Cardiogenic shock is a life threatening medical condition resulting from an inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively. Cardiogenic shock is a type of circulatory shock, where there is insufficient perfusion of tissue to meet the demands for oxygen and nutrients. Cardiogenic shock is a largely irreversible condition and as such is more often fatal than not. The condition involves increasingly more pervasive cell death from oxygen starvation (hypoxia) and nutrient starvation (low blood sugar). Because of this, it may lead to cardiac arrest, which is an abrupt stopping of cardiac pump function.
Cardiogenic shock is defined by sustained low blood pressure with tissue hypoperfusion despite left ventricular filling pressure. Signs of tissue hypoperfusion include low urine production (<30 mL/hr), cool extremities, and altered level of consciousness.
Signs and Symptoms
Anxiety, restlessness, altered mental state due to decreased blood flow to the brain and subsequent hypoxia
Low blood pressure due to decrease in cardiac output
A rapid, weak, thready pulse due to decreased circulation combined with tachycardia
Cool, clammy, and mottled skin due to vasoconstriction and subsequent hypoperfusion of the skin
Distended jugular veins due to increased jugular venous pressure
Oliguria due to inadequate blood flow to the kidneys if the condition persists
Rapid and deeper respirations due to sympathetic nervous system stimulation and acidosis
Fatigue due to hyperventilation and hypoxia
Absent pulse in fast and abnormal heart rhythms
Pulmonary edema, involving fluid back up in the lungs due to insufficient pumping of the heart
Causes
Cardiogenic shock is caused by the failure of the heart to pump effectively. It can be due to any of the following
Myocardial infarction
Abnormal heart rhythms
Cardiomyopathy, Cardiac valve problems
Aortic valve stenosis, aortic dissection
Cardiac tamponade
Constrictive pericarditis
Systolic anterior motion
Hypertrophic cardiomyopathy
Sudden decompressurization (aircraft)
Risk Factors
Old age
History of heart failure or heart attack
Coronary artery disease
Diabetes and/or HTN
Diagnosis
Electrocardiogram - helps establishing the exact diagnosis and guides treatment, it may reveal:
Abnormal heart rhythm
Myocardial infarction
Signs of cardiomyopathy
Ultrasound - may show poor ventricular function, rupture of the interventricular septum, an obstructed outflow tract or cardiomyopathy.
Swan-Ganz Catheter - or PA catheter may assist in the diagnosis by providing information on the hemodynamics.
Biopsy - when cardiomyopathy is suspected as the cause of cardiogenic shock, a biopsy of heart muscle may be needed to make a definite diagnosis.
Pancreatitis is inflammation in the pancreas. The pancreas is a long, flat gland that sits tucked behind the stomach in the upper abdomen. The pancreas produces enzymes that assist digestion and hormones that help regulate the way your body processes sugar (glucose). Pancreatitis can occur as acute pancreatitis — meaning it appears suddenly and lasts for days. Or pancreatitis can occur as chronic pancreatitis, which describes pancreatitis that occurs over many years. Mild cases of pancreatitis may go away without treatment, but severe cases can cause life-threatening complications.
Signs and Symptoms
Signs and symptoms of pancreatitis may vary, depending on which type you experience.
Acute pancreatitis signs and symptoms include:
Upper abdominal pain
Abdominal pain that radiates to your back
Abdominal pain that feels worse after eating
Nausea
Vomiting
Tenderness when touching the abdomen
Chronic pancreatitis signs and symptoms include:
Upper abdominal pain
Losing weight without trying
Oily, smelly stools (steatorrhea)
Causes
Pancreatitis occurs when digestive enzymes produced in your pancreas become activated while inside the pancreas, causing damage to the organ.
During normal digestion, the inactivated pancreatic enzymes move through ducts in your pancreas and travel to the small intestine, where the enzymes become activated and help with digestion. In pancreatitis, the enzymes become activated while still in the pancreas. This causes the enzymes to irritate the cells of your pancreas, causing inflammation and the signs and symptoms associated with pancreatitis.
With repeated bouts of acute pancreatitis, damage to the pancreas can occur and lead to chronic pancreatitis. Scar tissue may form in the pancreas, causing loss of function. A poorly functioning pancreas can cause digestion problems and diabetes.
A number of causes have been identified for acute pancreatitis and chronic pancreatitis, including:
Alcoholism
Gallstones
Abdominal surgery
Certain medications
Cigarette smoking
Cystic fibrosis
Endoscopic retrograde cholangiopancreatography (ERCP), when used to treat gallstones
Family history of pancreatitis
High calcium levels in the blood (hypercalcemia), which may be caused by an overactive parathyroid gland (hyperparathyroidism)
High triglyceride levels in the blood (hypertriglyceridemia)
Infection
Injury to the abdomen
Pancreatic cancer
Complications
Pseudocyst. Acute pancreatitis can cause fluid and debris to collect in cyst-like pockets in your pancreas. A large pseudocyst that ruptures can cause complications such as internal bleeding and infection.
