Which of the following would be the best diagnostic test to confirm the diagnosis?
Anonymous Poll
43%
a) Salivary gland biopsy
19%
b) Schirmer test
15%
c) CT scan of the neck
11%
d) Ultrasound scan of the swelling
12%
e) ANA
👍1🤔1
⏳ Case-based MCQ | #Case_355 | #answer
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✅ A
Sjogren syndrome is a chronic inflammatory disease characterized by lymphocytic infiltration and fibrosis of exocrine glands, especially lacrimal and salivary glands. The disease is much more prevalent in women (female/male - 9:1), with the usual age of onset being in the 4 and 5 decades of life. Sjogren syndrome for which no underlying etiology can be identified is termed primary, whereas when it is secondary to other connective tissue disorders, it is called secondary Sjogren syndrome.
🔎 Autoimmune diseases associated with Sjogren syndrome include:
▫Rheumatoid arthritis
▫Systemic lupus erythematosus
▫Scleroderma
Considering the overlap of Sjogren syndrome with many other rheumatic disorders,it is sometimes difficult to determine whether a clinical manifestation is solely a result of Sjogren syndrome or is due to one of its overlapping disorders.
Clinical features of the disease include the following:
• Dry eyes and keratoconjunctivitis sicca due to
decreased tear production- the patient may complain of feeling as sand under the eyelid or itchy eyes.
• Dry mouth (xerostomia) due to decreased salivation - dry mouth can lead to following manifestations:
▪Red smooth and dry tongue
▪Severe and progressive dental caries
▪Cracks at the corners of the mouth
▪Chronic oral Candidiasis
▪Parotid gland swelling
🔔 NOTE - Dry eyes and mouth are the most common presenting features in adults, whereas, children often present with parotid gland enlargement.
🔻Other clinical features of Sjogren disease include:
➕ Nasal dryness - can result in discomfort and bleeding
➕ Vaginal dryness - can result in dyspareunia, vaginitis and pruritus
➕ Myalgia and fatigue
➕ Arthralgia or arthritis - similar to that of SLE with symmetrical
involvement of small joints, arthritis is of non-erosive nature
➕ Raynaud's phenomenon
➕ Recurrent miscarriages or stillbirths in women and history of venous or arterial thrombosis related to the presence of antiphospholipid antibodies (e.g. lupus anticoagulant or anticardiolipin antibodies)
➕ Leukopenia, anemia
➕ Lymphadenopathy
➕ Non-Hodgkin lymphoma
Currently, minor salivary gland biopsy is the best single test to establish a diagnosis of Sjogren syndrome. In this procedure, an incision is made on the inner lip, and some minor salivary glands are removed for examination.
In patients with a possible diagnosis of this disease but with severe extraglandular symptoms, a lip biopsy is often performed to firmly establish the diagnosis of Sjogren syndrome.
While this is the most definitive test,performing it is not absolutely necessary from a clinical standpoint. Patients with Sjogren syndrome are essentially treated symptomatically and are observed for the development of other rheumatic disorders or lymphoma. This can be initiated without performing a biopsy. If, however, the diagnosis is in doubt or if a definitive diagnosis is needed, biopsy is the best test.
⚠ (Option B) Schirmer test shows decreased tear production. A strip of filter paper is put under the lower eye lid, and the distance along the paper that tears are absorbed is measured. Less than 5mm in 5 minutes is considered positive. It is one of the tests routinely performed when Sjogren disease suspected but it is not diagnostic.
⚠ (Options C and D) Imaging studies are not diagnostic; however they may be sometimes needed, particularly with extraglandular manifestations of the disease.
⚠ (Option E) ANA, particularly anti-Ro (SSA) and anti-La (SSB) may be positive, but again these could be elevated in other conditions as well.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ A
Sjogren syndrome is a chronic inflammatory disease characterized by lymphocytic infiltration and fibrosis of exocrine glands, especially lacrimal and salivary glands. The disease is much more prevalent in women (female/male - 9:1), with the usual age of onset being in the 4 and 5 decades of life. Sjogren syndrome for which no underlying etiology can be identified is termed primary, whereas when it is secondary to other connective tissue disorders, it is called secondary Sjogren syndrome.
🔎 Autoimmune diseases associated with Sjogren syndrome include:
▫Rheumatoid arthritis
▫Systemic lupus erythematosus
▫Scleroderma
Considering the overlap of Sjogren syndrome with many other rheumatic disorders,it is sometimes difficult to determine whether a clinical manifestation is solely a result of Sjogren syndrome or is due to one of its overlapping disorders.
