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Potassium-Sparing Diuretics
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Potassium-sparing diuretics are weak diuretics. They are most often prescribed in combination with thiazides or loop diuretics, to prevent hypokalemia or to increase the amount of fluid removed from the body.

Definition
A diuretic is a medicine which increases the amount of water that is excreted from the kidneys. There are different types of diuretics. Potassium-sparing diuretics are one type; they include amiloride and triamterene. There is one other medicine which is also a potassium-sparing diuretic: spironolactone. This medicine works in a slightly different way to amiloride and triamterene. It is referred to as an aldosterone antagonist.

Mechanism of Action
Amiloride and triamterene work by making the kidneys pass out more fluid. They do this by interfering with the transport of salt and water across certain cells in the kidneys. As more fluid is passed out by the kidneys, less fluid remains in the bloodstream. So any fluid which has accumulated in the tissues of the lungs or body is drawn back into the bloodstream to replace the fluid passed out by the kidneys. This eases symptoms such as edema (fluid retention in legs) and breathlessness caused by the congestion of fluid. As well as increasing the amount of water that is excreted by the kidneys, potassium-sparing diuretics also help the kidneys retain potassium in the body.

Spironolactone works in a slightly different way to amiloride and triamterene. This medicine blocks the action of a hormone called aldosterone and this causes the kidney to pass out more fluid and keep potassium. This is why it is sometimes referred to as an aldosterone antagonist.

Potassium-sparing diuretics are often combined with either a loop diuretic or a thiazide diuretic. This is because they help to keep the right amount of potassium in your blood and they help other diuretics to remove fluid from the body.

Usage
Potassium-sparing diuretics (amiloride, and triamterene) are weak diuretics, most often prescribed in combination with thiazides or loop diuretics, to prevent hypokalemia.

An aldosterone antagonist (spironolactone) is prescribed with other diuretics to increase the amount of fluid removed from the body and to prevent hypokalemia.

Diuretics are commonly used in the treatment of heart failure. Diuretics are also used to treat other conditions which cause fluid to build up in the body, such as certain liver and kidney disorders and high blood pressure.

Side-Effects
Side-effects are uncommon when routine low doses are used. The higher the dose, the greater the risk of side-effects developing.

Amiloride and triamterene
Possible side effects include: stomach upset, stomach ache or cramp, dry mouth, dizziness or feeling faint, especially when getting up from sitting or lying down (due to too low blood pressure). Other side-effects that have been reported include: skin rash, feeling sleepy or confused, headache, aches and pains, muscle cramps, weakness, diarrhea or constipation.

Spironolactone
Possible side effects include: feeling or being sick, sexual problems, enlargement of the breasts (both in men and women), irregular menstrual periods, confusion and skin rash.

Contraindications
They should not be taken by anyone who has high levels of potassium in their blood, severe kidney problems, or Addison's disease. In addition, potassium supplements should not be taken with these medicines.

CLINICAL VIGNETTES

A 55-year-old man consults a physician because of episodic weakness and paresthesias. On one occasion, he experienced transient paralysis. The patient has also been experiencing polyuria and polydipsia. Vital signs demonstrate a blood pressure of 140/100 mm Hg with normal temperature, pulse, and respirations. The remainder of the physical examination is unremarkable and specifically shows no significant abnormal neurologic findings and no peripheral edema. Routine screening chemistry studies are remarkable only for a serum potassium of 2.1 mEq/L. CT scan demonstrates a small adrenal mass. Which of the following is the most appropriate pharmacotherapy to treat this patient's hypertension?

A. Captopril 
B. Furosemide 
C. Hydrochlorothiazide 
D. Propanolol 
E. Spironolactone 

E. Hypertension with an adrenal mass should bring to mind two distinct conditions: an epinephrine/norepinephrine-secreting pheochromocytoma, or an aldosterone-secreting adrenocortical tumor (which can produce Conn syndrome). Although both of these can produce hypertension, other aspects of the clinical presentation are quite different. Pheochromocytoma can produce either episodic severe hypertension or continuous hypertension. In either situation, electrolyte studies are usually normal. In contrast, Conn syndrome (which this patient has) often shows prominent symptoms related to hypokalemia, including weakness, paresthesias, and transient paralysis. The treatment of hypertension related to high aldosterone levels is to block the aldosterone activity with the potassium-sparing diuretic (and aldosterone antagonist) spironolactone. 

Captopril (choice A) is an angiotensin converting enzyme (ACE) inhibitor that works well to reduce blood pressure in many patients by blocking the renin-angiotensin system; however, it is less effective when there is already an excess of aldosterone present. 

Furosemide (choice B), a loop diuretic, and hydrochlorothiazide (choice C), a thiazide type diuretic, would tend to make the patient's hypokalemia worse. 

Propanolol (choice D) is a beta blocker that would reduce blood pressure but would not specifically counter the cause of this patient's hypertension. 

A 68-year-old woman presents for a routine check-up. Her only complaint is that she occasionally experiences a little swelling in her ankles. Her serum potassium is 3.5 mEq/L, so the physician wants to avoid unnecessary potassium losses. Which of the following diuretics would be most appropriate for this patient? 

A. Furosemide
B. Hydrochlorothiazide
C. Indapamide
D. Metolazone
E. Triamterene

The correct answer is E. Potassium is responsible for maintenance of intracellular tonicity, transmission of nerve pulses, contraction of muscle (striated and smooth), and maintenance of renal function. The normal blood level of potassium ranges from 3.5 to 5.0 mEq/L. In potassium depletion, a decrease in the blood potassium level by 1 mEq/L equals a loss of 100-200 mEq from potassium stores in the body. Depletion can result in the development of muscular weakness, paralysis, and mental confusion. Since this patient is borderline hypokalemic, she should receive a potassium-sparing diuretic, such as spironolactone, amiloride, or triamterene. These agents are all indicated for the treatment of edematous states as well as the prophylaxis and treatment of hypokalemia. These agents are commonly combined with other non-potassium-sparing diuretics to prevent the appearance of hypokalemia during therapy.

Furosemide (choice A) is a loop diuretic indicated for the treatment of edematous states in hypertension and is commonly associated with the development of hypokalemia. 

Hydrochlorothiazide (choice B), indapamide (choice C), and metolazone (choice D) are thiazide diuretics indicated for the treatment of edematous states in hypertension and are also commonly associated with the development of hypokalemia.

You are seeing a 79-year-old woman with hypertension, diabetes, coronary artery disease, and rheumatoid arthritis in your office for a routine follow-up visit. Her meds include spironolactone, amiloride, NPH insulin, aspirin, prednisone, and ketorolac. Her temperature is 37 C (98.6 F), blood pressure is 99/56 mm Hg, pulse is 58/min, and respirations are 19/min. Physical examination is unremarkable. An electrocardiogram shows a sinus rhythm and non-specific ST and T wave abnormalities. Her serum sodium is 136 mEq/L and serum potassium is 5.8 mEq/L. A review of her laboratory values over the past 6 months indicates that her serum potassium has been gradually increasing. The most appropriate management at this time would be to

A. add clonazepam to her current therapy
B. add metoprolol to her current therapy
C. discontinue the amiloride
D. discontinue the ketorolac
E. discontinue the prednisone

The correct answer is C. Spironolactone, an aldosterone antagonist, causes an increase in serum potassium. Amiloride, a potassium sparing diuretic, has a similar effect. The use of both these agents can lead to potentially dangerous hyperkalemia. If hyperkalemia does manifest, one of them should be discontinued.

Clonazepam (choice A), a benzodiazepine anxiolytic, is not warranted since there is no evidence that the patient is anxious.

Metoprolol (choice B) will not decrease serum potassium. Infact, beta-blockers can increase serum potassium. The patient's heart rate and blood pressure also do not mandate a beta-blocker at this juncture.

Discontinuation of ketorolac (choice D), a nonsteroidal antiinflammatory agent, is unnecessary since it is not associated with hyperkalemia.

Discontinuation of prednisone (choice E) is not needed, since prednisone does not cause or worsen hyperkalemia.
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Post-Streptococcal Glomerulonephritis 
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Postistreptococcal glomerulonephritis occurs after infection, usually with a nephritogenic strain of group A β-hemolytic streptococcus (Streptococcal Pyogenes). Diagnosis is suggested by history and urinalysis and confirmed by finding a low complement level and sometimes by antibody testing. Prognosis is excellent. Treatment is supportive.

Etiology
Poststreptococcal glomerulonephritis, a nephritic syndrome, is the most common cause of a glomerular disorder in children between 5 and 15 yr.

Most cases are caused by nephritogenic strains of group A β-hemolytic streptococci - Streptococcus pyogenes, most notably type 12 (which causes pharyngitis) and type 49 (which causes impetigo); an estimated 5 to 10% of patients with streptococcal pharyngitis and about 25% of those with impetigo develop this condition. A latency period of 6 to 21 days between infection and GN onset is typical, but latency may extend up to 6 wk.

The mechanism is unknown, but microbial antigens are thought to bind to the glomerular basement membrane and activate primarily the alternate complement pathway both directly and via interaction with circulating antibodies, causing glomerular damage, which may be focal or diffuse. Alternatively, circulating immune complexes could precipitate on the glomerular basement membrane.

Symptoms and Signs
Symptoms and signs range from asymptomatic hematuria (in about 50%) and mild proteinuria to full-blown nephritis with microscopic or gross hematuria (cola-colored, brown, smoky, or frankly bloody urine), proteinuria, oliguria, edema, hypertension, and renal insufficiency. Severe, late disease is a relatively uncommon cause of nephrotic syndrome. Renal failure that causes fluid overload with heart failure and severe hypertension requiring dialysis affects 1 to 2% of patients and may manifest as a pulmonary-renal syndrome with hematuria and hemoptysis.

Diagnosis
• Clinical evidence of recent infection
• Urinalysis typically showing dysmorphic RBCs, proteinuria, WBCs, and renal tubular cells
Often hypocomplementemia

Poststreptococcal glomerulonephritis is suggested by history of pharyngitis or impetigo plus either typical symptoms or incidental findings on urinalysis. Tests done to confirm the diagnosis depend on clinical findings. Antistreptolysin O, antihyaluronidase, and antideoxyribonuclease (anti-DNAase) antibodies are commonly measured. Serum creatinine and complement levels (C3 and total hemolytic complement activity) are also usually measured. Biopsy confirms the diagnosis but is rarely necessary; demonstration of hypocomplementemia is essentially confirmatory.

Anti-streptolysin O (ASO is the antibody made against streptolysin O, a hemolytic toxin produced by most strains of group A including Strep Pyogenes.

Antistreptolysin O level, the most common laboratory evidence of recent streptococcal infection, increases and remains elevated for several months in about 75% of patients with pharyngitis and in about 50% of patients with impetigo, but it is not specific. An increase in antihyaluronidase and antideoxyribonuclease titers is more specific for detecting recent streptococcal skin infection but is not widely available.

Urinalysis typically shows proteinuria (0.5 to 2 g/m2/day); dysmorphic RBCs; WBCs; renal tubular cells; and possibly RBC, WBC, and granular casts.