Infection. Acute pancreatitis can make your pancreas vulnerable to bacteria and infection. Pancreatic infections are serious and require intensive treatment, such as surgery to remove the infected tissue.
Breathing problems. Acute pancreatitis can cause chemical changes in your body that affect your lung function, causing the level of oxygen in your blood to fall to dangerously low levels.
Diabetes. Damage to insulin-producing cells in your pancreas from chronic pancreatitis can lead to diabetes, a disease that affects the way your body uses blood sugar.
Kidney failure. Acute pancreatitis may cause kidney failure, which can be treated with dialysis if the kidney failure is severe and persistent.
Malnutrition. Both acute and chronic pancreatitis can cause your pancreas to produce fewer of the enzymes that are needed to break down and process nutrients from the food you eat. This can lead to malnutrition, diarrhea and weight loss, even though you may be eating the same foods or the same amount of food.
Pancreatic cancer. Long-standing inflammation in your pancreas caused by chronic pancreatitis is a risk factor for developing pancreatic cancer.
Acute renal failure occurs when your kidneys suddenly lose the ability to eliminate excess salts, fluids, and waste materials from the blood. This elimination is the core of your kidney's main function. Body fluids can rise to dangerous levels when the kidneys lose their filtering ability. The condition will also cause electrolyte and waste material to accumulate in your body, which can also be life-threatening.
Acute renal failure is also known as acute kidney injury or acute kidney failure. It's most common for people who are already in the hospital. It may develop rapidly over a few hours. It can also develop over a few days to weeks. People who are critically ill and need intensive care have the highest risk of developing acute kidney failure.
Signs and Symptoms
Bloody stools, breath odor
Slow, sluggish movements
Generalized swelling or fluid retention
Fatigue, hand tremor
Pain between ribs or hips
Bruising easily, Nausea, Vomiting
Mental status change
Seizures, HTN
A metallic taste in your mouth
Causes
Acute renal failure can occur for many reasons. Among the most common reasons are:
Acute tubular necrosis
Severe or sudden dehydration
Toxic kidney injury from poisons or certain medications
Autoimmune kidney diseases, such as acute nephritic syndrome and interstitial nephritis
Urinary tract obstruction
Reduced blood flow can damage your kidneys. The following conditions can lead to decreased blood flow to your kidneys:
Low blood pressure
Burns
Dehydration
Hemorrhage
Injury
Septic shock
Serious illness
Surgery
Certain disorders can cause clotting within your kidney's blood vessels, and this can lead to acute kidney failure. These conditions include:
Hemolytic uremic syndrome
Idiopathic thrombocytopenia purpura
Malignant hypertension
Transfusion reaction
Scleroderma
Risk Factors
The chances of acquiring acute renal failure are greater if you're an older person or if you have any of the following long-term health problems:
Kidney disease
Liver disease
Diabetes
Hypertension
Heart failure
Morbid obesity
Complications
Potential complications of acute kidney failure include:
Fluid buildup
Chest pain
Muscle weakness
Permanent kidney damage
Death
Treatment
IV fluids
Treat the electrolyte imbalances such as hyperkalemia, hypocalcemia
The PCCN Exam outline includes a host of content that will be included on the national exam. Including but not limited to Hematology. The Hematology section of the PCCN exam will include roughly 5 to 8 questions. Although this section does not account for a large percentage of the exam, it would be wise to try and answer all of the questions in the section appropriately so as to give yourself a better chance in other areas. In this article we will cover the outline of the Hematology section, an overview of Hematology (broad), and some PCCN Hematology practice questions with rationales.
Hematology Outline
Blood Products and Plasma
HIV, AIDS, Neoplasms
Life Threatening Coagulopathies
Organ Transplantation
Sickle Cell Crisis (Trait, Anemia)
Hematology Overview
Hematology is the branch of medicine concerned with the study, diagnosis, treatment, and prevention of diseases related to blood. Hematology involves treating diseases that affect the production of blood and its components, such as blood cells, hemoglobin, blood proteins, bone marrow, platelets, blood vessels, spleen, and the mechanism of coagulation. Hematologists also conduct studies in oncology and work with oncologists.
