Test 3, NP 614 - Sheet1 Flashcards
Labs to order for a 54-yo female experiencing unusual fatigue, Hct 38%, and fasting glucose of 130
Chemistry panel, fasting LFT, CK, Hgb A1C, and TSH
Best medication/rationale for a female with BMI of 50
Metformin / improves insulin sensitivity
Why does even a small weight loss (as little as 10 lbs) help diabetes
Helps improve sensitivity to insulin receptors
According to the ADA, a HbgA1c should be at least
<7
A common side effect of metformin therapy is
Gastrointestinal problems
The goal for someone with diabetes and HTN is
Treatment to a systolic blood pressure goal of less than 140 mmHg and diastolic pressure less than 80 mmHg
Besides a beta-blocker (that a patient has taken for years), what other HTN medication should be started
ACE inhibitor
Annual screenings for a patient who has had diabetes for 5 years includes
Fasting LFT, urine albumin, serum creatinine, dilated and comprehensive eye exam, neuropathy screening, comprehensive foot exam
Appropriate pharmacological management for a 77 yo female who has stable angina, increased TSH and normal T4
Levothyroxine 12.5 mcg q d
Diagnosis of 32 yo female who reports menstrual irregularities, fatigue, elevated TSH, normal free T4 and normal T3
Sub-clinical hypothyroidism
Consideration of Graves disease
Should be considered if patient has a-fib
Length of time to take medication for a patient diagnosed with Grave’s disease who elects treatment with anti-thyroid medications
6-12 months
The main reason for goiter in the U.S. is
Chronic autoimmune thyroiditis disease
A 56 yo man who reports fatigue, loss of weight, nausea and vomiting, muscle cramps, with hyperpigmentation at the elbows and knees would lead you to do a work-up for:
Addison’s disease
Initial medication for a patient who is hyperthyroid and complaining of fatigue and palpitations
Atenolol 50 mg daily
The response to a patient who asks you to increase her synthroid in order for her to lose weight
Excessive thyroid medication can lead to osteoporosis
Caution to tell patients regarding medication for hypothyroidism
This medication can increase the risk of fracture years from now if not monitored
Is insulin ever used for first-line treatment of Type II diabetes?
Yes
Early work-up for a suspected thyroid nodule includes:
TSH and serum free T4, ultrasound of suspected nodule, and a fine-needle biospy
Indication of elevated TSH
Hypothyroid
Indication of low TSH
Hyperthyroid
A gland
Anything in the endocrine system that sends out hormones
Hormones
Diffuse throughout the body and bump into cells
Water soluble hormones
Example - epinephrine. Docks on the surface of a cell and set up a signal transmission pathway in order to cause the desired effect
Lipid soluble hormones
Exampe - testosterone. Is transported directly into the cell membrane and can be moved into the nucleus
Pineal - hormone and action
Melatonin and circardian rhythm. Only secreted at night
Anterior pituitary - one hormone and action
Growth hormone and cell growth
Posterior pituitary - one hormone and action
ADH (antidiuretic hormone) and water balance
Thyroid gland - hormones and actions
T3/T4 - metabolism: calcitonin - lowers blood calcium and calcium goes back into the bones
Parathyroid gland - one hormone and action
PTH (parathyroid hormone) and raises blood calcium if calcium level gets too low
Pancreas - hormones and actions
Insulin - lowers blood sugar. Glucagon - raises blood sugar
Adrenal cortex - one hormone and action
Glucocorticoids - anti-inflammatory response
Adrenal medulla - one hormone and action
Epinephrine - fight or flight response
Ovaries - one hormone and action
Estrogen - female sex characteristics
Testes - one hormone and action
Testosterone - male sex characteristics
Hypothalamus
A member of the brain and the endocrine system. Nerve signals funnel into the brain and this gland sends them into the pituitary gland. Makes ADH and oxytocin.
Pituitary gland
Called the Master Gland because it takes the stimulation from hypothalamus and directs them to most of the other endocrine glands.