C3 and total hemolytic complement activity (CH50) levels fall during active disease and return to normal within 6 to 8 wk in 80% of cases; C1q, C2, and C4 levels are only minimally decreased or remain normal.

The complement system is a part of the immune system that helps or complements the ability of antibodies and phagocytic cells to clear pathogens from an organism. Hypocomplementemia may be used more generally to refer to decreased complement levels. The total hemolytic complement CH50 level in the blood will be low or undetectable with complement deficiencies.

Biopsy specimens show enlarged and hypercellular glomeruli, initially with neutrophilic infiltration and later with mononuclear infiltration. On electron microscopy, these deposits are semilunar or hump-shaped and are located in the subepithelial area. The presence of these deposits and of small subendothelial and mesangial deposits initiates a complement-mediated inflammatory reaction that leads to glomerular damage.

Prognosis
Normal renal function is retained or regained by 85 to 95% of patients. GFR usually returns to normal over 1 to 3 mo, but proteinuria may persist for 6 to 12 mo and microscopic hematuria for several years.

Treatment
• Supportive care
Treatment is supportive and may include restriction of dietary protein, Na, and fluid and, in more severe cases, treatment of edema and hypertension. Dialysis is occasionally necessary. Antimicrobial therapy is preventive only when given within 36 h of infection and before GN becomes established.

Key Points
• Consider post streptococcal glomerulonephritis in young patients who have had pharyngitis or impetigo plus signs of GN.
• Biopsy confirms the diagnosis but is rarely necessary; demonstration of hypocomplementemia is essentially confirmatory.
• Supportive treatment usually leads to recovery of kidney function.

CLINICAL VIGNETTES

A 7-year-old boy is brought to the emergency department by his mother because of "tea-colored urine" for the last several days. He has also had some nausea and vomiting, and his eyes appear swollen when he wakes up in the morning. The eye swelling tends to resolve over the course of the day. He is generally very healthy and there is no family history of any chronic diseases. His temperature is 36.7 C (98.0 F), blood pressure is 130/90 mm Hg, pulse is 96/min, and respiratory rate is 16/min. Physical examination is unremarkable. A urinalysis shows red cell casts. At this time the most appropriate study to confirm your diagnosis is 
             
A. antistreptolysin O antibody
B. renal biopsy
C. renal ultrasound
D. urine culture

The correct answer is A. Poststreptococcal glomerulonephritis is the most common cause of acute glomerulonephritis in children. Itusually follows a streptococcal pharyngitis by 1-2 weeks and a streptococcal skin infection by 2-3 weeks. It most commonly occurs in school-age children and has a male to female predominance of 2:1. It is most commonly characterized by hematuria (microscopic or gross) with red cell casts, proteinuria, hypertension (from fluid overload secondary to decreased glomerular filtration rate), and edema (from retention of salt and water). Laboratory values are usually significant for markedly decreased complement levels (C3 and C4),  hypo- or hypernatremia, and a blood urea nitrogen elevated disproportionately to the creatinine. In order to diagnose poststreptococcal glomerulonephritis with certainty, there needs to be evidence of a preceding streptococcal infection such as an elevated ASO or streptozyme.

At this time, a renal biopsy (choice B) is not indicated. A renal biopsy is an invasive procedure with inherent risks. As this patient fits the perfect description for post streptococcal glomerulonephritis a renal biopsy would only be indicated if the complement level does not return to normal within 8 weeks, and the gross hematuria does not resolve over several weeks. If one was to do a renal biopsy on a patient with post-streptococcal glomerulonephritis, the findings would be: mesangial and capillary cell proliferation, inflammatory cell infiltration, and granular "humps" of IgG and C3 below the glomerular basement membrane.

A renal ultrasound (choice C) is useful in evaluating parenchymal disease, urinary tract abnormalities, or renal blood flow. In the case of post-streptococcal glomerulonephritis, the changes are microscopic and therefore would not be seen on ultrasound.

Urinary tract infections are a common cause of hematuria. Therefore, it is a good idea to do a urine culture (choice D) in all cases of hematuria. Unfortunately, the child in this case has red cell casts which indicate the kidneys are the source for the blood. So, although a urine culture should be sent on this child, it will probably not help with the diagnosis.

A 7-year-old boy presents to the pediatrician because his mother noticed a "smoky" color to his urine. Upon questioning the mother, it is revealed that the child suffered a sore throat several weeks ago that was left untreated. Physical examination reveals hypertension and mild generalized edema. Urinalysis is significant for red blood cell casts. Which of the following is the microorganism responsible for this child's illness?

A. Streptococcus pneumoniae
B. Streptococcus viridans
C. Streptococcus pyogenes
D. Streptococcus agalactiae

The correct answer is C. This is one of the "second order" questions. In this case, you need to figure out what disease the child has,  and then what organism causes the disease. The disease in question is poststreptococcal glomerulonephritis, as evidenced by the smoky urine, hypertension, edema, and red blood cell casts in the urine sediment. The history of the prior sore throat is a tip-off that this is a nonsuppurative sequela of an infection due to Streptococcus pyogenes (group A beta-hemolytic Streptococci).
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Mesenteric Ischemia 
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Retinoblastoma  
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Retinoblastoma is a cancer arising from the immature retina. Symptoms and signs commonly include leukocoria (a white reflex in the pupil), strabismus, and, less often, inflammation and impaired vision. Diagnosis is based on ophthalmoscopic examination and ultrasonography, CT, or MRI. Treatment of small cancers and bilateral disease may include photocoagulation, cryotherapy, and radiation therapy. Treatment of larger cancers is enucleation. Chemotherapy is sometimes used to reduce cancer volume and to treat cancers that have spread beyond the eye.

Retinoblastoma occurs in 1/15,000 to 1/30,000 live births and represents about 3% of childhood cancers. It is usually diagnosed in children < 2 yr; < 5% of cases are diagnosed in those > 5 yr. The cancer may be hereditary. About 25% of patients have bilateral disease, which is always heritable. Another 15% of patients have heritable unilateral disease, and the remaining 60% have nonhereditary unilateral disease.

The pathogenesis of inheritance appears to involve mutational deactivation of both alleles of a retinoblastoma suppressor gene located on chromosome 13q14. In the hereditary form, a germline mutation alters one allele in all cells, and a later somatic mutation alters the other allele in the retinal cells (the 2nd hit in this 2-hit model), resulting in the cancer. The nonhereditary form probably involves somatic mutation of both alleles in a retinal cell.

Symptoms and Signs
Patients typically present with leukocoria (a white reflex in the pupil, sometimes referred to as cat's-eye pupil) or strabismus. Much less often, patients present with inflammation of the eye or impaired vision. Rarely, the cancer has already spread, via the optic nerve or the choroid or hematogenously, resulting in an orbital or soft-tissue mass, headache, anorexia, or vomiting.

When the diagnosis is suspected, both fundi must be closely examined by indirect ophthalmoscopy with the pupils widely dilated and the child under general anesthesia. The cancers appear as single or multiple gray-white elevations in the retina; cancer seeds may be visible in the vitreous.

Diagnosis
• Orbital ultrasonography, CT, or MRI
• Sometimes bone scan, bone marrow aspirate and biopsy, and lumbar puncture

Diagnosis is usually confirmed by orbital ultrasonography or CT. In almost all cancers, calcification can be detected by CT. However, if the optic nerve appears abnormal during ophthalmoscopy, MRI is better for finding cancer extension into the optic nerve or choroid. Whenever extraocular spread is suspected, testing should include a bone scan, a bone marrow aspirate and biopsy, and lumbar puncture.

Children who have a parent or sibling with a history of retinoblastoma should be evaluated by an ophthalmologist shortly after birth and then every 4 mo until age 4 yr. Patients with retinoblastoma require molecular genetic testing, and if a germline mutation is identified, parents should also be tested for the same mutation. If subsequent offspring of parents have the germline mutation, the same genetic testing and regular ophthalmologic examination are required. Recombinant DNA probes may be useful for detecting asymptomatic carriers.

Prognosis
If the cancer is treated when it is intraocular, > 90% of patients can be cured. Prognosis for patients with metastatic disease is poor.

In patients with hereditary retinoblastoma, incidence of 2nd cancers is increased; about 50% arise within the irradiated area. These cancers can include sarcomas and malignant melanoma. Within 30 yr of diagnosis, 70% develop a 2nd cancer.

Treatment
Unilateral retinoblastoma is managed by enucleation with removal of as much of the optic nerve as possible.

For patients with bilateral cancer, vision can usually be preserved. Options include bilateral photocoagulation or unilateral enucleation and photocoagulation, cryotherapy, and irradiation of the other eye. Radiation therapy is by external beam or, for very small cancers, brachytherapy (attachment of a radioactive plaque to the eye wall near the cancer).

Systemic chemotherapy, such as carboplatin plus etoposide, or cyclophosphamide plus vincristine, may be helpful to reduce the size of large cancers or to treat cancer that has disseminated beyond the eye. However, chemotherapy alone can seldom cure this cancer.

Ophthalmologic reexamination of both eyes and retreatment, if necessary, are required at 2-mo to 4-mo intervals.

CLINICAL VIGNETTES

A young mother is at the pediatrician's office for a routine well-baby visit for her 18-month-old son. It is immediately noticed that one of the baby's pupils is white, while the other one is black. When asked about it, the mother relates that she saw that curious situation for the first time 1 week ago, but since the baby was otherwise asymptomatic, she did not think it merited special attention. Which of the following is the most appropriate course of action? 

A. Do nothing, this is a normal anatomic variant
B. Inquire if the father is an albino, and do appropriate genetic counseling
C. Seek an ophthalmologic consultation for suspected congenital cataract
D. Seek an emergency ophthalmologic consultation for possible retinoblastoma
E. Treat the child with antibacterial eye drops and re-check in 2 weeks

D. A newly developed white pupil in a child raises the possibility of retinoblastoma. This tumor is so deadly that immediate diagnosis and treatment are imperative. Ignoring the finding (choice A) could prove to be lethal, and the same can be said for any delays caused by pursuing bizarre considerations, such as looking for albinos in the family (choice B) or treating for an eye infection that is not there (choice E). It could be argued that if an ophthalmologic consultation is obtained, even if it is for a wrong diagnosis (choice C), the true nature of the problem will eventually be recognized. But an appointment to check for cataracts (which would have been present since birth) will not be made with the same urgency that the situation requires.

A 2-year-old girl is evaluated because of deteriorating vision. On physical examination, a whitish hue is noted in the right pupil, along with strabismus. Palpation of the eye elicits apparent pain and tenderness. The patient is referred to an ophthalmologist, who schedules surgery, and removes a multifocal tumor from the right eye. The pathology report notes the presence of rosettes composed of cuboidal-to-columnar cells surrounding a central lumen in the tumor. In all likelihood, this child's condition stems from a mutation in a gene on chromosome

A. 5
B. 7
C. 9
D. 13
E. 21

The correct answer is D. The description of this case is classic for retinoblastoma, the most common malignant eye tumor of childhood. Retinoblastoma presents as in the question, and microscopically is composed of neuroepithelial cells that form characteristic rosettes (Flexner-Wintersteiner rosettes). Familial retinoblastoma is often bilateral or multifocal, as in this case. A preexisting mutation of a tumor suppressor gene, Rb, located on chromosome 13 (13q14) is present, but causes no symptoms. A second, somatic mutation in a retinal cell leads to loss of a nuclear protein that prevents the retinal cell from exiting G1, allowing development of the tumor. In cases of sporadic retinoblastoma, mutations must occur in both chromosomes 13 of a somatic cell, a rare event, hence sporadic retinoblastoma is always unifocal and unilateral.