Sickle Cell Anemia
Sickle Cell Anemia is an inherited form of anemia; a condition in which there aren't enough healthy red blood cells to carry adequate oxygen throughout your body. Normally, your red blood cells are flexible and round, moving easily through your blood vessels. In sickle cell anemia, the red blood cells become rigid and sticky and are shaped like sickles or crescent moons. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block flow and oxygen to parts of the body. There's no cure for most people with sickle cell anemia. However, treatments can relieve pain and help prevent further problems associated with sickle cell anemia.
Sickle Cell Anemia S/S
Signs and symptoms of sickle cell anemia often don't appear until an infant is at least 4 months old and may include; anemia, episodes of pain, hand foot syndrome, frequent infections, delayed growth, and vision problems.
Sickle Cell Anemia Causes
Sickle cell anemia is caused by a mutation in the gene that tells your body to make hemoglobin; the red, iron rich compound that gives blood its red color. Hemoglobin allows red blood cells to carry oxygen from your lungs to all parts of your body. In sickle cell anemia, the abnormal hemoglobin causes red blood cells to become rigid, and sticky. The sickle cell gene is passed from generation to generation in a pattern of inheritance called autosomal recessive inheritance. This means that both the mother and father must pass on the defective form of the gene for a child to be affected. With each pregnancy, two people with sickle cell traits have: a 25% chance of having an unaffected child with normal hemoglobin; a 50% chance of having a child who also is a carrier; and a 25 % chance of having a child with sickle cell anemia. The risk of inheriting sickle cell anemia comes down to genetics. For a baby to be born with sickle cell anemia, both parents must carry a sickle cell gene. Sickle cell anemia most commonly affects African Americans.
Sickle Cell Anemia Complications
Sickle cell anemia can lead to a host of complications, including; stroke, acute chest syndrome, pulmonary hypertension, organ damage, blindness, skin ulcers, gallstones and priapism. Treatment is aimed at treating the signs and symptoms.
PCCN Hematology Practice Questions
1) In the early stages of idiopathic thrombocytopenic purpura, (ITP), nursing interventions primarily focus on
A) Maintaining a patent airway
B) Controlling the respiratory rate
C) Replenishing circulating blood volume
D) Coping with alterations in body image
2) A patient with neutropenia has been placed in protective isolation. When providing care for this patient, it is important the nurse keeps in mind that the most common source of infection in immunocompromised patients is
A) Hospital equipment contaminated with pathogens
B) Poorly cleansed hands of health care workers
C) Normal flora and fauna from the patient's body
D) Family members coughing or sneezing on the patient
3) A patient experiencing renal transplantation has been having an unremarkable recovery over the previous 4 days. Which of the following findings would the nurse need to report to the physician immediately?
A) Abdominal discomfort and bladder distention
B) Increasing urinary output with decreasing serum creatinine
C) RUQ tenderness with elevated serum bilirubin
D) Elevated glucose and decreasing LOC
4) A patient about to receive a bone marrow transplant is in strict isolation and expressing feelings of anxiety. Nursing measures appropriate to this situation include
A) Playing music the patient enjoys and allowing photographs at the bedside
B) Allowing the patient's cat to visit for a pet therapy session
C) Encouraging the patient's school aged grandchildren to visit
D) Asking family members to bring in fresh produce as comfort food
5) A patient with HIV/AIDS is admitted complaining of weakness, weight loss of 25 pounds over the past month, fever, chills, and diarrhea. The patient's CD 4 count is 40. While taking the admission history, the nurse learns that the patient has two pet cats and a parrot. Which of the following opportunistic pathogens could be contributing to this patient's current clinical picture?
A) Pneumocystis carini
B) Cryptococcus
C) Toxoplasmosis
D) Mycobacterium avium
PCCN Hematology Practice Questions Answer with Rationale
1) Correct Answer - C) Replenishing circulating blood volume
Rationale - ITP is a deficiency of platelets with measurable amounts of antiplatelets antibodies resulting in bleeding into the skin and other organs. Acute ITP is generally a disease that affects children, while chronic ITP is generally experienced by adolescents and adults. Because of blood loss, replacing circulating blood volume is the primary goal when managing patients with ITP.
2) Correct Answer - C) Normal flora and fauna from the patient's body
Rationale - As the patient's natural immunity declines, his or her own normal body flora and fauna become the major source of opportunistic infections. While all of the other choices may contribute to the development of illness, they pose danger to the patient transiently and episodically rather than continually.
3) Correct Answer - A) Abdominal discomfort and bladder distention
Rationale - Abdominal discomfort and bladder distention indicate urinary tract obstruction, which could progress to renal transplant graft failure. An increase in urinary output and decreasing serum creatinine indicate improved renal function.