Clinical features of the disease include the following:
• Dry eyes and keratoconjunctivitis sicca due to
decreased tear production- the patient may complain of feeling as sand under the eyelid or itchy eyes.
• Dry mouth (xerostomia) due to decreased salivation - dry mouth can lead to following manifestations:
▪Red smooth and dry tongue
▪Severe and progressive dental caries
▪Cracks at the corners of the mouth
▪Chronic oral Candidiasis
▪Parotid gland swelling
🔔 NOTE - Dry eyes and mouth are the most common presenting features in adults, whereas, children often present with parotid gland enlargement.
🔻Other clinical features of Sjogren disease include:
➕ Nasal dryness - can result in discomfort and bleeding
➕ Vaginal dryness - can result in dyspareunia, vaginitis and pruritus
➕ Myalgia and fatigue
➕ Arthralgia or arthritis - similar to that of SLE with symmetrical
involvement of small joints, arthritis is of non-erosive nature
➕ Raynaud's phenomenon
➕ Recurrent miscarriages or stillbirths in women and history of venous or arterial thrombosis related to the presence of antiphospholipid antibodies (e.g. lupus anticoagulant or anticardiolipin antibodies)
➕ Leukopenia, anemia
➕ Lymphadenopathy
➕ Non-Hodgkin lymphoma
Currently, minor salivary gland biopsy is the best single test to establish a diagnosis of Sjogren syndrome. In this procedure, an incision is made on the inner lip, and some minor salivary glands are removed for examination.
In patients with a possible diagnosis of this disease but with severe extraglandular symptoms, a lip biopsy is often performed to firmly establish the diagnosis of Sjogren syndrome.
While this is the most definitive test,performing it is not absolutely necessary from a clinical standpoint. Patients with Sjogren syndrome are essentially treated symptomatically and are observed for the development of other rheumatic disorders or lymphoma. This can be initiated without performing a biopsy. If, however, the diagnosis is in doubt or if a definitive diagnosis is needed, biopsy is the best test.
⚠ (Option B) Schirmer test shows decreased tear production. A strip of filter paper is put under the lower eye lid, and the distance along the paper that tears are absorbed is measured. Less than 5mm in 5 minutes is considered positive. It is one of the tests routinely performed when Sjogren disease suspected but it is not diagnostic.
⚠ (Options C and D) Imaging studies are not diagnostic; however they may be sometimes needed, particularly with extraglandular manifestations of the disease.
⚠ (Option E) ANA, particularly anti-Ro (SSA) and anti-La (SSB) may be positive, but again these could be elevated in other conditions as well.
⏳ Case-based MCQ | #Case_356
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A 28-year-old man is brought to the Emergency Department after he had an accident while driving a motorcycle and had his right ankle injured. On examination, his vital signs are stable. The right ankle joint is laterally displaced and there is a laceration over the joint.
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A 28-year-old man is brought to the Emergency Department after he had an accident while driving a motorcycle and had his right ankle injured. On examination, his vital signs are stable. The right ankle joint is laterally displaced and there is a laceration over the joint.
Which one of the following is the most important initial step in management?
Anonymous Poll
15%
a)Wound debridment
23%
b)Tetanus immunization
8%
c)Intravenous antibiotics
31%
d)Reduction of the displacement
24%
e)X-ray of the joint
👍1
⏳ Case-based MCQ | #Case_356 | #answer
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ D
Open fractures and/or dislocations are defined as the bone and/or joint being exposed to the external environment, or when the fracture or dislocation is caused by blunt or penetrating forces sufficient to disrupt or penetrate skin, subcutaneous tissue, muscle fascia, muscle, and/ or the bone or joint. Open fractures are often contaminated by foreign material (e g., clothing, grass, dirt, gravel), dead or devitalized tissue, and bacteria.
Always follow the following rules in open fractures/ dislocations:
• Remove any gross contamination off the wound. No provisional irrigation or debridement is performed at this stage.
• Take photographs of the wound and dress it with wet sterile cover (the photographs are taken, so that other treating physicians do not need to uncover the wound to see it)
• Give patient analgesic (preferably intravenously to both control the pain and prepare for a reduction in the emergency department). Morphine is a good option.
• By gentle traction, reduce the fracture and correct misalignments as much as possible.