A 5-month-old girl has bilateral retinoblastoma. Neither parent has a history of having had retinoblastoma. Chromosomal analysis of the patient's stimulated peripheral blood lymphocytes is done; the photograph is of a representative karyotype. Which of the following critical events has most likely resulted from an aberration involving chromosome 13?

A. Proto-oncogene activation
B. Proto-oncogene amplification
C. Proto-oncogene loss
D. Tumor-suppressor gene activation
E. Tumor-suppressor gene loss

Answer E. The pathogenesis of inheritance appears to involve mutational deactivation of both alleles of a retinoblastoma suppressor gene located on chromosome 13q14. In the hereditary form, a germline mutation alters one allele in all cells, and a later somatic mutation alters the other allele in the retinal cells (the 2nd hit in this 2-hit model), resulting in the cancer. 

A young mother is at the pediatrician's office for a routine well-baby visit for her 18-month-old son. The mother recalls that a child in his daycare program had to be sent home 9 days ago because of "pink eye," but none of the other children seem to have been affected. Physical examination reveals stable vital signs. He has appropriate growth curves for both height and weight. The baby has a white reflex in the left eye with no evidence of discharge. Which of the following is the most appropriate course of action?

A. Provide antibacterial eye drops and follow up in 2 weeks
B. Provide genetic counseling
C. Routine followup
D. Seek an emergency ophthalmologic consultation
E. Seek a surgery consultation for the next available appointment

The correct answer is D. A newly developed white pupil (leukocoria) in a child raises the possibility of retinoblastoma. This tumor is so deadly that immediate diagnosis and treatment are imperative. The first step is referral for emergent ophthalmologic examination under anesthesia. The eyes are examined with pupillary dilation that will most likely reveal a chalky, white-gray retinal mass with a soft and friable consistency. Examination also allows for identifying seeding or multifocaltumors. After ophthalmologic examination, a CT scan, ultrasound, or MRI of the head may be performed for staging. Do not biopsy, because this results in easy seeding of the tumor. Treatment is individualized and involves enucleation, external beam radiotherapy , cryotherapy, or laser photocoagulation. After determining the presence and extent of the tumor, surgical intervention (choice E) by the ophthalmologist may be warranted.

Remember these pearls:
If the white reflex is bilateral and present at birth, it is most likely congenital.
If the white reflex is unilateral or present months after birth, it is most likely malignant.

Ignoring the finding (choice C) could prove to be lethal, and the same can be said for any delays caused by pursuing other considerations, such as looking for albinos in the family and providing genetic counseling (choice B) or treating for an eye infection that is not there (choice A).
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Parkland Formula for Burns    
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Burns are injuries of skin or other tissue caused by thermal, radiation, chemical, or electrical contact. Burns are classified by depth (1st-degree, superficial and deep partial-thickness, and full-thickness) and percentage of total body surface area (TBSA) involved. Complications and associated problems include hypovolemic shock, inhalation injury, infection, scarring, and contractures. Patients with large burns require fluid resuscitation. Treatments for burn wounds includes topical antibacterials, regular cleaning, elevation, and sometimes skin grafting. Intensive rehabilitation, consisting of range-of-motion exercises and splinting, is often necessary.

Intravenous fluids: IV fluids are given to patients in shock or with burns > 10% TBSA. A 14- to 16-gauge venous cannula is placed in 1 or 2 peripheral veins through unburned skin if possible. Venous cutdown, which has a high risk of infection, is avoided. 

Initial fluid volume is guided by treatment of clinically evident shock. If shock is absent, fluid administration aims to replace the predicted deficit and supply maintenance fluids.The Parkland formula (4 mL x kg  x % TBSA burned) is used to estimate fluid volume needs in the first 24 h after the burn (not after presentation to the hospital) and determines the rate of IV fluid administration. Fluid is given as lactated Ringer solution because large amounts of normal saline could result in hyperchloremic acidosis. 

Parkland Formula for Burns = [4 mL/kg] x [weight in kg]  x [% TBSA burned]

For example, in a 100-kg man with a 50% TBSA burn, fluid volume by the Parkland formula would be 

4 x 100 x 50 = 20,000 mL

Half of the volume, 10 L, is given in the first 8 h after injury as a constant infusion (1250 mL/hr), and the remaining 10 L is given over the following 16 h (625 mL/hr). In practice, this formula is only a starting point, and infusion rates are adjusted based on clinical response. Urine output, typically measured with an indwelling catheter, is the usual indicator of clinical response; the goal is to maintain output between 30 and 50 mL/h in adults and between 0.5 and 1.0 mL/kg/h in children. When giving typical large volumes of fluid, it is also important to avoid fluid overload and consequent heart failure. Clinical parameters, including urine output and signs of shock or heart failure, are recorded at least hourly on a flow chart. 

Some clinicians give colloid after 12 h to patients who have larger burns, are very young or very old, or have heart disease and require large fluid volumes. 

If urine output is inadequate despite administration of a large volume of crystalloid, consultation with a burn center is necessary. Such patients may respond to an infusion of colloid or other measures. Patients with inadequate urine output despite administration of a large volume of crystalloid are at risk of resuscitation complications including compartment syndrome. 

For patients of any age with rhabdomyolysis, fluid should be given to maintain urine output between 0.5 and 1 mL/kg/h. Some authorities recommend alkalinizing the urine by adding 50 mEq NaHCO3 (one 50-mL ampule of 8.4% solution) to a liter of IV fluid. 

Key Points

• If burns are > 10% TBSA, give IV lactated Ringer solution, at an initial rate guided by the Parkland formula ([4 mL/kg] x [weight in kg]  x [% TBSA burned] during the 1st 24 h after the burn) and adjusted based on hourly urine output.

• In the "rule of nines," in an adult, the head and neck represent 9% of the body surface. Each arm represents 9%. The anterior trunk represents 18% and the posterior truck represents 18%. Each lower extremity represents 18% of the body surface. The final 1% is represented by the genital area.

CLINICAL VIGNETTES

A man who weighs 65 kg sustains second and third degree burns over both of his lower extremities when his pants catch on fire. When examined shortly thereafter, it is ascertained that virtually all of the skin from both groins to the tip of the toes, front and back, has been burned. According to the modified Parkland formula, which of the following is the approximate total amount of IV fluid that he can be expected to require during the first 24 hours post-burn? 

A. 3460 mL
B. 4960 mL
C. 6760 mL
D. 8160 mL
E. 11,360 mL

E. The modified Parkland formula calls for 4 mL of Ringer's lactate per kilogram of body weight, times the percentage of the body surface that has been burned; plus an additional 2000 mL of dextrose 5% in water to cover maintenance fluid needs. In the "rule of nines," each lower extremity represents 18% of the body surface. Thus, this patient has sustained a 36% body burn: 4 × 65 × 36 = 9360, plus 2000 = 11,360 None of the other options provide enough fluid, although in the real world the formula calculations are used only to help determine a "ballpark figure" and a rate of initial infusion. Once fluid is going in, the fine tuning is done on the basis of hourly urinary output and central venous pressure. 

After suitable calculations have been made using the modified Parkland formula, a 70-kg man with extensive third-degree burns is receiving Ringer's lactate at the calculated rate, which happens to be 750 mL/hr. The infusion was started within 30 minutes of the time when the burn occurred. Over the next 3 hours, his urinary output is recorded as 15 mL, 22 mL, and 18 mL. It is verified that the Foley catheter is open and draining freely. The urine is dark yellow, without blood, and has a specific gravity of 1040 and a sodium concentration of 10 mEq/L. The patient's blood pressure is 100/70 mm Hg, his pulse is 98/min, and his central venous pressure is 2 cm H2O. On the basis of these findings, which of the following is the most appropriate next step in management?

A. Diuretics should be given
B. Fluid administration should continue at the present rate
C. The rate of fluid administration should be decreased
D. The rate of fluid administration should be increased
E. Treatment is needed for renal failure 

The correct answer is D. The calculations made by standard formulas are only an educated guess. Once fluid administration begins, we judge its adequacy by the information provided by urinary output and central venous pressure, aiming for an output of 1-2 mL/kg/hr, while not exceeding a venous pressure of 10 or 15. In this case, our calculations fell short of the mark, and the patient needs more fluids at a faster rate.
Diuretics (choice A) are not the answer when all indicators show fluid need: his venous pressure is low, his blood pressure and pulse rate are marginal, and he has very concentrated urine. He needs fluids!
The present rate (choice B) may follow the "formula," but it is clearly inadequate.
Decreasing the rate (choice C) is the very opposite of what is needed.
And as for renal failure (choice E), it is indeed part of the differential diagnosis whenever urinary output is not as high as it should be. However, the vignette told you that his urine is highly concentrated and has well less than 20 mEq/L of sodium: evidence of superb kidneys trying to conserve fluid to the best of their ability.

A 68-year-old woman is brought to the emergency department after being rescued from her burning apartment building. She was found unconscious in her bedroom, which was full of smoke and flames. On presentation, she has extensive second and third degree burns over her legs and torso with an estimated TBSA burn of 25%. The patient is stable with a blood pressure of 160/70 mm Hg and a pulse of 100/min. The body temperature is 36 C (96.8 F). The plan is to initiate fluid replacement. The most appropriate management is to

A. infuse 1ml/kg x TBSA % burn of colloid solution on post burn day 2 for 24 hours
B. infuse 1ml/kg x TBSA % burn of colloid solution over 24 hours
C. infuse 4ml/kg x TBSA % burn of lactated ringers solution over 8 hours
D. infuse 4ml/kg x TBSA % burn of lactated ringers solution over 24 hours
E. infuse 4ml/kg x TBSA % burn of lactated ringers solution with one half in the first 8 hours

The correct answer is E. 

Crystalloid solutions include isotonic or hypertonic saline or Ringer lactate solutions.

Colloid solutions included red blood cells, fresh frozen plasma or albumin solutions.

Burn patients are acutely hypovolemic secondary to massive capillary leak and tissue sequestration of fluid. Many formulas for administering fluid resuscitation have been described, all in proportion to the %TBSA burned. One half of the calculated resuscitation volume for the first 24 hours is given in the first 8 hours. The formula in this answer is the Parkland formula, the most widely used resuscitation formula. Most centers use crystalloid (normal saline or lactated ringers solution) for volume resuscitation.

Infusing 1ml/kg x TBSA % burn of colloid solution on post burn day 2 for 24 hours (choice A) or 1ml/kg x TBSA % burn of colloid solution over 24 hours (choice B) are colloid based resuscitation formulas. There is abundant evidence that outcome in burn patients is not influenced by early colloid administration. If colloid has any role in the management of acute thermal injury it is after the initial 24-hour post-burn period.