4) Correct Answer - A) Playing music the patient enjoys and allowing photographs at the bedside
Rationale - Allowing the patient to have things that make him or her feel more at home helps to reduce anxiety. Cats tend to carry many pathogens, owing to their bathing habits and litter box use, that could become opportunistic for this patient.
5) Correct Answer - D) Mycobacterium avium
Rationale - The symptoms evidenced (diarrhea, weight loss, fever with chills, and weakness) as well as contact with birds suggest the likelihood of Mycobacterium avium infection.
In this featured article, we will focus primarily on Bacterial Meningitis. Although there are other forms forms of meningitis, bacterial meningitis poses the biggest threat.
Bacterial Meningitis Overview
Meningitis is an infection of the membranes (meninges) surrounding the brain and spinal cord. Meningitis can be caused by a bacterial, fungal or viral infection. Meningitis can be acute, with a quick onset of symptoms, it can be chronic, lasting a month or more, or it can be mild or aseptic. Anyone experiencing symptoms of meningitis should see a doctor immediately.
Acute bacterial meningitis is the most common form of meningitis. Approximately 80 percent of all cases are acute bacterial meningitis. Bacterial meningitis can be life threatening. The infection can cause the tissues around the brain to swell. This in turn interferes with blood flow and can result in paralysis or even stroke.
Signs and Symptoms
Sudden high fever
Stiff neck
Severe headache that seems different than normal
Nausea and vomiting
Confusion, Seizures
Sleepiness or difficulty waking up
Sensitivity to light
No appetite or thirst
Skin rash
Causes
Streptococcus pneumoniae (pneumococcus)
Neisseria meningitidis
Haemophilus influenza
Listeria monocytogenes
Risk Factors
Skipping Vaccinations
Age - more common when <20 y/o
Living in a community setting - college life
Pregnancy
Compromised immune system - AIDS
Complications
Hearing loss
Memory difficulty
Learning disabilities
Brain damage
Gait problems
Seizures
Kidney failure
Shock and death
Diagnosis
Positive Blood cultures
CT scan or MRI, X-rays
Lumbar puncture
Treatment
Acute bacterial meningitis must be treated with antibiotics and more recently corticosteroids. The antibiotics or combination of antibiotics depends on the type of bacteria causing the infection.
A basilar skull fracture (or basal skull fracture) is a fracture of the base of the skull, typically involving the temporal bone, occipital bone, sphenoid bone, and/or ethmoid bone. This type of fracture is rare, occurring as the only fracture in just 4% of severe head injury patients. Such fractures can cause tears in the membranes surrounding the brain, or meninges, with resultant leakage of the cerebrospinal fluid (CSF). The leaking fluid may accumulate in the middle ear space, and dribble out through a perforated eardrum (CSF otorrhea) or into the nasopharynx via the eustachian tube, causing a salty taste. CSF may also drip from the nose (CSF rhinorrhea) in fractures of the anterior skull base, yielding a halo sign. These signs are characteristic for basilar skull fractures.
Basilar skull fractures include breaks in the posterior skull base or anterior skull base. The former involve the occipital bone, temporal bone, and portions of the sphenoid bone; the latter, superior portions of the sphenoid and ethmoid bones. The temporal bone fracture is encountered in 75% of all basilar skull fractures and may be longitudinal, transverse or mixed, depending on the course of the fracture line in relation to the longitudinal axis of the pyramid.
Bones may be broken around the foramen magnum, the hole in the base of the skull through which the spinal cord exits and becomes the brain stem, creating the risk that blood vessels and nerves exiting the hole may be damaged.
Due to the proximity of the cranial nerves, injury to those nerves may occur. This can cause palsy of the facial nerve or oculomotor nerve or hearing loss due to damage of cranial nerve VIII.
Signs and symptoms
Battle's sign -- bruising of the mastoid process of the temporal bone.
Raccoon eyes -- bruising around the eyes, i.e. "black eyes"
Cerebrospinal fluid rhinorrhea
Cranial nerve palsy
Bleeding (sometimes profuse) from the nose and ears
Hemotympanum
Conductive or perceptive deafness, nystagmus, vomitus
In 1-10% of patients, optic nerve entrapment occurs. The optic nerve is compressed by the broken skull bones, causing irregularities in vision.
Serious cases usually result in death
Treatment
Surgical Intervention
Adults with simple linear fractures who are neurologically intact do not require any intervention and may even be discharged home safely and asked to return if symptomatic. Infants with simple linear fractures should be admitted for overnight observation regardless of neurological status.[25] Neurologically intact patients with linear basilar fractures also are treated conservatively, without antibiotics. Temporal bone fractures are managed conservatively, at least initially, because tympanic membrane rupture usually heals on its own.