Thyroid gland
Wraps around the trachae and it helps in regularing metabolism by using T3 and T4
Parathyroid glands
Main role is reguation of blood calcium levels.
Adrenal glands
Located on top of kidneys
Adrenal cortex responsibility
Makes the adrenocorticosteroids - cortisol (stress hormone and increases blood sugar) and aldosterone (major regulator of blood fluid volume)
Adrenal medulla responsibility
Makes catecholamines - epinephrine and norepi and are involved in the body’s fight or flight response
Gonads - ovaries and testes
Release sex hormones that are involved in making the secondary sex characteristics and progressing us through the life stages
Pancreas
Located in upper abdomen and is uses hormones to stimulate control of the blood sugar through hormones insulin and glucoagan
Hormones and receptors
The receptors and their locations respond specifically to certain hormones
Autocrine hormones
Function at the cell that makes them. Example T-cells and the immune system
Paracrine hormones
Function regionally. Example - hormones released by hypothalamus that direct the thyroid
Endocrine hormones
Function at a distance - example pituitary gland stimulating the gonads
Incretin hormones
Located in the gut and are glucagon-like peptide-1 and glucose-dependent insulin-otropic polypeptide that regulate the secretion of insulin by stimulating beta cells to produce and secrete insulin, but only when glucose levels are increased.
Incretin hormone medications
Januvia - taken once daily with metformin. Byetta - injectable twice daily and causes nausea - biggest side effect pancreatitis.
When to start insulin as first-line glucose treatment
When Hgb A1C >9.0% and they are taking no meds.
Aspirin for CAD prevention in diabetics
Little evidence, focus on minimizing risks.
Facts about diabetes
7th leading cause of death, leading cause of blindness and kidney failure, >60% have nerve damage and amputations secondary to diabetes, 2x more likely to have periodontal disease and depression
Criteria for diagnosis of diabetes
A1C >6.5% or FPG > 126 mg/dl or 2-h plasma glucose > 200 or a random plasma glucose of >200 in a patient with classic symptoms of hyperglycemia
Categories of increased risk for Prediabetes
FPA 100-125 mg/dL or 2-h plasma glucose in the 75-g OGTT 140-199 mg/dl or A1C 5.7-6.4%
Testing in asymptomatic patients
All patients with BMI > 25 who have any additional risk factors. Begin testing at age 45 if BMI is normal (If normal and not diabetic or prediabetic recheck in 3 years). If patient is prediabetic, screen annually for progression to diabetes.
Test patients with a BMI >25 and any of the following risk factors for diabetes
Sedentary: first degree relative: high-risk ethnicity; previous GDM; delivery of infant >9 lbs; HTN; HDL 250; PCOS; prediabetes; clinical conditions associated with insulin resistance; history of CVD
Prevention of type 2 diabetes
Screen for any modifiable risk factors. At least 150 min/week of moderate physical activity. Weight loss of 7% of body weight. Appropriate referrals. Consider metformin for any prediabetics 35.
Microvascular considerations of patient with diabetes
Assess for retinopathy, nephropathy, and neuropathy
Sensory neuropathy considerations of patient with diabetes
Include history of foot lesions
Autonomic neuropathy considerations of patient with diabetes
Include sexual dysfunction and pastroparesis
Macrovascular considerations of patient with diabetes
CHD, CVA, PAD
Other medical conditions to consider in patient with diabetes
Psychosocial problems and dental disease
Comprehensive foot exams in patient with diabetes
Inspection. Palpation of dorsalis pedis and posterior tibial pulses. Presense/absence of patellar adn Achilles reflexes. Determination of proprioception, vibration, and monofilament sensation
Diagnostics to consider in patient with diabetes
A1C if not avaialble within last 3 months. Each year - fasting lipids, LFTs, urine albumin, serum creatinine with GFR, TSH in type 1 or dyslipidemic patients or women over 50
When to order A1C
At initial assessment. Every 6 months in patients at goal and who are stable. Every 3 months in patients not at goal. Use point of care if avaialble
A1C goal in non-pregnant adult
7%
Preprandial (fasting glucose) ideal reading
70-130 mg/dL
Postprandial (1-2 hr after meal) ideal reading
<180
Pt centered approach to diabetes - Key points
Glycemic targets and glucose lowering therapies must be individualized. Diet, exercise, and education remain the foundation of therapy. Metformin is 1st line. After metformin data is iffy. Most pts will require insulin alone or in combo with oral agents. All treatment decisions must be made with the patient. CVD risk reducation is overall goal.