Infusing 4ml/kg x TBSA % burn of lactated ringers solution over 8 hours (choice C) and over 24 hours (choice D) are incorrect because of the duration of infusions.
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Scabies 
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Scabies is an infestation of the skin with the mite Sarcoptes scabiei. Scabies causes intensely pruritic lesions with erythematous papules and burrows in web spaces, wrists, waistline, and genitals. Diagnosis is based on examination and scrapings. Treatment is with topical scabicides or, sometimes, oral ivermectin.

Etiology
Scabies is caused by the mite Sarcoptes scabiei, an obligate human parasite that lives in burrowed tunnels in the stratum corneum. Scabies is easily transmitted from person to person through physical contact; animal and fomite transmission probably also occurs. The primary risk factor is crowded conditions (as in schools, shelters, barracks, and some households); there is no clear association with poor hygiene.

Symptoms and Signs
The primary symptom is intense pruritus, classically worse at night, although that timing is not specific to scabies.

Classic scabies: Erythematous papules initially appear in finger web spaces, flexor surfaces of the wrist and elbow, axillary folds, along the belt line, or on the lower buttocks. Papules can affect any area of the body, including the breasts and penis. The face remains uninvolved in adults. Burrows, usually on the wrists, hands, or feet, are pathognomonic for disease, manifesting as fine, wavy, and slightly scaly lines several mm to 1 cm long. A tiny dark papule—the mite—is often visible at one end. In classic scabies, people usually have only 10 to 12 mites. Secondary bacterial infection commonly occurs. 

Signs of classic scabies may be atypical. In infants, the palms, soles, face, and scalp may be involved, especially in the posterior auricular folds. In elderly patients, scabies can cause intense pruritus with subtle skin findings, making it a challenge to diagnose. In immunocompromised patients, there may be widespread nonpruritic scaling (particularly on the palms and soles in adults and on the scalp in children). 

A hallmark of scabies is the appearance of track-like burrows in the skin. These raised lines are usually grayish-white or skin-colored. They are created when female mites tunnel just under the surface of the skin. After creating a burrow, each female lays 10 to 25 eggs inside.

Diagnosis
• Clinical evaluation
Burrow scrapings

Diagnosis is suspected by physical findings, especially burrows, and itching that is out of proportion to physical findings and similar symptoms among household contacts. Confirmation is by finding mites, ova, or fecal pellets on microscopic examination of burrow scrapings; failure to find mites is common and does not exclude scabies. Scrapings should be obtained by placing glycerol, mineral oil, or immersion oil over a burrow or papule (to prevent dispersion of mites and material during scraping), which is then unroofed with the edge of a scalpel. The material is then placed on a slide and covered with a coverslip; potassium hydroxide should be avoided because it dissolves fecal pellets.

Treatment
• Topical permethrin or lindane
• Sometimes oral ivermectin

Primary treatment is topical or oral scabicides. Permethrin is the 1st-line topical drug.

Older children and adults should apply permethrin or lindane to the entire body from the neck down and wash it off after 8 to 14 h. Permethrin is often preferred because lindane can be neurotoxic. Treatments should be repeated in 7 days.

For infants and young children, permethrin should be applied to the head and neck, avoiding periorbital and perioral regions. Special attention should be given to intertriginous areas, fingernails, toenails, and the umbilicus. Mittens on infants can keep permethrin out of the mouth. Lindane is not recommended in children < 2 yr and in patients with a seizure disorder because of potential neurotoxicity.

Ivermectin is indicated for patients who do not respond to topical treatment, are unable to adhere to topical regimens, or are immunocompromised with Norwegian scabies. Ivermectin has been used with success in epidemics involving close contacts, such as nursing homes.

Close contacts should also be treated simultaneously, and personal items (eg, towels, clothing, bedding) should be washed in hot water and dried in a hot drier or isolated (eg, in a closed plastic bag) for at least 3 days.

Symptoms and lesions take up to 3 wk to resolve despite killing of the mites, making failed treatment due to resistance, poor penetration, incompletely applied therapy, reinfection, or nodular scabies difficult to recognize. Skin scrapings can be done periodically to check for persistent scabies.

Key Points
• Risk factors for scabies include crowded living conditions and immunosuppression; poor hygiene is not a risk factor.
• Suggestive findings include burrows in characteristic locations, intense itching (particularly at night), and clustering of cases among household contacts.
• Confirm scabies when possible by finding mites, ova, or fecal pellets.
• Treat scabies usually with topical permethrin or, when necessary, oral ivermectin.

CLINICAL VIGNETTES

An 18-year-old college student comes to the clinic because of an "extremely itchy rash" on her hands, abdomen, and legs. She says that she was home for spring break a couple of weeks earlier and her younger brother had a similar rash. She says that she first noticed the symptoms after taking a "nice, hot shower" when she returned to her dormitory after vacation. She says that she is having trouble sleeping because the pruritus is most severe at night. Physical examination shows papules, vesicles, and plaques symmetrically distributed on her wrists, underneath her breasts, around the naval, her buttocks and inner thighs. There are dark, wavy lines that end in a pearly bleb in between her fingers. The most appropriate next step is to

A. place a drop of mineral oil on a bleb and unroof it with a needle or scalpel, then examine the scrapings under the microscope
B. prescribe a high potency hydrocortisone cream applied twice a day to the affected area
C. take an excisional biopsy of one of the most prominent lesions and send it to pathology for histologic evaluation
D. tell her to wash all of her clothing and bedding in hot water and have her roommate come in to be examined

The correct answer is A. This patient most likely has scabies, which is an infestation with Sarcoptes scabiei. The mite is acquired by direct contact with an infected person and penetrates the skin, producing burrows that are visible on close examination (dark, wavy lines that end in a pearly bleb). The areas most frequently affected are axillary and genital regions, waistline, fingerwebs, underneath the breasts, and around the umbilicus. The most effective way to confirm the diagnosis is to place a drop of mineral oil on a suspected area, and unroof the burrow hole with a needle or scalpel and examine the scrapings under the microscope. The patient should be treated with permethrin cream and close contacts should be treated, even if asymptomatic.

A high potency hydrocortisone cream applied twice a day to the affected area (choice B) is the treatment for allergic contact dermatitis, not scabies. Allergic contact dermatitis typically presents with pruritus, vesicles, and erythema, due to an exogenous agent such as poison ivy or nickel in jewelry. It typically occurs in the area where the offending agent had contact with the skin.

An excisional biopsy (choice C) is not the best first step in evaluating a patient whose signs and symptoms are consistent with scabies. The diagnosis can usually be established based on history, physical findings, and scrapings of the lesion. A biopsy is not typically necessary.

It is appropriate to tell her to wash all of her clothing and bedding in hot water and have her roommate come in to be examined (choice D) after the diagnosis of scabies is established, but not before scraping the lesions and evaluating them under the microscope.

You care for a family that consists of a 38-year-old husband, a 36-year-old wife, and a 6-year-old daughter. The daughter is brought into the office because of "itchy skin" that is particularly intense at night. Examination shows gray, tortuous, threadlike lines in the interdigital folds and 3mm reddish-brown nodules on the groin and axilla. Mineral oil is placed on the lesions and scrapings from the lesions are examined under the microscope. Adult mites are seen. Examination of the other members of the family is unremarkable. The most appropriate next step in management is to 

A. advise them to wash all bedding in warm water and dry using a cool cycle
B. exclude the daughter from school for 1 week
C. biopsy one of the reddish-brown nodules in the axilla
D. prescribe permethrin lotion for all family members if they are not allergic to medication

The correct answer is D. This patient has scabies, which is an infestation caused by the mite, Sarcoptes scabiei, that causes an intensely pruritic eruption. Permethrin lotion should be given to the affected person and for all household members if they are not allergic.

Many believe that patients should be advised to wash all bedding in hot water and dry using a hot cycle, not warm water and dry using a cool cycle (choice A). Clothing worn next to the skin within a few days of initiating treatment should be washed the same way.  Others say that the mite cannot exist for more than a few minutes off the host, however either way, washing all bedding in warm water and drying using a cool cycle is incorrect.

Exclude the daughter from school for 1 week (choice B) or send the child back to school and recommend treatment before bedtime this evening are incorrect because the child should be excluded from school or daycare until after treatment has been given.

It is unnecessary to biopsy one of the reddish-brown nodules in the axilla (choice C) because they are most likely a granulomatous response to parts of the dead mite. The diagnosis has already been established with the visualization of the mite under the microscope.
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Osteoporosis
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Osteoporosis is a progressive metabolic bone disease that decreases bone density (bone mass per unit volume), with deterioration of bone structure. Skeletal weakness leads to fractures with minor or inapparent trauma, particularly in the thoracic and lumbar spine, wrist, and hip (called fragility fractures). Diagnosis is by dual-energy x-ray absorptiometry (DEXA scan) or by confirmation of a fragility fracture. Prevention and treatment involve risk factor modification, Ca and vitamin D supplements, exercises to maximize bone and muscle strength and minimize the risk of falls, and drug therapy to preserve bone mass or stimulate new bone formation.

Pathophysiology
Bone is continually being formed and resorbed. Normally, bone formation and resorption are closely balanced. Osteoblasts (cells that make the organic matrix of bone and then mineralize bone) and osteoclasts (cells that resorb bone) are regulated by parathyroid hormone (PTH), calcitonin, estrogen, vitamin D, various cytokines, and other local factors such as prostaglandins.

Peak bone mass in men and women occurs by the mid 20s. Men have higher bone mass than women. After achieving peak, bone mass plateaus for about 10 yr, during which time bone formation approximately equals bone resorption. After this, bone loss occurs at a rate of about 0.3 to 0.5%/yr. Beginning with menopause, bone loss accelerates in women to about 3 to 5%/yr for about 5 to 7 yr and then the rate of loss decelerates.

Osteoporotic bone loss affects cortical and trabecular (cancellous) bone. Loss of both types contributes to skeletal fragility and fractures.

Risk Factors
Because stress, including weight bearing, is necessary for bone growth, immobilization or extended sedentary periods result in bone loss. A low body mass index predisposes to decreased bone mass. Certain ethnicities, including whites and Asians, have a higher risk of osteoporosis. Insufficient dietary intake of Ca, P, Mg, and vitamin D predisposes to bone loss, as does endogenous acidosis. Tobacco and alcohol use also adversely affect bone mass. A family history of osteoporosis, particularly a parental history of hip fracture, also increases risk.

Symptoms and Signs
Patients with osteoporosis are asymptomatic unless a fracture has occurred. Nonvertebral fractures are typically symptomatic, but about two thirds of vertebral compression fractures are asymptomatic. A vertebral compression fracture that is symptomatic begins with acute onset of pain that usually does not radiate, is aggravated by weight bearing, may be accompanied by point spinal tenderness, and typically begins to subside in 1 wk. However, residual pain may last for months or be constant.

Multiple thoracic compression fractures eventually cause dorsal kyphosis, with exaggerated cervical lordosis (dowager's hump). Abnormal stress on the spinal muscles and ligaments may cause chronic, dull, aching pain, particularly in the lower back.