Simple depressed fractures in neurologically intact infants are treated expectantly. These depressed fractures heal well and smooth out with time, without elevation. Seizure medications are recommended if the chance of developing seizures is higher than 20%. Open fractures, if contaminated, may require antibiotics in addition to tetanus toxoid. Sulfisoxazole is a common recommendation.
Acute respiratory distress syndrome (ARDS), previously known as respiratory distress syndrome (RDS), adult respiratory distress syndrome, or shock lung, is a medical condition occurring in critically ill patients characterized by widespread inflammation in the lungs. ARDS is not a particular disease, rather it is a clinical phenotype which may be triggered by various pathologies such as trauma, pneumonia and sepsis.
The hallmark of ARDS is diffuse injury to cells which form the alveolar barrier, surfactant dysfunction, activation of the innate immune response, and abnormal coagulation. In effect, ARDS results in impaired gas exchange within the lungs at the level of the microscopic alveoli.
The syndrome is associated with a high mortality rate between 20 and 50%.The mortality rate with ARDS varies widely based on severity, the patient's age, and the presence of other underlying medical conditions.
Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in neonates, international consensus is that "acute respiratory distress syndrome" is the best moniker because ARDS can affect those of all ages.
Signs and Symptoms
The signs and symptoms of ARDS often begin within two hours of an inciting event, but can occur after 1–3 days. Signs and symptoms may include:
Severe shortness of breath
Labored and unusually rapid breathing
Low blood pressure
Confusion and extreme tiredness
Causes
The mechanical cause of ARDS is fluid leaked from the smallest blood vessels in the lungs into the tiny air sacs where blood is oxygenated. Normally, a protective membrane keeps this fluid in the vessels. Severe illness or injury, however, can cause inflammation that undermines the membrane's integrity, leading to the fluid leakage of ARDS.
The most common underlying causes of ARDS include
Sepsis
Inhalation of harmful substances
Severe pneumonia
Head, chest or other major injury
Trauma, lung contusion
Multiple blood transfusions
Risk Factors
Most people who develop ARDS are already hospitalized for another condition, and many are critically ill. You're especially at risk if you have a widespread infection in your bloodstream (sepsis).
People who have a history of chronic alcoholism are at higher risk of developing ARDS. They're also more likely to die of ARDS.
Complications
ARDS is extremely serious, but thanks to improved treatments, more people are surviving it. However, many survivors end up with potentially serious — and sometimes lasting — complications, including:
Scarring in the lungs (pulmonary fibrosis). Scarring and thickening of the tissue between the air sacs can occur within a few weeks of the onset of ARDS. This stiffens your lungs, making it even more difficult for oxygen to flow from the air sacs into your bloodstream.
Collapsed lung (pneumothorax). In most ARDS cases, a breathing machine called a ventilator is used to increase oxygen in the body and force fluid out of the lungs. However, the pressure and air volume of the ventilator can force gas to go through a small hole in the very outside of a lung and cause that lung to collapse.
Blood clots. Lying still in the hospital while you're on a ventilator can increase your risk of developing blood clots, particularly in the deep veins in your legs. If a clot forms in your leg, a portion of it can break off and travel to one or both of your lungs (pulmonary embolism) — where it blocks blood flow.
Infections. Because the ventilator is attached directly to a tube inserted in your windpipe, this makes it much easier for germs to infect and further injure your lungs.
Abnormal lung function. Many people with ARDS recover most of their lung function within several months to two years, but others may have breathing problems for the rest of their lives. Even people who do will usually have shortness of breath and fatigue and may need supplemental oxygen at home for a few months.
Memory, cognitive and emotional problems. Sedatives and low levels of oxygen in the blood can lead to memory loss and cognitive problems after ARDS. In some cases, the effects may lessen over time, but in others, the damage may be permanent. Most ARDS survivors also report going through a period of depression, which is treatable.
Diagnosis
There's no specific test to identify ARDS. The diagnosis is based on the physical exam, chest X-ray and oxygen levels and by ruling out other diseases and conditions — for example, certain heart problems — that can produce similar symptoms.
The Endocrine portion of the PCCN Exam will encompass roughly 5 to 8 questions on the national exam. In comparison to a lot of the other sections, this is a relatively small portion of the exam. Nevertheless, this is a significant portion in the event you get all of the Endocrine questions incorrect. It would be wise to put as much emphasis on this section as you do on the other sections of the exam. In this article, we will cover the PCCN Exam outline as it relates to the Endocrine section. We will also cover Diabetes Insipidus which is one of the areas of focus on the PCCN exam as well as some practice questions.