• Start the patient on intravenous prophylactic antibiotics.
• Give the patient tetanus prophylaxis If indicated
• Obtain X-rays
• Urgently arrange for transferring the patient to the operating room for surgical wound debridement and definite treatment of the fracture and dislocation
NOTE • Initial irrigation or debridement in the emergency department is not recommended and should be avoided. In this scenario the most appropriate initial management would be reduction of the dislocation by gentle traction after non-surgical removal of any gross contamination, and analgesia. The patient then should be started on intravenous antibiotics and receive tetanus prophylaxis.
⚠ X-ray of the joint (option E) is required pre-operatively to visualize the anatomical disruption. Wound debridement (option A) is crucial but should be performed in the operating room ideally with 1-2 hours of presentation.
NOTE - In open fractures, wound treatment may sometimes be more time-consuming and require more work than the treatment of the fracture itself.
Debridement may be carried out several times before and after definitive fracture treatment is performed.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ D
Open fractures and/or dislocations are defined as the bone and/or joint being exposed to the external environment, or when the fracture or dislocation is caused by blunt or penetrating forces sufficient to disrupt or penetrate skin, subcutaneous tissue, muscle fascia, muscle, and/ or the bone or joint. Open fractures are often contaminated by foreign material (e g., clothing, grass, dirt, gravel), dead or devitalized tissue, and bacteria.
Always follow the following rules in open fractures/ dislocations:
• Remove any gross contamination off the wound. No provisional irrigation or debridement is performed at this stage.
• Take photographs of the wound and dress it with wet sterile cover (the photographs are taken, so that other treating physicians do not need to uncover the wound to see it)
• Give patient analgesic (preferably intravenously to both control the pain and prepare for a reduction in the emergency department). Morphine is a good option.
• By gentle traction, reduce the fracture and correct misalignments as much as possible.
• Start the patient on intravenous prophylactic antibiotics.
• Give the patient tetanus prophylaxis If indicated
• Obtain X-rays
• Urgently arrange for transferring the patient to the operating room for surgical wound debridement and definite treatment of the fracture and dislocation
NOTE • Initial irrigation or debridement in the emergency department is not recommended and should be avoided. In this scenario the most appropriate initial management would be reduction of the dislocation by gentle traction after non-surgical removal of any gross contamination, and analgesia. The patient then should be started on intravenous antibiotics and receive tetanus prophylaxis.
⚠ X-ray of the joint (option E) is required pre-operatively to visualize the anatomical disruption. Wound debridement (option A) is crucial but should be performed in the operating room ideally with 1-2 hours of presentation.
NOTE - In open fractures, wound treatment may sometimes be more time-consuming and require more work than the treatment of the fracture itself.
Debridement may be carried out several times before and after definitive fracture treatment is performed.
👍4
⏳ Case-based MCQ | #Case_357
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During physical examination of a 3 kg full-term male newborn, you notice that the baby's oxygen saturation decreases when he is laid. The fall in oxygen saturation is sometimes associated with mild cyanosis. However, when the baby starts crying the oxygen saturation increases again.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
During physical examination of a 3 kg full-term male newborn, you notice that the baby's oxygen saturation decreases when he is laid. The fall in oxygen saturation is sometimes associated with mild cyanosis. However, when the baby starts crying the oxygen saturation increases again.
Which one of the following will be the next best step in management?
Anonymous Poll
28%
a)Oxygen via nasal cannula
22%
b)Chest X-ray
10%
c) Surgery
20%
d) Intubation and ventilation
20%
e) Rigid nasogastric tube
❤1👍1
⏳ Case-based MCQ | #Case_357 | #answer
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ E
The presentation is classic for choanal atresia. Choanal atresia is a congenital abnormality in which there is failure of canalization of the bucconasal membrane. This can be either unilateral or bilateral and is usually due to a combination of bone and soft tissue anomalies.
It occurs in 1:5000 to 1:8000 births. Unilateral atresia is more common, with a predilection for females.
🔆 CHARGE Syndrome (coloboma, heart defect, atresia choanae, retarded growth and development, genital abnormality and ear abnormality) or other congenital abnormalities are present in 50% of patients with bilateral choanal atresia.
Bilateral choanal atresia is a relatively rare anomaly of the upper airway. As neonates are obligatory nasal breathers, presentation may be with life-threatening respiratory distress, retractions and paradoxical cyanotic episodes which are relieved by crying as the infant begins to breathe via the mouth. Unilateral choanal atresia does not usually produce severe symptoms.