Diagnosis
• Dual-energy x-ray absorptiometry (DEXA)
Bone density should be measured using DEXA to screen people at risk and to follow patients with documented low bone density, including those undergoing treatment.

Typically, DEXA is done in all women ≥ 65 yr, women between menopause and 65 who have risk factors, including a family history of osteoporosis, a low body mass index (eg, previously defined as body weight < 127 lb), and use of tobacco and/or drugs with a high risk of bone loss (eg, glucocorticoids). DEXA is also recommended for both men and women of any age who have had fragility fractures, older adults with unexplained sudden onset of back pain, patients with decreased bone density or asymptomatic vertebral compression fractures incidentally noted on imaging studies.

Bone density measurement: DEXA is used to measure bone mineral density (g/cm2); it is suggestive of osteopenia or osteoporosis (in the absence of osteomalacia), predicts the risk of fracture, and can be used to follow treatment response. Bone density is ideally measured at three sites, including the lumbar spine and both hips.

DEXA results are reported as T-scores and Z-scores. The T-score corresponds to the number of standard deviations that the patient's bone density differs from the peak bone mass of a healthy, young person of the same sex and ethnicity. The WHO establishes cutoff values for T-scores that define osteopenia and osteoporosis. A T-score < -1.0 and > -2.5 defines osteopenia. A T-score ≤ -2.5 suggests osteoporosis. 

The Z-score corresponds to the number of standard deviations that the patient's bone mineral density differs from that of a person of the same age and sex and should be used for children, premenopausal women, or men < 50 yr. If the Z-score is ≤ -2.0, bone density is low for the patient's age and secondary causes of bone loss should be considered. 

In patients being treated for osteoporosis, DEXA should be repeated, usually about every 2 yr, but sometimes more frequently in patients taking glucocorticoids. Patients with as significantly decreased bone mineral density should be evaluated for drug adherence and secondary causes of bone loss. 

Treatment
• Risk factor modification
• Ca and vitamin D supplements
• Antiresorptive drugs (eg, bisphosphonates, hormone replacement therapy)

The goals of treatment are to preserve bone mass, prevent fractures, decrease pain, and maintain function.

Risk factor modification can include increasing weight-bearing exercise, minimizing caffeine and alcohol intake, and smoking cessation. The optimal amount of weight-bearing exercise is not established, but an average of 30 min/day is recommended.

All men and women should consume at least 1000 mg of elemental Ca daily. An intake of 1200 to 1500 mg/day (including dietary consumption) is recommended for postmenopausal women and older men and for periods of increased requirements, such as pubertal growth, pregnancy, and lactation. Diet alone is rarely adequate; Ca supplements are needed, most commonly as Ca carbonate or Ca citrate. Ca should be taken in divided doses of 500 to 600 mg bid or tid. 

Vitamin D supplementation is recommended with 800 to 1000 IU/day. Patients with vitamin D deficiency may need even higher doses. Supplemental vitamin D is usually given as cholecalciferol, the natural form of vitamin D, although ergocalciferol, the synthetic plant-derived form, is probably also acceptable. The 25-hydroxy vitamin D level should be ≥ 30 ng/mL. 

Bisphosphonates are first-line drug therapy. By inhibiting bone resorption, bisphosphonates preserve bone mass and can decrease vertebral and hip fractures by 50%. They can be given orally or IV. Oral bisphosphonates include alendronate (10 mg once/day or 70 mg once/wk) and risedronate (5 mg once/day, 35 mg once/wk, or 150 mg once/mo). Zoledronic acid is given IV (5 mg once/yr). Ibandronate can be given orally (150 mg once monthly) or IV (3 mg once every 3 mo). Oral bisphosphonates must be taken on an empty stomach with a full (8-oz, 250 mL) glass of water, and the patient must remain upright for at least 30 min (60 min for ibandronate).

Estrogen can preserve bone density and prevent fractures. Most effective if started within 4 to 6 yr of menopause, estrogen may slow bone loss and possibly reduce fractures even when started much later. Use of estrogen increases the risk of thromboembolism and endometrial cancer and may increase the risk of breast cancer. The risk of endometrial cancer can be reduced in women with an intact uterus by taking a progestin with estrogen.

CLINICAL VIGNETTES

A 67-year-old woman comes to your office because she is concerned about osteoporosis. She went through menopause at 56, has no history of bone fractures, no smoking history, and no known family history of hip fractures. Her weight is 51 kg and height is 60 cm. Physical examination is unremarkable. A dual X-ray absorptiometry shows: Average Z-score= -1.6 SD, Average T-score= -0.9 SD. Now that you have completed a basic screening for osteoporosis, your patient returns to your office for an interpretation of her tests results. At this time, it is most appropriate to inform the patient that:

A. Because of her risk factors, treatment with calcium and alendronate should be initiated
B. Because of her risk factors, treatment with calcium should be initiated
C. Compared to aged matched controls, her bone density is 0.9 SDs below the mean
D. Compared to healthy young adults, her bone density is 1.6 SDs below the mean

The correct answer is B. All individuals should ensure that they consume adequate amounts of calcium. Premenopausal, non-pregnant women should consume about 1,000 mg/day of calcium. Postmenopausal women should consume 1,200-1,500 mg/day of calcium and pregnant women should consume about 1,300 mg/day of calcium.

Treatment with alendronate (choice A) or any other approved osteoporosis medication should generally be reserved for the following women with post menopausal osteoporosis: women who suffered low impact trauma, women with T-Scores < 2.5, women with T-scores < 1.5 and risk factors, and women who continue to lose bone mass despite preventive intervention.

Compared to aged matched controls, her bone density is 0.9 standard deviations below the mean (choice C) and compared to healthy young adults, her bone density is 1.6 standard deviations below the mean (choice D) are incorrect interpretations of BMD. A patient's T-score compares women to healthy young adults. It is used to make the diagnosis of osteoporosis. T-scores between 1 and 2.5 SD below the mean are defined as osteopenia. A t-score of less than 2.5 SD below the mean defines osteoporosis. The Z-score compares BMD of age and race matched controls. A low Z-score (<-2.0 SD below the mean) may be consistent with secondary cause of osteoporosis (e.g., hyperthyroidism or hyperparathyroidism).

A 17-year-old female comes to your office with an 8-month history of amenorrhea. Menarche occurred at age 12 and her menses were regular until the past year. The patient’s vital signs are in the normal range for her age except for a BMI of 16.1 kg/m2 (below the third percentile for age). She practices dance several hours a day and works out regularly. She admits that she follows a strict 800-calorie/day diet to keep in shape for ballet. You order a CBC, a complete metabolic profile, a urine Beta-hCG level, FSH and LH levels, and a TSH level. Which one of the following is also recommended as part of the workup?

A. An EKG
B. Pelvic ultrasonography
C. Abdominal/pelvic CT
D. A DEXA scan

ANSWER: D. The female athlete triad is a relatively common condition in athletes, and is characterized by amenorrhea, disordered eating, and osteoporosis. It is more common in sports that promote lean body mass. Female athletes should be screened for the disorder during their preparticipation evaluations. Individuals who present with one or more components of the triad should be evaluated for the other components. This patient evidences disordered eating (low BMI for age) and secondary amenorrhea, and should be screened for osteoporosis using a DEXA scan. The International Society for Clinical Densitometry recommends using the Z-score, rather than the T-score, when screening children or premenopausal women. The T-score is based on a comparison to a young adult at peak bone density, whereas the Z-score uses a comparison to persons of the same age as the patient. A Z-score less than –2.0 indicates osteoporosis.

An EKG is not required in this patient since she has normal vital signs. Pelvic ultrasonography is not necessary unless an abnormal finding is identified on a pelvic examination. Abdominopelvic CT would be inappropriate given the patient’s age and lack of abdominopelvic symptoms such as pain or a mass. 

A 55-year-old woman comes to the office for a periodic health maintenance examination. Her review of systems is positive for fatigue, recent weight gain, temperature intolerance with hot flashes being frequent, and some mild pruritus over her hands. Her last menstrual period was seven months prior. She smokes one-half pack of cigarettes per day. She appears her stated age, is well and in no distress. Her temperature is 37.0 C (98.6 F), blood pressure is 110/80 mm Hg, and pulse is 65/min. Physical examination is unremarkable. Concerning her post-menopausal status, the most appropriate intervention to reduce long-term morbidity and mortality is

A. annual bone density surveys
B. estrogen and progesterone replacement
C. estrogen and progesterone replacement and bisphosphonate therapy
D. estrogen replacement and bisphosphonate therapy

The correct answer is C. This patient is postmenopausal and not on hormone replacement therapy (HRT). Accelerated bone loss and osteoporosis are top among the increased risks that such women have. Bisphosphonates are a class of drugs that are taken orally and act to inhibit osteoblast formation and/or function. Their precise mechanism(s) of action are unknown. This, in addition to estrogen and progesterone replacement will reduce her long-term morbidity and mortality.

Annual bone density surveys (choice A) are a monitoring tool. These tests are not therapeutic in any way and in order to reduce long-term morbidity, some intervention is required. Bone density surveys are the standard monitoring tool for following the progression of osteoporosis.

It is appropriate to treat with estrogen and progesterone replacement (choice B) together since the progesterone offsets the unopposed estrogen. However bisphosphonate therapy is absent from this regimen.

Because the beneficial effects of progesterone on estrogen action is lost with estrogen replacement and bisphosphonate therapy (choice D) alone, it is incorrect.

A 58-year-old woman comes to the office for a periodic health maintenance examination. You notice in her chart that her last menstrual period was two years ago, and at that time, she was not interested in discussing hormone replacement therapy. Now she says that she has noticed that a few of her friends have been "shrinking" and she is ready to take something "for osteoporosis." She read that women with thromboembolic disease should not take estrogen. She vaguely remembers having a few "blood clots" many years ago. Dual energy absorptiometry (DEXA) shows a bone mineral density that is more than 2.5 standard deviations below the mean. Alendronate is prescribed. The patient should be advised to

A. avoid weight-bearing exercise
B. return to the office in one week for a complete blood count (CBC)
C. take the alendronate, along with calcium, after breakfast
D. take the alendronate first thing in the morning, on an empty stomach, with a full glass of water, and remain upright for at least 30 minutes

The correct answer is D. Alendronate (Fosamax), is a biphosphate that is used to treat and prevent osteoporosis. Because esophageal irritation and ulceration are side effects, it is necessary to advise patients that after taking the pill, they must remain sitting upright or standing for at least 30 minutes. Also, it must be taken with a full glass of water on an empty stomach because it may interact with other substances. Alendronate works by reducing the activity of osteoclasts, which decreases the rate of bone loss and increases the amount of mineral density.

It would be incorrect to advise this patient to avoid weight-bearing exercise (choice A). It is actually important to advise the patient to engage in weight-bearing exercise to help maintain bone density.