PCCN Exam Endocrine Outline
Endocrine Hormones
Diabetes Insipidus
Diabetic Ketoacidosis
Hyperglycemic Hyperosmolar Nonketotic Coma (HHNK)
Endocrine Anatomy & Physiology
The Endocrine system refers to the collection of glands of an organism that secrete hormones directly into the circulatory system to be carried towards distant target organs. The major endocrine glands include the pineal gland, pituitary gland, pancreas, ovaries, testes, thyroid gland, parathyroid gland, hypothalamus, gastrointestinal tract and adrenal glands. The endocrine system is in contrast to the exocrine system, which secretes its hormones to the outside of the body using ducts. Special features of endocrine glands are, in general, their ductless nature, their vascularity, and commonly the presence of intracellular vacuoles or granules that store their hormones. In contrast, exocrine glands, such as salivary glands, sweat glands, and glands within the GI tract, tend to be much less vascular and have ducts or a hollow lumen.
Diabetes Insipidus
DI is a condition characterized by excessive thirst and excretion of large amounts of severely dilute urine, with reduction of fluid intake having no effect on the concentration of urine. There are different types of DI, each with a different set of causes. The most common type is central DI, which involves a deficiency of vasopressin, also known as antidiuretic hormone (ADH). The second common type of DI is nephrogenic DI, which is due to kidney or nephron dysfunction caused by an insensitivity of the kidneys or nephrons to ADH. DI can also be gestational, or caused by alcohol or some types of drug abuse. DI should not be confused with nocturia.
Signs & Symptoms of DI
Excessive urination
Extreme thirst
Blurred vision
Diagnosis of DI
Water deprivation test
Urinalysis
MRI of brain
Genetic screening
Classification of DI
Neurogenic DI - more commonly known as central diabetes insipidus, is due to the lack of vasopressin production in the hypothalamus due to a range of causes. The underlying causes of central DI can include vascular, autoimmune, infection, sarcoidosis, some drugs, surgery, head trauma, benign or metastatic pituitary-hypothalamic tumor, although 50% of cases are found to be idiopathic.
Nephrogenic DI - is due to the inability of the kidney to respond normally to vasopressin.
Primary Polydipsia or Dipsogenic DI - results from excessive intake of fluids as opposed to deficiency of arginine vasopressin. It may be due to a defect or damage to the thirst mechanism, located in the hypothalamus, or due to mental illness. Treatment with DDAVP may lead to water intoxication.
Gestational DI - occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placenta, which breaks down ADH. Gestational DI is thought to occur with excessive production and/or impaired clearance of vasopressinase.
Treatment of DI
Central DI (Neurogenic) - because the cause of this form of DI is a lack of anti-diuretic hormone (ADH), treatment is usually with a synthetic hormone called desmopressin. You can take desmopressin as a nasal spray, as oral tablets or by injection.
Nephrogenic DI - this condition is the result of your kidneys not properly responding to ADH, so desmopressin is not a treatment option. Instead, your doctor may prescribe a low salt diet to help reduce the amount of urine your kidneys make. You'll also need to drink enough water to avoid dehydration.
Gestational DI - treatment for most cases of gestational DI is with the synthetic hormone desmopressin.
Primary polydipsia - there is no specific treatment for this form of DI, other than decreasing the amount of fluid intake. However, if the condition is caused by mental illness, treating the mental illness may relieve the symptoms.
PCCN Endocrine Practice Questions
1) Which of the following statements regarding fluid management is correct, regarding patients with diabetes insipidus?
A) Electrolyte levels must be monitored to determine the correct IV fluids to administer
B) If the diabetes insipidus is nephrogenic, vasopressin will need to be administered
C) If the diabetes insipidus is neurogenic, only fluids will need replacement
D) The patient's output must exceed his intake in order to prevent complications
2) The nurse is performing an admission health assessment on a newly diagnosed 54 year old male admitted with diabetes insipidus. Which of the following assessment findings would the nurse expect to see in a patient with that condition?
A) Elevated SBP, tachycardia, decreased urinary output
B) Elevated serum potassium, bradycardia, numbness in hands
C) Polyuria, extreme thirst, decreased urinary specific gravity
D) Widened pulse pressures, dilated pupils, decerebrate posturing
3) Which of the following signs are characteristic of diabetes insipidus?
A) Low urine output, low serum osmolality, hyponatremia, and low urine sodium
B) Elevated urine output, low serum osmolality, hyponatremia, and low urine sodium
C) Low urine output, low serum osmolality, hypernatremia, and elevated urine sodium
D) Elevated urine output, elevated serum osmolality, hypernatremia, and low urine sodium
PCCN Endocrine Practice Questions Answer with Rationale
1) Correct Answer - A) Electrolyte levels must be monitored to determine the correct IV fluids to administer
Rationale - Regardless of the cause or type of diabetes insipidus, the patients electrolyte values will govern appropriate treatment for this disorder. In nephrogenic diabetes insipidus, the kidney has been damaged and no longer responds to vasopressin, so aggressive replacement of fluids is required to sustain life.