When choanal atresia is suspected the diagnosis can be confirmed with trying to pass a nasogastric tube. It is not possible to pass a nasogastric tube through the nares and choanae if there is choanal atresia.
⚠ In the presence of bilateral choanal atresia, as the history and physical suggest, oxygen through nasal cannula will be of no benefit.
➕ Other measures to consider as parts of management plan include:
• Oxygen
• Oropharyngeal airway
• Intubation and ventilation if there is life-threatening hypoxemia
• CT scan
• ENT consultation and referral for surgical treatment
Since the manifestation is typical of choanal atresia, chest X-ray is not indicated now, but it may be obtained to exclude other possible associated respiratory conditions or anomalies
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ E
The presentation is classic for choanal atresia. Choanal atresia is a congenital abnormality in which there is failure of canalization of the bucconasal membrane. This can be either unilateral or bilateral and is usually due to a combination of bone and soft tissue anomalies.
It occurs in 1:5000 to 1:8000 births. Unilateral atresia is more common, with a predilection for females.
🔆 CHARGE Syndrome (coloboma, heart defect, atresia choanae, retarded growth and development, genital abnormality and ear abnormality) or other congenital abnormalities are present in 50% of patients with bilateral choanal atresia.
Bilateral choanal atresia is a relatively rare anomaly of the upper airway. As neonates are obligatory nasal breathers, presentation may be with life-threatening respiratory distress, retractions and paradoxical cyanotic episodes which are relieved by crying as the infant begins to breathe via the mouth. Unilateral choanal atresia does not usually produce severe symptoms.
When choanal atresia is suspected the diagnosis can be confirmed with trying to pass a nasogastric tube. It is not possible to pass a nasogastric tube through the nares and choanae if there is choanal atresia.
⚠ In the presence of bilateral choanal atresia, as the history and physical suggest, oxygen through nasal cannula will be of no benefit.
➕ Other measures to consider as parts of management plan include:
• Oxygen
• Oropharyngeal airway
• Intubation and ventilation if there is life-threatening hypoxemia
• CT scan
• ENT consultation and referral for surgical treatment
Since the manifestation is typical of choanal atresia, chest X-ray is not indicated now, but it may be obtained to exclude other possible associated respiratory conditions or anomalies
👍2
⏳ Case-based MCQ | #Case_358
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 37-year-old African American woman was diagnosed with diffuse type of scleroderma and was prescribed an antihistamine and prednisolone 5 mg/day to control the pruritus. Two months later, the patient came to you with severe headache, chest pain, and blurred vision. Her BP is 210/118 mmHg. Urinalysis showed proteinuria and microscopic hematuria. Blood urea nitrogen was 11 mmol/L (N 2.9-7.1 mmol/L), and serum creatinine was 124 pmol/L (N 50-90 pmol/L). Your patient was still taking prednisolone 5 mg/day prescribed earlier. You diagnosed your patient with sclerodermal renal crisis and decided to put her on an ACE inhibitor.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 37-year-old African American woman was diagnosed with diffuse type of scleroderma and was prescribed an antihistamine and prednisolone 5 mg/day to control the pruritus. Two months later, the patient came to you with severe headache, chest pain, and blurred vision. Her BP is 210/118 mmHg. Urinalysis showed proteinuria and microscopic hematuria. Blood urea nitrogen was 11 mmol/L (N 2.9-7.1 mmol/L), and serum creatinine was 124 pmol/L (N 50-90 pmol/L). Your patient was still taking prednisolone 5 mg/day prescribed earlier. You diagnosed your patient with sclerodermal renal crisis and decided to put her on an ACE inhibitor.
👍2
In addition to this, what should you also do?
Anonymous Poll
9%
a) Continue steroids at the 5 mg daily dose
19%
b) Increase the dose of prednisolone
21%
c) Reduce the dose of prednisolone
19%
d) Replace prednisolone with the equivalent dexamethasone dose.