It is not necessary for the patient to return to the office in one week for a complete blood count (CBC), (choice B). Common side effects of alendronate are esophagitis, gastrointestinal upset, headache, bone and joint pain, a rash, and an altered sense of taste. Agranulocytosis, which is a rare side effect of the antipsychotic agent clozapine, is not typically associated with alendronate. Therefore, regular monitoring of the CBC is unnecessary.
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Mastitis 
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Mastitis occurs in approximately 10 percent of mothers who are breastfeeding, and it can lead to the cessation of breastfeeding. The risk of mastitis can be reduced by frequent, complete emptying of the breast and by optimizing breastfeeding technique. Sore nipples can precipitate mastitis. The diagnosis of mastitis is usually clinical, with patients presenting with focal tenderness in one breast accompanied by fever and malaise. Treatment includes changing breastfeeding technique, often with the assistance of a lactation consultant. When antibiotics are needed, those effective against Staphylococcus aureus (e.g., dicloxacillin, cephalexin) are preferred. As methicillin-resistant S. aureus becomes more common, it is likely to be a more common cause of mastitis, and antibiotics that are effective against this organism may become preferred. Continued breastfeeding should be encouraged in the presence of mastitis and generally does not pose a risk to the infant. Breast abscess is the most common complication of mastitis. It can be prevented by early treatment of mastitis and continued breastfeeding. Once an abscess occurs, surgical drainage or needle aspiration is needed. Breastfeeding can usually continue in the presence of a treated abscess.

Mastitis is defined as inflammation of the breast. Although it can occur spontaneously or during lactation, this discussion is limited to mastitis in breastfeeding women, with mastitis defined clinically as localized, painful inflammation of the breast occurring in conjunction with flu-like symptoms (e.g., fever, malaise).

Mastitis is especially problematic because it may lead to the discontinuation of breast-feeding, which provides optimal infant nutrition. Mastitis is most common during the second and third weeks postpartum.

Prevention of Mastitis
Because mastitis is thought to result partly from inadequate milk removal from the breast, optimizing breastfeeding technique is likely to be beneficial.

Risk Factors
Sore nipples may be an early indicator of a condition that may predispose patients to mastitis. In the early weeks of breastfeeding, sore nipples are most often caused by a poor latch by the feeding infant.

Nipple fissures (cracks) can cause pain and can serve as a portal of entry for bacteria that result in mastitis.

Blocked milk ducts can also lead to mastitis. This condition presents as localized tenderness in the breast from inadequate milk removal from one duct. A firm, red, tender area is present on the affected breast, and a painful, white, 1-mm bleb may be present on the nipple. This bleb is thought to be an overgrowth of epithelium or an accumulation of particulate or fatty material. Removal of the bleb with a sterile needle or by rubbing with a cloth can be beneficial.

Diagnosis
The diagnosis of mastitis is generally made clinically. Patients typically present with localized, unilateral breast tenderness and erythema, accompanied by a fever of 101°F (38.5° C), malaise, fatigue, body aches, and headache.

Culture is rarely used to confirm bacterial infection of the milk because positive cultures can result from normal bacterial colonization, and negative cultures do not rule out mastitis. Culture has been recommended when the infection is severe, unusual, or hospital acquired, or if it fails to respond to two days' treatment with appropriate antibiotics.

Treatment
• Antistaphylococcal antibiotics

Treatment includes encouragement of fluid intake and antibiotics aimed at Staphylococcus aureus, the most common causative pathogen. Examples are dicloxacillin 500 mg po q 6 h for 7 to 10 days and, for women allergic to penicillin, erythromycin 250 mg po q 6 h. If women do not improve and do not have an abscess, vancomycin 1 g IV q 12 h or cefotetan 1 to 2 g IV q 12 h to cover resistant organisms should be considered. Breastfeeding should be continued during treatment because treatment includes emptying the affected breast.

Breast abscesses are treated mainly with incision and drainage. Antibiotics aimed at S. aureus are often used.

It is not clear whether antibiotics aimed at methicillin-resistant S. aureus are necessary for treatment of mastitis or breast abscess

Treatment of mastitis begins with improving breastfeeding technique. If the mother stops draining the breast during an episode of mastitis, she will have increased milk stasis and is more likely to develop an abscess.

Complications
One of the most common complications of mastitis is the cessation of breastfeeding. Mothers should be reminded of the many benefits of breastfeeding and encouraged to persevere. Another potential complication is the development of an abscess, which presents similarly to mastitis except that there is a firm area in the breast, often with fluctuance. An abscess can be confirmed by ultrasonography and should be treated with surgical drainage or needle aspiration, which may need to be repeated. Fluid from the abscess should be cultured, and antibiotics should be administered. Breastfeeding usually can continue, except if the mother is severely ill or the infant's mouth must occlude the open incision when feeding.

CLINICAL VIGNETTES

A 29-year-old woman who is 3 weeks postpartum, comes to the clinic because of left breast pain, body aches, and fever. She had a normal vaginal delivery and an uneventful postpartum period. Four days ago, she started feeling feverish with diffuse body aches. She is concerned, because she is breast-feeding her infant and her left breast has also been tender for the last 4 days. She denies cough, sore throat, or rhinorrhea. Vital signs are: temperature 39.3 C (102.7 F), blood pressure 120/65 mm Hg, and pulse 90/min. Breast examination reveals a moderately erythematous left breast with diffuse tenderness. The right breast is normal. The rest of the physical examination is normal. The most likely diagnosis is

A. Breast Abscess
B. Benign breast mass
C. Breast Cancer
D. Cellulitis
E. Acute Mastitis

Acute mastitis (choice E) is a disease of nursing women in which bacteria gain entry to the breast tissue via cracks in the traumatized nipple. It is characterized by acute inflammation and tissue necrosis.

Seven days after delivering a healthy full-term infant, a 27-year-old woman comes to the office because of fever, "body aches," and intense right-sided breast pain "just above the nipple." She is breast-feeding and says it has been "going pretty well" until she developed this "breast pain." Her temperature is 39.5 C (103.1 F). Physical examination shows a 3-cm area of erythema and induration 4-cm above the right nipple. This area is warm to the touch, has a "brawny" texture, and is very tender. Her left breast is nontender and appears unremarkable. The most appropriate next step in management is to 

A. prescribe a penicillinase-resistant antibiotic and advise her to stop breast-feeding
B. prescribe a penicillinase-resistant antibiotic and encourage her to continue breast feeding 
C. send her home with analgesic therapy and warm compresses and encourage her to continue to breast-feed
D. send her home with analgesic therapy and warm compresses and have her express milk with a breast pump 
E. send her home with vitamin A and D ointment and encourage her to continue to breast-feed

The correct answer is B. This patient most likely has mastitis,a breast infection that typically presents with a fever, malaise, generalized body aches, and a unilateral painful, erythematous, firm breast. It is often caused by Staphylococcus aureus, most likely  from the infant's mouth, and should be treated with a penicillinase-resistant antibiotic. The mother can continue to breast feed as long as the antibiotic prescribed is not contraindicated during breast-feeding.

This patient most likely has mastitis, which is treated with a penicillinase-resistant antibiotic. It is incorrect to advise her to stop breast-feeding (choice A).

Engorgement is treated with analgesic therapy, warm compresses, and the continuation of breast-feeding (choice C). Engorgement typically presents with bilateral breast tenderness and generalized breast swelling. These patients are typically afebrile and lack the systemic symptoms that the patient in this case suffers from. 

A plugged duct is often treated with analgesic therapy, warm compresses, and a breast pump (choice D). A plugged duct is characterized by unilateral breast tenderness and localized swelling. Patients with a plugged duct are afebrile, and lack systemic symptoms unlike the woman in this case.

Vitamin A and D ointment (choice E) is part of the typical nipple care for all breast-feeding women with tender nipples. Breast-feeding women often complain of nipple tenderness and they should be given water-based creams, vitamin A and D ointment, and should be encouraged to continue breast-feeding. Fever, generalized body aches, and a unilateral tender breast are usually signs of an infection. They are not a normal part of breast-feeding.
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Rabies
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Rabies is a viral encephalitis transmitted by the saliva of infected bats and certain other infected mammals. Symptoms include depression and fever, followed by agitation, excessive salivation, and hydrophobia. Diagnosis is by serologic tests or biopsy. Vaccination is indicated for people at high risk of exposure. Postexposure prophylaxis involves wound care and passive and active immunoprophylaxis and, if promptly and meticulously executed, almost always prevents human rabies. Otherwise, the disorder is almost universally fatal. Treatment is supportive.

Rabies causes > 55,000 human deaths worldwide annually, mostly in Latin America, Africa, and Asia, where canine rabies is endemic. In the US and Canada, vaccination of domestic animals has drastically reduced rabies cases in people, mostly transmitted by infected bats. Infected raccoons, skunks, and foxes can also transmit rabies.

Rabid animals transmit the infection through their saliva, usually by biting. Rarely, the virus can enter through a skin abrasion or across mucous membranes of the eyes, nose, or mouth. The virus travels from the site of entry via peripheral nerves to the spinal cord (or to the brain stem when the face is bitten), then to the brain. It then spreads from the CNS via peripheral nerves to other parts of the body. Involvement of the salivary glands and oral mucosa is responsible for transmissibility.

Symptoms and Signs
Pain or paresthesias may develop at the site of the bite. Rapidity of progression depends on the viral inoculum and proximity of the wound to the brain.

Initial symptoms are nonspecific: fever, headache, and malaise. Within days, encephalitis (furious rabies; in 80%) or paralysis (dumb rabies; in 20%) develops. Encephalitis causes restlessness, confusion, agitation, bizarre behavior, hallucinations, and insomnia. Salivation is excessive, and attempts to drink cause painful spasms of the laryngeal and pharyngeal muscles (hydrophobia). In the paralytic form, ascending paralysis and quadriplegia develop without delirium and hydrophobia.

Diagnosis
• Skin biopsy
• Sometimes PCR testing of fluid or tissue samples
Rabies is suspected in patients with encephalitis or ascending paralysis and a history of an animal bite or exposure to bats; bat bites may be superficial and overlooked.

Direct fluorescence antibody testing of a biopsy specimen of skin from the nape of the neck is the diagnostic test of choice. Diagnosis can also be made by PCR of CSF, saliva, or tissue. Specimens tested for rabies antibodies include serum and CSF. CT, MRI, and EEG are normal or show nonspecific changes.

Treatment
• Supportive care
Treatment is only supportive and includes heavy sedation (eg, with ketamine and midazolam) and comfort measures. Death usually occurs 3 to 10 days after symptoms begin. Few patients have survived; many received immunoprophylaxis before onset of symptoms. There is evidence that giving rabies vaccine and immune globulin after clinical rabies develops may cause more rapid deterioration.

Prevention
Rabid animals can often be recognized by their strange behavior; they may be agitated and vicious, weak, or paralyzed and may show no fear of people. Nocturnal animals (eg, bats, skunks, raccoons) may be out during the day. Bats may make unusual noises and have difficulty flying. An animal suspected of having rabies should not be approached. Local health authorities should be contacted to remove the animal.

Preexposure: Human diploid cell rabies vaccine (HDCV) is safe and recommended for preexposure prophylaxis for people at risk, including veterinarians, animal handlers, spelunkers, workers who handle the virus, and travelers to endemic areas. A total of three 1-mL doses are given IM, one each on days 0, 7, and between day 21 and 28. 