Weight loss and diabetes
All pts with prediabetes or diabetes should receive nutritional counseling. Modest weight loss produces significant benefit. Limit ETOH, limit sodium, and increase fiber
Immunizations recommended for diabetics
Influenza, pneumococcal, and Hep B
BP >140-80 treatment and diabetes
Should be advised on lifestyle changes and began on med - ACE is 1st line
Consider low dose ASA for these diabetic patients
History of CVD or other major risk factors such as: FH or CVD, HTN, smoking, dyslipidemia or albuminuria. Increased risk for stroke. Most men >50. Most women >60
When to refer a diabetic patient with chronic kidney disease based on GFR
<30
LDL goals of patient with known CVD diabetes
<70
LDL goals of patient without CVD with risk factors and diabetes
<100
5 clinical manifestations of metabolic syndrome
Central obesity (waist >39 in men, >35 women), elevated fasting glucose >100 or drug treatment for elevated glucose, elevated triglyceridea >150 or treatment, reduced HDL-C 130 systolic or >85 diastolic or treatment
Number of clinical manifestations required for diagnosis of metabolic syndrome
3 of 5
Microvascular changes in diabetes
Caused by the long-standing hyperglycemia and results in neuropathy, nephropathy, and retinopathy. They are not part of metabolic syndrome.
Risk of CV disease in diabetics
2-4 fold increased risk
Primary prevention of CV in diabetics patients
Aspirin (75-162 mg/d) especially in pts >40 with additional risk factors (family hx of CVD, HTN, smoking, dyslipidemia, or albuminuria)
Possible best combo for patients with type 2 DM
Basal insulin and 1-2 daytime oral medications - Metformin with insulin
Race with greater insulin resistance
Latinos
Danger of hypoglycemia
Exacerbates MI and may cause dysrhythmias and possibly brain dysfunction with repeated episodes
Adverse effects of diabetes
Cardiovascular disease, renal failue, blindness, and nontraumatic lower limb amputation. Lower life expectancy and significant morbidity
Target organ damage of diabetes
Eyes, kidneys, heart, blood vessels, and nerves
Pathophysiology of type 1 diabetes
Caused by the autoimmune destruction of the beta cells within the islets of Langerhans in the pancreas in a genetically predisposed individual
Pathophysiology of type 2 diabetes
More obscure and hallmarks are insulin resistance and impaired beta cell function
Typical symptoms of untreated type 1 diabetes
Polyuria, polydipsia, polyphagia, weight loss, blurred vision, and fatigue
Signs of ketoacidosis
Glycosuria increases, nausea, vomiting, abdominal pain, rapid shallow breathing, hypotension, and dehydration
Symptoms of untreated type 2 diabetes
May have no symptoms or subtle ones that last for weeks to years. Polyuria, polydipsia, blurred vision, fatigue, slowly healing wounds, and frequent infections.
Focus of physical exam in diagnosis of diabetes
Dehydration, weight loss, and precipitating causes, such as illness, infection, or stress. May appear dry and flushed. Assess skin, eyes, heart, lungs, thyroid.
Labs related to diagnosis of diabetes
Serum glucose (random or fasting), oral glucose tolerance test, HbA1C, and urinalysis
Treatment of diabetes
Health diet, regular exercse, medication, monitoring, self-care education, and periodic follow-up by the PCP and diabetes care team.
Goal of nutritional therapy regarding diabetes
Development of a meal plan, balancing insulin with food intake and activity to achieve glycemic control
Exercise and type 2 diabetes
Decreases insulin resistance and increases glucose uptake into the cell. This can cause the exercise lag effect and can last up to 48 hrs after exercise.