2) Correct Answer - C) Polyuria, extreme thirst, decreased urinary specific gravity
Rationale - Patients with diabetes insipidus would be expected to be thirsty and produce large volumes of dilute urine. They will usually exhibit a decrease in BP and increase in HR related to hypovolemia.
As a part of our continued review of the human body, we decided to take an in-depth look at Cerebrospinal fluid. Within this article, we will cover in great detail the structure and make-up of cerebrospinal fluid.
Cerebrospinal Fluid (CSF) Overview
Cerebrospinal fluid (CSF) is a clear, colorless body fluid found in the brain and spine. It is produced in the choroid plexuses of the ventricles of the brain. It acts as a cushion or buffer for the brain's cortex, providing basic mechanical and immunological protection to the brain inside the skull. The CSF also serves a vital function in cerebral autoregulation of cerebral blood flow.
The CSF occupies the subarachnoid space (between the arachnoid mater and the pia mater) and the ventricular system around and inside the brain and spinal cord. It constitutes the content of the ventricles, cisterns, and sulci of the brain, as well as the central canal of the spinal cord.
Production of CSF
The brain produces roughly 500 mL of cerebrospinal fluid per day. This fluid is constantly reabsorbed, so that only 100-160 mL is present at any one time.
Ependymal cells of the choroid plexus produce more than two thirds of CSF. The choroid plexus is a venous plexus contained within the four ventricles of the brain, hollow structures inside the brain filled with CSF. The remainder of the CSF is produced by the surfaces of the ventricles and by the lining surrounding the subarachnoid space.
Ependymal cells actively secrete sodium into the lateral ventricles. This creates osmotic pressure and draws water into the CSF space. Chloride, with a negative charge, moves with the positively charged sodium and a neutral charge is maintained. As a result, CSF contains a higher concentration of sodium and chloride than blood plasma, but less potassium, calcium and glucose and protein
Circulation of CSF
CSF circulates within the ventricular system of the brain. The ventricles are a series of cavities filled with CSF, inside the brain. The majority of CSF is produced from within the two lateral ventricles. From here, the CSF passes through the interventricular foramina to the third ventricle, then the cerebral aqueduct to the fourth ventricle. The fourth ventricle is an outpouching on the posterior part of the brainstem. From the fourth ventricle, the fluid passes through three openings to enter the subarachnoid space – these are the median aperture, and the lateral apertures. The subarachnoid space covers the brain and spinal cord. There is connection from the subarachnoid space to the bony labyrinth of the inner ear making the cerebrospinal fluid continuous with the perilymph.
Reabsorption of CSF
It had been thought that CSF returns to the vascular system by entering the dural venous sinuses via the arachnoid granulations (or villi). However, some have suggested that CSF flow along the cranial nerves and spinal nerve roots allow it into the lymphatic channels; this flow may play a substantial role in CSF reabsorbtion, in particular in the neonate, in which arachnoid granulations are sparsely distributed. The flow of CSF to the nasal submucosal lymphatic channels through the cribriform plate seems to be especially important.
CSF Contents
The CSF is created from blood plasma and is largely similar to it, except that CSF is nearly protein-free compared with plasma and has some modified electrolyte levels. CSF contains approximately 0.3% plasma proteins, or approximately 15 to 40 mg/dL, depending on sampling site,and it is produced at a rate of 500 ml/day. Since the subarachnoid space around the brain and spinal cord can contain only 135 to 150 ml, large amounts are drained primarily into the blood through arachnoid granulations in the superior sagittal sinus. Thus the CSF turns over about 3.7 times a day. This continuous flow into the venous system dilutes the concentration of larger, lipid-insoluble molecules penetrating the brain and CSF.
Healthy cerebrospinal fluid is free of red blood cells, and at most contains only a few white blood cells. Any cell count higher than that constitutes pleocytosis, an excess of cells.
Development of CSF
Around the third week of development, the embryo is a three-layered disc, covered on the dorsal surface by a layer of endoderm. In the middle of this surface is a linear structure called the notochord. As the endoderm proliferates, the notochord is dragged into the middle of the developing embryo and becomes the neural canal.
As the brain develops, by the fourth week of embryological development three swellings have formed within the embryo around the canal, near where the head will develop. These swellings represent different components of the central nervous system: the prosencephalon, mesencephalon and rhombencephalon.