Postexposure: Exposure is considered to be a bite that breaks the skin or any contact between mucous membrane or broken skin and animal saliva. If exposure occurs, prompt, meticulously executed prophylaxis almost always prevents human rabies. The wound is cleansed immediately and thoroughly with soap and water or benzalkonium chloride.

Postexposure prophylaxis (PEP) with rabies vaccine and rabies immune globulin (RIG) is given depending on the biting animal and circumstances. PEP is begun, and the animal's brain is tested for virus.

General Guidelines for Post-Exposure Prophylaxis (PEP): 

[A] Domestic Animals (Pets) that are non-symptomatic  - observe the animal for 10 (ten) days for signs/symptoms of rabies. If animal shows signs/symptoms of rabies, give patient PEP

[B] Domestic Animals (Pets) that are symptomatic for rabies - a veterinarian checks the animal to confirm signs of rabies. Patient is given PEP. Domestic animals infected with rabies usually die within 10 days.

[C] Wild Animals - animal is captured, euthanized (killed) and the brain is tested for rabies. If positive for rabies, patient is given PEP. (PEP is painful and risky, so only given if necessary).

[D] Animal is not available for observation or testing - patient is given PEP.

Key Points
• Worldwide, rabies still causes tens of thousands of deaths yearly, mostly in Latin America, Africa, and Asia, where canine rabies is endemic.
• In the US, rabies kills only a few people yearly; it is usually transmitted by bats, but possibly by racoons, skunks, or foxes.
• Pain and/or paresthesias at the bite site are followed by encephalitis (causing restlessness and agitation) or by ascending paralysis.
• Biopsy neck skin or do PCR of saliva, CSF, or tissue if patients have unexplained encephalitis or ascending paralysis.
• Treat patients supportively.
• Before exposure, give the rabies vaccine to people at risk (eg, veterinarians, animal handlers, spelunkers, workers who handle the virus, travelers to endemic areas).
• After exposure, thoroughly clean and debride wounds, then give the rabies vaccine and rabies immune globulin.

CLINICAL VIGNETTES

A 20-year-old man comes to your office with a dog bite to his left thigh received after he and a friend taunted a neighbor's dog. He reports that the bite occurred about 36 hours ago and only came to your office after coworkers informed him that dog bites frequently become infected. His temperature is 37.0 C (98.6 F), blood pressure is 110/70 mm Hg, pulse is 63/min, and respirations are 13/min. On physical examination you notice a shallow abrasion on his left thigh, which is mildly tender. There is no surrounding edema or erythema. The most appropriate management of this patient is to

A. administer a rabies vaccination
B. prescribe amoxicillin-clavulanate
C. prescribe clindamycin
D. provide local wound care without antibiotic therapy

The correct answer is D. Only 5-20% of dog bites become infected. This patient does not seem to have any systemic signs of infection and his wound doesn't appear to be infected. Puncture wounds become infected more often than abrasion and this patient doesn't have any skin punctures. Local wound care including debridement, cleaning, and irrigation are essential. X-rays can be taken if fracture is suspected but a fracture would be unlikely in a superficial thigh wound.

Rabies vaccination (choice A) is not indicated now. Vaccination for rabies should be considered only when you have a strong suspicion of rabies. Rabies is always fatal so treatment is essential if the disease is seriously being considered (such as a bat, skunk, raccoon, fox, bat, etc.). In this case, the dog was a household pet, which probably indicates that it was vaccinated in the past. Also, the dog did not seem rabid (the dog bite occurred only after being provoked). If the dog spontaneously bit the patient, suspicion might be higher. If rabies is suspected, an attempt to contact the dog owner is a reasonable first step to determine the pet's vaccination status. Local wound care remains important.

Antibiotics would be indicated for patients with signs of local or systemic infection. Hand bites should also be treated with antibiotics since infection can be devastating to a patient. Amoxicillin-clavulanic acid (choice B) and clindamycin (choice C) would both be acceptable antibiotics since they have broad spectrums covering likely infectious organisms such as Pasteurella multocida, Staphylococcus, Streptococci, and anaerobes.

A 6-year-old girl is brought to the emergency department by her parents immediately after she was bitten on the hand by the neighbor's domestic dog. The father reports that the girl tried to pet the dog while it was eating. The dog has been vaccinated regularly. Examination shows three bite marks on the dorsum of the left hand with broken skin and dried blood. The wound is cleaned and bandaged. Which of the following is the most appropriate next step for rabies prophylaxis in this patient?

A. Rabies immunoglobulin
B. Rabies immunoglobulin and vaccine
C. Rabies vaccine
D. The dog should be killed and the brain examined for signs of rabies
E. The dog should be observed for behavioral changes suggestive of rabies

The correct answer is E. Disturbing a dog while it is eating and being bitten in response is considered to be a provoked attack, and thus not indicative of aggressive behavior in the dog. Among healthy domestic dogs, cats, and ferrets, those infected with rabies virus usually sicken and die within 10 days. It is thus considered safe to quarantine the animal for 10 days to observe it for signs of disease with rabies. Bites that are closer to the central nervous system carry a higher risk for transmission of the rabies virus.

Passive immunization with the rabies immunoglobulin alone (choice A) is never used in post-exposure prophylaxis.

Rabies immunoglobulin and vaccination (choice B) is the post-exposure prophylaxis of choice in individuals who have not previously been vaccinated. Indications for active and passive immunization with immunoglobulin and vaccine include high-risk wild animals such as bats, raccoons, and skunks, or domestic animals such as dogs, cats, or ferrets. When the animal is available for testing, the post-exposure prophylaxis can be held; if the animal is not available for testing, then post-exposure prophylaxis should be administered.

Active immunization with the vaccine alone (choice C) is reserved for individuals who have already been vaccinated (i.e., a veterinarian)

Killing the animal and examining the brain (choice D) is the norm for wild animals that are captured alive, because their behavior cannot be deemed to be "normal" or "abnormal." II is also the appropriate step if observation of a domestic animal by a veterinarian suggests that signs of rabies are developing in the animal.

During a hunting trip, a young man is bitten by a coyote. The animal is captured and brought to the authorities alive. Which of the following is the most important criterion to determine the patient's need for rabies prophylaxis? 

A. The patient's history of previous immunizations
B. The patient's clinical course over the next few weeks
C. Observing the animal's behavior over the next few days
D. Killing the animal and examining the brain
E. The events that took place have already established the need to proceed with rabies immunization

D. Examination of the animal's brain for signs of rabies will determine whether the painful and risky process of rabies passive and active immunization is required. 

History of previous immunizations (choice A) is used to determine what to do for tetanus prophylaxis, but it has no application for rabies, because virtually no one has ever received such immunization in the past. Waiting for signs of rabies to appear in the patient (choice B) would be a death sentence. We can prevent rabies, but once established we cannot cure it. Observation of the animal's behavior (choice C) is applicable when dealing with provoked bites by domestic pets. The behavior of a wild animal gives no clues to the presence or absence of rabies. If the animal had escaped, choice E would have been correct.
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Subdural Hematoma    
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The meninges are the connective tissue membranes that line the skull and vertebral canal. They enclose the brain and spinal cord. The outermost layer is the dura mater. The middle layer is the arachnoid mater. The inner layer is the pia mater. The subdural space is the space between the dura mater and the arachnoid mater.

A subdural hematoma (SDH) is a collection of clotting blood that forms in the subdural space. This may be: An acute SDH. A subacute SDH (this phase begins 3-7 days after the initial injury). A chronic SDH (this phase begins 2-3 weeks after the initial injury).

Pathophysiology
An acute SDH is caused by either:
Bleeding from a damaged cortical artery.
Bleeding from an underlying parenchymal injury.
Tearing of bridging veins from the cortex to one of the draining venous sinuses.
Blunt head trauma is the usual mechanism of injury but spontaneous SDH can arise as a consequence of clotting disorder, arteriovenous malformations/aneurysms or other conditions.

At-risk groups
• Infants
In the infant brain, SDHs are caused by tearing of the bridging veins in the subdural space and may result in significant brain injury. Some SDHs are due to physical abuse, so suspicion should be raised but SDH should not be assumed to be always due to this cause in children.

• The elderly
Cerebral atrophy can occur in people over the age of 60, causing tension on the veins, which may also be weaker and more susceptible to injury as a consequence of age. Chronic SDH is more common in this age group.

• Those with alcoholism
Alcohol misuse leads to a risk of thrombocytopenia, prolonged bleeding times and blunt head trauma and is a risk factor for SDH. Alcoholism also causes cerebral atrophy which can put tension on the bridging veins. People on anticoagulation treatment: Anticoagulation treatment (including with aspirin or warfarin) is another risk factor.

Presentation
• Acute SDH
Usually presents shortly after a moderate-to-severe head injury. Loss of consciousness may occur but not always. There may be a 'lucid interval' of a few hours after the injury where the patient appears relatively well and normal but subsequently deteriorates and loses consciousness as the hematoma forms.

• Chronic SDH
Usually presents about 2-3 weeks following the provoking trauma. The initial injury may be relatively trivial (or forgotten), particularly in an older patient on anticoagulants, or in the context of alcohol misuse. Symptoms tend to be gradually progressive. There is often a history of anorexia, nausea and/or vomiting.
There may be a gradually evolving neurological deficit such as focal limb weakness, speech difficulties, increasing drowsiness/confusion or personality changes. If there is accompanying and progressive headache, this should raise suspicion of the diagnosis. This is especially so in the context of coagulopathy, anticoagulant use or suspected alcohol misuse.

Examination
Assess consciousness level using the Glasgow Coma Scale. Check vital signs, looking for evidence of bradycardia and hypertension associated with raised intracranial pressure. Perform a full neurological examination, including examination for pupil size and reactivity and papilloedema (which can indicate raised intracranial pressure). Look for evidence of external trauma to the head or elsewhere.

It is important to survey for other injuries in children with suspected SDH, as there may be evidence of non-accidental injury. In babies, the fontanelles may be tense due to raised intracranial pressure. Look for evidence of bruising or purpura, indicating a bleeding diathesis or meningitis.

Investigations
Blood tests
CBC and LFTs may reveal alternative causes of impaired consciousness. Thrombocytopenia may indicate a bleeding diathesis. Coagulation screen should be checked to screen for coagulopathy. Take blood for group and save/cross-match if SDH seems likely, in anticipation of operative intervention.

Imaging
In patients with impaired consciousness, confusion, focal neurology or signs of possible raised intracranial pressure, that cannot be otherwise explained, urgent neuroimaging is mandatory. 

CT scan of the head is good for detecting acute SDH and mandatory in children with significant head injury. Subacute SDH may be more difficult to detect, so CT with contrast or MRI is preferred. Chronic SDH is usually detectable on non-contrast CT and is a quicker examination.

Management
In cases of severe trauma, immobilize the cervical spine and alert the trauma team. Assess and manage 'Airway, Breathing and Circulation’. Intubation and assisted ventilation may be needed depending on the level of consciousness. Obtain anesthetic or neurosurgical advice.

Stabilize the patient before transfer for any imaging and send an appropriately experienced member of staff to accompany them during investigations, in case of deterioration.
If the condition is strongly suspected or confirmed by investigation, refer urgently to the neurosurgical team.