Treatment of type 2 diabetes includes…
Management of dyslipidemia, hypertension, obesity, insulin resistance, and hypercoagulability as well as glycemic control, education, diet, exercise, adn achievement and maintenance of a desirable body weight.
The most common reason for use of insulin in type 2 diabetes
Failure to respond to the oral antihyperglycemic agents
Symptoms of mild hypoglycemia
Shaking/trembling, sweating, hunger, tachycardia, weakness, lightheadedhess, pallor, irritability, but no change in mental status: individual able to treat self
Symptoms of moderate hypoglycemia
Decreased thinking, increased emotions (anger, irritability), inability to complete tasks, some changes in mental status: individual may be able to treat self
Symptoms of severe hypoglycemia
Confusion, drowsiness; may progress to unconsciousness, impaired neurologic function; individual requires assistance
Diabetic ketoacidosis
Caused by insulin deficiency and is characterized by hyperglycemia, ketonemia, and acidemia
Clinical presentation of DKA
Rapid development of abdominal pain, nausea, vomiting, Kussmaul respirations, dehydration, fruity odor to breath, tachycardia, hypotension, and changes in consciousness
Treatment of DKA
Fluid resuscitation, IV insulin, electrolyte monitoring and replacement, and treatment of underlying illness or infection
Acanthosis nigricans
A diffuse, hyperpigmented, velvety thickening of the skin that is found on the neck and axillae. Sign of insulin resistance
How to calculate BMI
Weight divided by height squared
Labs of metabolic syndrome
Glucose tolerance test - fasting blood glucose, fasting plasma insulin concentration, fasting lipid profile, urinalysis (for protein), and C-reactive protein
Complications of metabolic syndrome
CVD, atherosclerotic vascular disease, ischemic heart disease, coronary artery disease, MI, and stroke
Causes of goiter
Hormonal or immunologic stimulation or may result from inflammatory, infiltrative, or metabolic conditions, including iodine deficiency or excess, neoplasia, Graves’ disease, and thyroiditis
Diagnosis of goiter
TSH, free T4, antimicrosomal antibodies, radionuclide scannin, thyroid ultrasound
Hyperthyroidism
A clinical syndrome caused by the excess production or release of thyroid hormone and its clinical manifestations
Most common cause of hyperthyroidism
Graves’ disease
Pathophysiology of Graves’ disease
An autoimmune disorder in which thyroid-stimulating antibodies compete with TSH for TSH receptors on the thyroid and activate the production of cyclic adenosine monophosphate, which increases the synthesis and release of thyroid hormones
Symptoms of hyperthyroidism
Dry eyes, SOA, palpitation, tachycardia, weight loss, goiter, amenorrhea, tremor, sweaty palms, anxiety, irritability, sleeplessness, anorexia
TSH level in hyperthyroidism
TSH will be low or undetectable
Pharmacological treatment of Graves’ disease
Beta blockers for tremor and tachycardia.
Medical treatment of Graves’ disease
PTU and radioiodine therapy
Subclinical hyperthyroidism
Suppressed TSH with normal serum T4 and T3 levels and most elderly patients have multinodular goiters
Clinical findings of thyroid storm or thyrotoxic crisis
Temp 102-105, profuse sweating, pulse above 120-140, a-fib, restlessness, confusion, agitation, coma, severe vomiting, diarrhea, and hepatomegaly, jaundice
Hypothyroidism
Results from synthesis of thyroid hormone that is insufficient to meet the body’s needs and is the most common disorder of the thyroid.
Clinical presentation of hypothyroidism
Myxedema, slowed mentation, the most comon is fatigue. Increased sensitivity to cold, weight gain, hoarseness, puffiness of the face and hands, heavy and irregular menstrual periods, dry skin, dry and brittle hair, depression, paresthesias, muscle aches, and constipation.