The developing forebrain surrounds the neural cord. As the forebrain develops, the neural cord within it becomes a ventricle, ultimately forming the lateral ventricles. Along the inner surface of both ventricles, the ventricular wall remains thin, and a choroid plexus develops, releasing CSF. The CSF quickly fills the neural canal.
Function of CSF
Buoyancy: The actual mass of the human brain is about 1400 grams; however, the net weight of the brain suspended in the CSF is equivalent to a mass of 25 grams. The brain therefore exists in neutral buoyancy, which allows the brain to maintain its density without being impaired by its own weight, which would cut off blood supply and kill neurons in the lower sections without CSF.
Protection: CSF protects the brain tissue from injury when jolted or hit. In certain situations such as motor vehicle crashes or sports injuries, the CSF cannot protect the brain from forced contact with the skull case, causing hemorrhaging, brain damage, and sometimes death.
Chemical stability: CSF flows throughout the inner ventricular system in the brain and is absorbed back into the bloodstream, rinsing the metabolic waste from the central nervous system through the blood–brain barrier. This allows for homeostatic regulation of the distribution of neuroendocrine factors, to which slight changes can cause problems or damage to the nervous system. For example, high glycine concentration disrupts temperature and blood pressure control, and high CSF pH causes dizziness and syncope. To use Davson's term, the CSF has a "sink action" by which the various substances formed in the nervous tissue during its metabolic activity diffuse rapidly into the CSF and are thus removed into the bloodstream as CSF is absorbed.[
Prevention of brain ischemia: The prevention of brain ischemia is made by decreasing the amount of CSF in the limited space inside the skull. This decreases total intracranial pressure and facilitates blood perfusion.
Clearing waste: CSF has been shown to be critical in the brain's glymphatic system, which plays an important role in flushing metabolic toxins or waste from the brain's tissues' cellular interstitial fluid (ISF). CSF flushing of wastes from brain tissue is further increased during sleep, which results from the opening of extracellular channels controlled through the contraction of glial cells, which allows for the rapid influx of CSF into the brain. These findings indicate that CSF may play a large role during sleep in clearing metabolic waste, like beta amyloid, that are produced by the activity in the awake brain.
Otitis media is a group of inflammatory diseases of the middle ear. The two main types are acute otitis media (AOM) and otitis media with effusion (OME). AOM is an infection of abrupt onset that usually presents with ear pain. In young children this may result in pulling at the ear, increased crying, and poor sleep. Decreased eating and a fever may also be present. OME is typically not associated with symptoms. Occasionally a feeling of fullness is described. It is defined as the presence of non-infectious fluid in the middle ear for more than three months.
Chronic suppurative otitis media (CSOM) is middle ear inflammation of greater than two weeks that results in episodes of discharge from the ear. It may be a complication of acute otitis media. Pain is rarely present. All three may be associated with hearing loss. The hearing loss in OME, due to its chronic nature, may affect a child's ability to learn.
Signs and Symptoms
An integral symptom of acute otitis media is ear pain; other possible symptoms include fever, and irritability (in infants). Since an episode of otitis media is usually precipitated by an upper respiratory tract infection (URTI), there often are accompanying symptoms like cough and nasal discharge.
Discharge from the ear can be caused by acute otitis media with perforation of the ear drum, chronic suppurative otitis media, tympanostomy tube otorrhea, or acute otitis externa. Trauma, such as a basilar skull fracture, can also lead to discharge from the ear due to cerebral spinal drainage from the brain and its covering (meninges).
Causes
The common cause of all forms of otitis media is dysfunction of the Eustachian tube. This is usually due to inflammation of the mucous membranes in the nasopharynx, which can be caused by a viral URI, strep throat, or possibly by allergies.
Because of the dysfunction of the Eustachian tube, the gas volume in the middle ear is trapped and parts of it are slowly absorbed by the surrounding tissues, leading to negative pressure in the middle ear.
Eventually the negative middle-ear pressure can reach a point where fluid from the surrounding tissues is sucked in to the middle ear's cavity (tympanic cavity), causing a middle-ear effusion.
By reflux or aspiration of unwanted secretions from the nasopharynx into the normally sterile middle-ear space, the fluid may then become infected — usually with bacteria. The virus that caused the initial URI can itself be identified as the pathogen causing the infection.
Risk Factors
Risk factors for otitis media include:
Age. Children between 6 to 36 months are most likely to get ear infections.
Attending daycare
Recent illness, such as a cold or sinus infection.
History of allergies, like hay fever, also called allergic rhinitis, or sinusitis.
Exposure to secondhand smoke
Having family members who are prone to ear infections; studies show a clear genetic component for recurrent otitis media.
Using a pacifier
Having a history of gastroesophageal reflux disease (GERD).
