopressin)
Adequate hydration
IV fluids, Force Fluids
Daily weights
I/O
Lifelong vasopressinInterventions for SIADH
Fluid restriction Diuretics Check fluid overload Declomycin -antibiotic Hypertonic saline Daily weights I/O Assess neuro status
True or false
Administration of hypertonic saline in SIADH is to raise serum sodium levels
True
Adrenal insufficiency
Chronic insufficiency is also referred to as Addison’s Disease
Chronic insufficiency is also referred to as Addison’s Disease
Acute insufficiency is referred to Addisonian Crisis
A severe or total loss of mineralcorticoids and glucocorticoids
Symptoms of adrenal insufficiency
Clinical Manifestations ↑ ACTH Hypoglycemia Hyperkalemia Neurologic changes Lethargy Confusion
Pathophysiology of cushings
Pituitary tumor Adrenal tumor Excessive stimulation of ACTH Adrenocortical hyperplasia Excessive amounts of glucocorticoids Iatrogenic causes: administration of steroid therapy (Cushing’s Syndrome)
Symptoms of cushings syndrome
Central type obesity Buffalo hump Moon face Thin fragile skin Muscle wasting Hirsutism Hypertension (from water & sodium retention) Pink/purple stretch marks Emotional labile
Treatment goals for cushings
Reduce plasma cortisol levels
Remove tumors
Prevent complications
Restore normal or acceptable body appearance
MAngment for cushings
Drug Therapy
Periactin: reduce ACTH production
Metopirone: reduce cortisol levels
Pituitary tumors: hypophysectomy or radiation
Adrenal tumors: adrenalectomy
Iatrogenic causes: taper or stop steroids if possible
Glucocorticoid replacement therapy
Mineralcorticoids
Acutely critical for maintenance of life
Aldosterone is principle mineralcorticoid
Major target organ for aldosterone is the kidney
-Increases absorption of Na+
-Increases absorption of H2O
-Increases excretion of K+
Hyperaldostreonsim
Increased secretion of aldosterone results in mineralocorticoid excess.
Primary hyperaldosteronism (Conn’s syndrome) is a result of excessive secretion of aldosterone from one or both adrenal glands
Cause: adrenal adenoma
Pheochromocytoma
Tumors of the adrenal medulla that produce excess adrenaline
Can be deadly because of the severe elevation in BP it causes
Is the cause of high BP in a small percentage of clients with HTN
Is the one form of HTN that can be cured with surgery
Fatal if not detected and treated
Diagnosing pheochromocytoma
Suspect with the following clients:
Difficult to control HTN
Taking 4 or more anti-HTN meds
Exhibit the “5 H’s”
The five Hs
Headache Hypertension Hyperhydrosis Hypermetabolism Hyperglycemia Must have HTN to make diagnosis of Pheochromocytoma
Criteria for selection of organ recipient
Life expectancy of less than 1 year
Age generally less than 65 years old
Absence of active infection
Stable psychological status
No evidence of drug or alcohol abuse
Ability to follow instructions regarding meds and self care
Cardiac –
New York Heart Association class III or IV
Normal of slightly increased pulmonary vascular resistance
Corneal transplant
Potential eye donor at time of death Head of Bed 30 degrees Antibiotic drops Close eyes and place small ice pack on eyes Discuss eye donation with family
Heart transplantation
Match comparable body weight and blood ABO compatibility in recipient less than 6 hours after procurement
Posterior wall of recipient atria left to anchor the donor heart
Watch carefully for concealed postop bleeding
Transplanted heart is denervated and unresponsive to vagal stimulation (HR about 100). Responds slowly to exercise or position change
75% survival after 3 years
To detect rejection – endomyocardial biopsies
Complications of organ transplant
Rejections:
Hyperacute: remove organ (48 hrs after surgery)
Acute: Increased immunosuppressives
(Important to continue taking immuno- suppressive meds a life time)
Chronic: conservative management
Immunosuppresant drugs
Cyclosporin (Sandimmune, Neoral)—inhibit T-cell activation prevent T-cell attack organ
Azathioprines (Imuran)–disrupt DNA/ RNA synthesis & cell division
Monoclonal antibodies (Simulect, Zenpax) inhibit interleukin-2 binding slows T-cell production
Corticosteroids: (Deltasone, Orasone) suppress inflammation r/t rejection
Others: Prograf in liver, kidney transplant; CellCept in kidney, liver & heart transplant
Rapanume in kidney transplant