Lab tests of hypothyroidism
Elevated TSH
Treatment of hypothyroidism
Levothyroxine
Subclinical hypothyroidism
Elevated TSH in the presence of normal thyroid hormone levels
Myxedema coma
Hypothermic stuporous state that may be characterized by respiratory depression and eventually death is the result of untreated hypothyroidism and can be triggered by environmental stressors such as cold exposure or trauma and infection
Thyroid hormone and metabolism
Stimulates metabolic activities in cells, leading to increased basal metabolic rate
Lipids and thyroid hormone
Increased thyroid hormone leads to an increased concentration of fatty acids in plasma
Cholesterol levels and thyroid hormone
Cholesterol and triglycerides are inversely realted to thyroid hormone levels
Carbohydrates and thyroid hormone
Stimulates their metabolism, and stimulates the insulin-dependent entry of glucose into cells
Glucose production and thyroid hormone
Increased levels result in increased gluconeogenesis and glycogenolysis resulting in increased production of glucose
Growth hormone and thyroid hormone
Closely related to the effects of growth hormone and is necessary for normal growth and development in children
Thyroid hormone and cardiovascular effects
It increases HR, contractility and cardiac output
Thyroid hormone and CNS effects
Derangements in thyroid hormone can lead to changes in mental statue; fatigue if too low and anxiety if too high
Thyroid hormone and reproductive system effects
Normal levels are necessry for the functioning of the reproductive system, and low levels are associated with infertility
T4 and T3
Hormones released by the thyroid gland itself and circulates through the bloodstream to other “target cells”. 80% if T4 and most of T4 is converted to T3
Feedback loop of thyroid hormone production
Negative loop
Diagnosing Graves’ disease
The TSH will be low and the free T4 will be high. No further workout needed especially if ophthalmic signs and symptoms are present
Toxicosis
Low TSH, low T4 and high T3
Radioiodine uptake patterns
High update - Graves’ disease. Low uptake - thyroiditis
Treatment of hyperthyroidism
Depends on multiple factors: age of pt, size of goiter, other medical conditions, severity of symptoms, and wishes of pt
Iodine preparations and treatment of Graves’ disease
Dose is 1 gm/day for up to 12 weeks and not used long-term because can increase thyroid hormone release
Low term effects of thyroxine
Decreased bone density, cardiac arrhythmias
TSH and disgnosis of hypothyroidism
TSH elevated and free T4 decreased
Diseases classified under Alzheimer’s disease
Parkinson’s-associated dementia, Lewy Body Dementia, Frontal Lobe Dementia
Questions to ask yourself when considering dementia
Is this a reversible problem? How best to treat the patient and the family?
Changes in brain regarding Alzheimer’s
Senile plaques develop between neurons. Neurofibrillary tangles develop within the neurons
Pathophysiology of Alzheimer’s
Involvement of cholinergic neurons causes level of acetylcholine within synapses to drop. Levels of acetylcholinesterase also drop. Butylcholinesterase levels increase which metabolizes acetylcholinesterase and the disease progresses. Glutamate is also thought to be involved, is a chemical that causes brain cell death.
Vascular dementia - clinical manifestations
Caused by multi-infarcts. Sudden onset, stepwise deterioration. Difficulty retrieving works, organizing and solving complex problems. Relatively preserved language skills. More depressed component. Numerous CV risk factors. MRI - periventricular white matter disease
Lewy Body Dementia - clinical manifestations
Dementia presents first followed by physical changes. Recurrent visual hallucinations and delusions. Often walks with a stoop (similiar to Parkinson’s). Frequent falls are common. More flactuating attention problems. Increased sensitivity to conventional anti-psychotics. Performs better on verbal recall than Alzheimer’s pts. Poor organizational skills
Progression of Alzheimer’s
Mild cognitive impairment- 7 yrs - short-term memory loss. Mild - 2 yrs - problems reading, poor object recognition, poor directional sense. Moderate - 2 yrs - poor judgment, impulsivity, short attention. Severe - 2 yrs - visual problems
Diagnosis of Alzheimer’s dementia
Memory impairment and one or more of the following - asphasia, apraxia, agnosia, and disturbances in planning, organizing, sequencing, abstracting
Diagnostic studies to consider when diagnosing Alzheimer’s
CBC - anemia or infection. Vit B12 - anemia. Folate - anemia. Homocystine - supports B12 and folate. Thyroid function - reversible cause. Metabolic panel - rule out liver or renal and is reversible. Electrolytes and calcium - hypo/hypernatremia or hypo/hypercalcemia. Glucose. Lipid - vascular cause. ECG - a-fib. RPR - latent syphilis
Prevelance of stroke
Major cause of permanent disability and 3rd leading cause of death in U.S.