Hypertonic saline or mannitol may be considered if there is raised intracranial pressure. Burr holes may be considered if there is rapid deterioration. Any coagulopathy also needs treating.

If there is a small, asymptomatic, acute SDH, this can be managed by observation, serial examinations, and serial CT scanning. Surgery is needed if there are focal signs, deterioration, a large hematoma, raised intracranial pressure or midline shift. SDH is treated by emergency craniotomy and clot evacuation.

Prevention
Avoidance of over-anticoagulation in patients taking warfarin.
Avoidance of falls in older people, especially if on anticoagulants.
Treatment for alcoholism.

CLINICAL VIGNETTES

A 71-year-old man has been in excellent health, and practicing competently as an attorney. He is brought to the emergency room following a motor vehicle accident. A workup, including imaging of the spine, thorax, and head, is negative, but the patient is admitted for overnight observation. His injuries include several lacerations to the face and extremities as well as several contusions to the thorax. Three weeks later, he is admitted to the hospital for confusion. A neurologic exam is normal except that he is not oriented to time or place, and can recall only 1 out of 6 objects after 3 minutes. Which of the following is the most likely diagnosis?

A. Alzheimer's disease
B. Brain metastases
C. Epidural hematoma
D. Normal pressure hydrocephalus
E. Subdural hematoma

The correct answer is E. This is a classic history and presentation of a subdural hematoma, which usually occurs several days to weeks following a traumatic head injury. Often the patient will have had a hospital admission with a negative workup, including x-rays and CT scans of the head. Either gradually or abruptly, the patient can experience decreasing mental status, sleepiness, focal neurologic deficits, seizures, etc. The bleeding originates from the bridging veins of the meninges and blood collects beneath the dural layer. A CT or MRI of the brain will show a semicircular, crescent-shaped opacity (blood) just below the cranium impinging on the brain tissue.

Alzheimer's disease (choice A) usually develops more gradually, typically over several years (although some cases can develop over a few months). Brain metastases (choice B) could very well present like this, however, the patient will often have constitutional symptoms of cancer such as fatigue and weight loss. In a patient with a recent traumatic event, however, subdural hematoma is more likely.

An epidural hematoma (choice C) differs from a subdural hematoma in that it occurs much more rapidly, usually over several hours or less. The bleed originates from the middle meningeal artery, which runs right next to the anterolateral cranium and often gets injured with a skull fracture in this location. A CT or MRI will show a circular opacity within the cranium compressing the brain tissue. Normal pressure hydrocephalus (choice D) occurs in the elderly and is associated with urinary incontinence, new onset of confusion, and gait disturbances.

A 77-year-old man becomes "senile" over a period of 3 or 4 weeks. He used to be active and managed all of his financial affairs. Now, he stares at the wall, barely talks, and sleeps most of the day. His daughter recalls that he fell from a horse about a week before the mental changes began. It is suspected that this fall led to an intracranial bleed. Which of the following is the most likely source of the bleeding?

A. AV malformation
B. Bridging veins
C. Charcot-Bouchard aneurysm
D. Circle of Willis
E. Middle meningeal artery

B. People who are very old or alcoholic have smaller brains in a skull that has not changed in size; thus, very minimal trauma can make the brain "rattle around" and tear a venous sinus, from which a subdural hematoma very slowly forms. Senility does not occur in a 3-week period. Such marked changes in someone with recent trauma should trigger a search for chronic subdural hematoma. Rupture of bridging veins (choice B) produces a subdural hematoma.

Subarachnoid hemorrhages are most often the result of bleeding from berry aneurysms. The berry aneurysms develop at sites of congenital weakness (near branch points) of the relatively unsupported vessels of the circle of Willis (choice D). AV malformations (choice A) tend to produce mixed parenchymal and subarachnoid hemorrhages.

Rupture of Charcot-Bouchard aneurysms (choice C) can be seen with hypertension (which may
complicate adult polycystic kidney disease). Such rupture produces intraparenchymal hemorrhage, which if severe, may spread to the subarachnoid space. Rupture of the middle meningeal artery (choice E) produces epidural hematoma.

An 82-year-old man is admitted to the hospital after he started dragging his right leg today. Workers at the nursing home where he resides also noticed that he was not as talkative as usual. His temperature is 37.0 C (98.6 F). His speech pattern is non-fluent. On the right side, hip flexion, knee flexion, dorsiflexion, and abductor hallucis longus were weaker than other lower extremity muscles. Cell counts, chemistries, and coagulation studies are normal. A CT scan of the head shows a 1.5 cm left-sided subdural hematoma. His granddaughter arrives after he returns to his room from the CT scan and is very concerned about her grandfather's condition. The most appropriate next step is to

A. arrange for an emergent cerebral angiogram
B. call a neurosurgical consult
C. give fresh frozen plasma
D. order an immediate MRI of the head
E. tell the granddaughter that the patient is too old for any treatment and send him back to the nursing home

The correct answer is B. This is a neurosurgical emergency and a neurosurgical consult needs to be called. There is no age that is an absolute contraindication for surgery and it would be wrong to tell the family he is too old for any treatment and send him back to the nursing home (choice E).

A cerebral angiogram (choice A) would be indicated if you had strong suspicion for an aneurysm or vascular malformation. This is not the usual cause of a subdural hematoma. Since his coagulation studies were already normal, there is no reason to give fresh frozen plasma (choice C). A brain MRI (choice D) will not provide any further useful diagnostic information right now.

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Morton Neuroma (Interdigital neuralgia)   
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Interdigital neuralgia (Morton Neuroma)

Interdigital nerve irritation (neuralgia) or persistent benign enlargement of the perineurium (neuroma) can cause pain, which may be nonspecific, burning, or lancinating, or a foreign body sensation. Diagnosis is usually clinical. Treatment may involve correction of footwear, local injection, or sometimes surgical excision.

Interdigital neuralgia is a common cause of metatarsalgia. The interdigital nerves of the foot travel beneath and between the metatarsals, extending distally to innervate the toes. Neuralgia of the interdigital nerve along its distal innervation near the ball of the foot develops primarily as a result of improper or constrictive footwear or, less commonly, nerve traction resulting from abnormal foot structure (eg, splayfoot deformity). As a result of chronic repetitive trauma, a benign thickening of the nerve develops (Morton neuroma).

Symptoms and Signs
Interdigital neuralgia is characterized by pain around the metatarsal heads or the toes. Early interdigital neuralgia often causes an occasional mild ache or discomfort in the ball of the foot, usually when wearing a specific shoe, such as those that are too narrow at the front. Neuralgia is usually unilateral. As the condition progresses, the nerve thickens. The pain becomes worse, often with a burning or lancinating quality or paresthesias. In time, patients are unable to wear most closed-toe shoes. While walking, patients often falsely sense a pebble in their shoes, which they take off for relief. Neuroma most frequently affects the 3rd interspace. Only slightly less common is involvement of the 2nd interspace. Sometimes both interspaces or feet are involved simultaneously.

Diagnosis
• Clinical evaluation
The symptoms are often specific, and the diagnosis is confirmed by tenderness on plantar palpation of the interdigital space and by reproduction of the radiating burning pain, often accompanied by a notable click, by squeezing the space (Mulder sign). Although MRI does not usually confirm neuroma, it may be useful to rule out other interspace lesions or arthritis causing similar symptoms.

Treatment
• Modification of footwear and injection
• Neuralgia of recent onset usually resolves quickly with properly fitting shoes and insoles or with local anesthetic injection. Using a metatarsal pad placed proximally to the metatarsal heads of the affected interspace may also help reduce symptoms.

Neuromas may require one or more perineural infiltrations of long-acting corticosteroids with a local anesthetic. Injection is at a 45° angle to the foot, into the interspace at the level of the dorsal aspect of the metatarsophalangeal joints. Orthotics with neuroma pads, rest, cold packs, and properly fitting shoes often relieve symptoms. Nerve ablation techniques, such as injecting 20% alcohol with a local anesthetic directly into the nerve with ultrasonographic guidance, or cryogenic freezing of the nerve may help relieve symptoms. If other treatments are ineffective, excision often brings complete relief. Another neuroma occasionally develops at the site of nerve excision (amputation or stump neuroma), which may require additional surgery.

Key Points
• Metatarsal pain can result from irritation or benign thickening of the interdigital nerves.
• Initially, mild pain caused by wearing narrow shoes can worsen and become lancinating, sometimes with paresthesias and/or a foreign body sensation.
• Diagnose the disorder by clinical findings, including tenderness and reproduction of symptoms with palpation of the interdigital space.
• Treat by modifying footwear, giving local anesthetic injections and sometimes corticosteroid injections, doing nerve ablation techniques, or doing surgery.

CLINICAL VIGNETTES

A 45-year-old woman, who wears high-heeled, pointed shoes, complains of pain in the forefoot after prolonged standing or walking. Occasionally, she also experiences numbness, a burning sensation, and tingling in the area. Physical examination shows no obvious deformities and a very tender spot in the third interspace, between the third and fourth toes. There is no redness, limitation of motion, or signs of inflammation. Which of the following is the most likely diagnosis? 

A. Gout
B. Hallux rigidus
C. Metatarsophalangeal articulation pain
D. Morton's neuroma
E. Plantar fasciitis

D. The location and circumstances are classic for Morton's neuroma, a benign neuroma of the third plantar interdigital nerve. Gout (choice A) happens to obese, elderly males, and redness and signs of inflammation in the affected joint are evident. Hallux rigidus (choice B) is osteoarthritis of the first metatarsophalangeal joint. There is deformity and limitation of motion. The joint is tender on physical examination. Metatarsophalangeal articulation pain (choice C) is likewise associated with misalignment of joint surfaces. There is pain when examining the joint, and there is no history of numbness, burning, or tingling. Plantar fasciitis (choice E) produces sharp pain on physical examination when pressing the plantar surface of the heel.

A 46-year-old woman presents with a chief complaint of pain in her toes. She describes it as an ache that occurs more when she wears any of her many shoes that are too narrow at the front. The pain is only on her right foot. Initially she states that she did not feel it was that severe but now the pain has become worse, often with a burning or lancinating quality. She even describes a sense of having a pebble in her shoe. On physical exam there is tenderness on plantar palpation of the interdigital space. Which of the following initial recommendations would be most appropriate for this patient?

A. Modification of footwear
B. Physical therapy
C. Ultrasound
D. Ice 

This is a classic description for Interdigital neuralgia (Morton Neuroma). Interdigital nerve irritation (neuralgia) or persistent benign enlargement of the perineurium (neuroma) can cause pain, which may be nonspecific, burning, or lancinating, or a foreign body sensation. Diagnosis is usually clinical. Treatment may involve correction of footwear, local injection, or sometimes surgical excision.
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I sold my 2012 Hyundai Accent today at Village Luxury Cars. The process was explained to me clearly by the sales person Omid Fard. The check was made out to me the same day. Very easy and pleasant experience. Great place to sell your car. They also have a very nice selection of vehicles, if you want to buy.
Public - 3 months ago
reviewed 3 months ago
1 review
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