Definition of stroke
Symptoms lasting 24 hrs or imaging of an acute clinically relevant brain lesion in patients with rapidly vanishing symptoms.
Definition of TIA
Brief episode of neurological dysfunction caused by a focal disturbance of brain or retinal ischemia, wich clinical symptoms typically lasting less than 1 hr and without evidence of infarction”. Important determinant of stroke with 90-day risk reported as high as 10.5% and greatest risk in first week.
Diagnosis of epilepsy
When they have had two unprovoked seizures and all other possible causes have been ruled out
Physiological signiture of Parkinson’s disease
Progressive death of neurons, and the presence of tiny dense structures called Lewy bodies, in the substantia nigra of the brain’s basal ganglia that produce dopamine
Cardinal signs of Parkinson’s disease
Non-intentional tremors at rest (pill-rolling), bradykinesis, muscle ridigity, and postural instability.
Early symptoms of Parkinson’s disease
Small handwriting, slowness in walking, reduced speech volume with montony, reduced arm swing, reduced blinking and swallowing, and seborrheic dermatitis
Later symptoms of Parkinson’s disease
A shuffling, stooped gait, instability, propulsive gait, retropulsion, and postural hypotention leads to falls, dysphagia, impotence, and urgent micturition or incontinence
Diagnosis of Parkinson’s
Made by history and physical exam. No specific labs
Pharmacologic therapy of Parkinson’s
Drugs that lower central dopamine concentrations - Levadopa, Requip, MAO inhibitors, Amantadine
Levadopa/Carbidopa
Often initial choice for Parkinson’s - greater effect on bradykinesia and rigidity. Sinemet
Where in the back does the spinal cord end?
T12-L1
Conus Medullaris
Lower end of the spinal cord
Cauda Equina
Division of multiple nerve roots beginning at the level of L1
Discs commonly involved in lower back problems
L4-L5 and L5-S1
Types of disc herniation
Protrusion/bulge, disc herniation, and sequestration
Protrusion/bulge of disc
A bulgin disc with intact annular and posterior longitudinal ligament fibers
Categories of disc herniation
Type A - disruption of inner annular fibers with intact outer annular fibers. Type B - disrupted annulus with tail of disc material extending into the disc space.
Sequestration
Free fragment without tail extending into disc space. Fragment may be reabsorbed spontaneously.
Typical locations of disc herniation
Central, posterolateral, and foraminal
Central disc herniation
Rare and affects multiple nerve roots, back pain more than leg, cause incontinence of bladder and bowel, requires immediate treatment.
Posterolateral disc herniation
Usual location, most commonly involving one nerve root (the lower one)
Foraminal disc herniation
Occurs in 8-10% of cases and involves the exiting nerve. Usually the top nerve
Discogenic back pain internal disc disruption
Annular tears. Early disc degeneration. Pain worsens with flexion/sitting. Slightly better with extension. Forward flexion limited on exam. No radicular symptoms.
Straight leg raise with back pain
Wanting to see if pt can actively lift leg more than 30 degrees. Passively lift pt leg until point of pain is reached. Looks for nerve root impingement
Braggard stretch leg test for back pain
Stop at point of pain with straight leg pain and lower until pain stops. Then dorsiflex the foot to reproduce the pain in the buttock and back
Hoover test for leg pain
Measures ability of pt to more or not be able to move leg. Put hands under heels and ask pt to lift leg. When they are faking, you will feel counter force to the opposite foot.
Benign essential tremors
Get worse with intentional activity and they respond really well to beta blockers
Goal of parkinson’s disease treatment
Reduce symptoms, minimize complications, maintain independence. The foundation of treatment is individualization and education.
Freezing phenomenon with Parkinson’s
A motor block, is a transient inability to perform active movements. Usually affects legs, but can involve eyelid opening, speaking, and writing
Wearing off effect of parkinson’s
The period of effectiveness after each dose may begin to shorten
On/off effect of Parkinson’s
Sudden fluctuations in movement, from normal or dyskinesia to parkinsonian slowness and stiffness and back again. The responses to a drug is changing as the disease progresses
Risk stratification for risk of early recurrence of stroke
ABCD - Age, blood pressure, clinical symptoms of focal weakness or speech impairment without weakness, diabetes.
When to discontinue anti-thrombotic therapy
When risks of bleeding become greater than the beneift. Pre-procedures - must weigh risk of hemorrhage about risk of thromboembolism. The decisions about stopping treatment pre-surgery/procedure are made on the basis of type of therapy, pts bleeding risk, and degree of inherent in the procedure. Consult
Type of dementia associated with neurofibrillary tangles
Alzheimer’s
Question to ask when assessing for memory loss
What did you have for dinner yesterday?
Acetylcholinesterase inhibitors works by…
Shown to slow progression of memory loss
Principle of antiepileptic drug therapy
Titrate medication slowly
A construction worker who suffered a new seizure should be advised…
To avoid work on any roof until fully evaluated
Earliest presentation of Parkinson’s Disease that is often misdiagnosed
Resting tremor in the distal extremities
Best way to diagnose Parkinson’s disease
Giving a small dose of Levadopa /carbidopa (Sinemet)
Spinal stenosis should be suspect when…
Walking or prolonged standing causes pain in legs
Diagnosis of a patient who suffered from right side facial and arm numbness for a few hrs and resolved
TIA
A nonmodifiable risk factor for stroke is
HTN
An appropriate antiplatelet therapy post TIA without a-fib and no other contraindications/risk factors
Low dose aspirin
Essential tremor
Benign, chronic neurologic condition that involves symmetric, rhythmic trembling of the upper extremities, head, or voice. Legs are less common. Emotional stress will increase symptoms.
Multiple sclerosis
Chronic progressive inflammatory and neurodegenerative disease affecting the CNS. Hallmark lesion is called a plaque
Onset of MS
Usually between 20-50, more women than men
Pathophysiology of MS
Thought to be triggered by an event, probably environment, that activates the inflammatory process outside the CNS
Four clinical courses of MS
Relapsing-remitting (RRMS), primary-progressive (PPMS), secondary-progressive (SPMS), and progressive-relapsing(PRMS). RRMS is most common
Common initial symptoms of MS
Sensory symptoms (paresthesias), optic neuritis, limb weakness, diplopia, nystagmus, unsteady gait, myelopathy, and trigeminal neuralgia
Diagnosis of MS
Clinical diagnosis. Events must be at least two distinct episodes lasting more than 24 hrs occuring at least 30 days apart and occur in two different locations. The symptoms must be not explained by another pathologic process.
Gold standard of MS diagnosis
MRI of brain
Drugs to treat MS
Interferons (Betaseron, extavia, avonex, rebif), copaxone, mitoxantrone
Pathophysiology of Parkinson’s
Develops after widespread depletion of dopamine in the substantia nigra and the nigrostriatal pathway to the caudate and putamen
Clinical presentation of Parkinson’s
Asymmetric or unilateral tremor, rigidity, bradykinesia with freezing, and flexed posture with loss of postural reflexes. Cogwheel feeling with passive movement of joint
Status epilepticus
Defined as more than 30 minutes of continuous seizure activity or two or more seizures without a baseline consciousness between attacks
Partial seizures
Begin in a limited region of one cerebral hemisphere and how focal EEG abnormalities. Consciousness may vary
Simple partial seizures
No alteration in consciousness and are usually the aura, or warning, that the patient experiences before a larger seizure
Complex partial seizure
The seizure activity spreads and involves the brainstem or both hemispheres, consciousness becomes altered
Primary generalized seizure
Occur when the initial electrical activity begins in both cerebral hemispheres. Consciousness is almost always imapired and may be convulsive or nonconvulsive
Clinical presentation of seizure
Accurate and detailed history is important New onset seizures require determination of any recent history of headache, illness, trauma, or focal neurologic deficit
Goal of seizure management
Control seizures with minimum adverse effects
Types of stroke
Ischemic (more prevalent) and hemorrhagic (more deadly)
Relapse of back pain
75% in the 12 months after recovery
Chronic low back pain
Defined as pain that lasts for more than 12 weeks, making the recovery time less certain
Categories of lumbar spine disorders
Axial low back pain and radicular pain
Mechanical back pain causes
Atrributed to direct injury, deformity, imbalance, or overuse of identifiable structures
Structural causes of mechanical low back pain
Intervertebral disks, facet joints, vertebral bodies, ligamentous structures, and sacroiliac joing as well as imbalances of the muscles supporting the lumbar spine
Neuropathic causes of low back pain
Typically attributed to direct compression of the spinal cord or spinal nerve roots as well as alteration of the neurologic pathways involving the brain and spinal cord.
Lumbar radiculopathy
Refers to involvement of the spinal nerve root with resultant neurologic symptoms, such as pain, weakness, numbness, tingling, and change in reflexes involving a specific dermatomal or myotomal distribution associated with an affected lumbar spinal nerve root
Clinical presentation of lumbar radiculopathy
Often present with significant leg and thigh pain greater than low back pain and may include neurologic symptoms
Clinical presentation of spinal stenosis
Typically present with thigh, calf, and back pain, typically worsened by standing and walking and alleviated with sitting
Most widely used imaging study for back pain
MRI of brain
Management of back pain
Bed rest for no more than 2 days with frequent position changes
Acute cerebral vascular syndreom (ACVS)
Used to be called TIA and refers to events that are manifested as neurologic deficits that resolve completely within a few hrs but no more than 24 hrs.
Population typically affected by ischemic strokes
Typically older persons with other disease processes
Population typically affected by hemorrhagic strokes
Typically healthy individuals between 40-60
Risk factors for ischemic stroke
HRN, age, smoking, male, family history, race, previous stroke, carotid stenosis of more than 80%, a-fib, CHF, mitral stenosis, prosthetic cardiac valves, MI, and cocaine use, diabetes, sedentary lifestyle, and elevated cholesterol
Risk factors for hemorrhagic stroke
Intracranial vascular anomalies, HTN, family history, PCOS, Ehler-Danlos syndrome, lupus, neurofibromatosis, tuberous schlerosis, pregnancy, smoking, atherosclerosis, acute ETOH intoxication, and cocaine use.
Most common cause of hemorrhagic stroke
Trauma
Common signs and symptoms of stroke
Hemiparesis, hemisensory loss, visual field defects, ataxia, dysarthria, relfex asymmetry, and Babinski’ssign
Presentation of ischemic stroke
May occur over a few hours in a stepwise or shuttering fashion involving one area and progressing until the stroke is fully developed
Presentation of hemorrhagic stroke
Usually begins with the abrupt onset of a severe headache (“worst headache of my life”), nausea and vomiting, signs of meningeal irritation, and varying degrees of neurologic dysfunction, loss of consciousness, dizziness, seizures, with or without neurologic dysfunction
Presentation of HTN intracerebral hemorrhage
May have no warning signs, HTN, headache, followed within a few minutes by unilateral facial sag, slurred speech, weakness in an arm and leg, and eye deviation away from the paretic limbs occurring during 5-30 minutes
Preferred diagnostic test for stroke
CT
Management of TIA
If seen days after event and has no current signs or symptoms - out-pt management is adequate. If symptoms, should be treated as a medical emergency
Management of ischemic stroke
Careful monitoring of BP - labetalol. tPA for selected pts if administered within 3 hrs of onset. Antiplatelet agents - ASA, Coumadin, Plavix
Patient education regarding stroke
Risk factor reduction and stroke symptom recognition and emergency treatment. HTN is most important independent and modifiable risk factor