32%
e) Stop prednisolone completely
⏳ Case-based MCQ | #Case_358 | #answer
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ E
Systemic sclerosis (SS) is a chronic systemic disorder of unknown cause. It is characterized by the thickening of the skin and the involvement of multiple internal organs. Thickening of skin distinguishes this disease from other connective tissue diseases. The disease has two distinct phases: an inflammatory and fibrotic phase. Patients with disease can be classified into two major subsets according to the degree of clinically involved skin. Diffuse cutaneous systemic sclerosis is more severe with prominent internal organ involvement, while in the limited form, it is less severe but is more likely to be associated with pulmonary arterial hypertension. Systemic sclerosis affects 9-19 per 100,000 and is more common in women. African Americans are more susceptible to disease. The age of onset is between 30 and 50 years. Development of sclerodermal renal crisis has been associated with glucocorticoid use, and indeed, the use of these drugs should be avoided in scleroderma. They can, however, be used in small doses to control the early skin symptoms, for myositis associated with scleroderma and for cardiac involvement. Thus, in this patient, prednisolone should be stopped completely (choice E) because it is used for non-life-threatening skin lesions. Other glucocorticoids, including dexamethasone, should be avoided in this patient.
🔖 Key point: Development of sclerodermal renal crisis has been associated with glucocorticoid use, which is managed by glucocorticoid discontinuation.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ E
Systemic sclerosis (SS) is a chronic systemic disorder of unknown cause. It is characterized by the thickening of the skin and the involvement of multiple internal organs. Thickening of skin distinguishes this disease from other connective tissue diseases. The disease has two distinct phases: an inflammatory and fibrotic phase. Patients with disease can be classified into two major subsets according to the degree of clinically involved skin. Diffuse cutaneous systemic sclerosis is more severe with prominent internal organ involvement, while in the limited form, it is less severe but is more likely to be associated with pulmonary arterial hypertension. Systemic sclerosis affects 9-19 per 100,000 and is more common in women. African Americans are more susceptible to disease. The age of onset is between 30 and 50 years. Development of sclerodermal renal crisis has been associated with glucocorticoid use, and indeed, the use of these drugs should be avoided in scleroderma. They can, however, be used in small doses to control the early skin symptoms, for myositis associated with scleroderma and for cardiac involvement. Thus, in this patient, prednisolone should be stopped completely (choice E) because it is used for non-life-threatening skin lesions. Other glucocorticoids, including dexamethasone, should be avoided in this patient.
🔖 Key point: Development of sclerodermal renal crisis has been associated with glucocorticoid use, which is managed by glucocorticoid discontinuation.
👍4❤3
⏳ Case-based MCQ | #Case_359
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 52-year-old lady presents to your GP clinic for breast cancer screening. She has been on combined hormone replacement therapy (HRT) for the past year. Mammogram is the only available method of screening for breast cancer and because of HRT she is expected to have dense breast tissue.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 52-year-old lady presents to your GP clinic for breast cancer screening. She has been on combined hormone replacement therapy (HRT) for the past year. Mammogram is the only available method of screening for breast cancer and because of HRT she is expected to have dense breast tissue.
Which one of the following is the best recommendation to this patient regarding HRT and breast cancer screening?
Anonymous Poll
20%
a)Stop HRT six months before mammography
7%
b) Stop HRT lone year before mammography
44%
c) Continue HRT and perform mammography as recommended for other women
19%
d) Change combined HRT to estrogen-only hormone replacement therapy
10%
e) Decreasethe dose of combined hormone replacement therapy
⏳ Case-based MCQ | #Case_359 | #answer
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ C
About 10% of women on combined HRT will have extremely dense breasts; nonetheless, presently, there is not enough evidence to recommend that patients on combined hormone replacement therapy should stop HRT for any length of time before their mammography in an attempt to reduce breast density.
Therefore, this patient should continue HRT and have mammography based on current recommendations for other women. Women making decisions as to whether to commence combined HRT should be aware of the fact that HRT may lead to inaccurate mammography results. Furthermore, they should be informed about the increased risk of breast cancer if HRT extends beyond the recommended period (3 to 5 years).
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ C
About 10% of women on combined HRT will have extremely dense breasts; nonetheless, presently, there is not enough evidence to recommend that patients on combined hormone replacement therapy should stop HRT for any length of time before their mammography in an attempt to reduce breast density.
Therefore, this patient should continue HRT and have mammography based on current recommendations for other women. Women making decisions as to whether to commence combined HRT should be aware of the fact that HRT may lead to inaccurate mammography results. Furthermore, they should be informed about the increased risk of breast cancer if HRT extends beyond the recommended period (3 to 5 years).
👍2
⏳ Case-based MCQ | #Case_360
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 56-year-old man presents to the emergency department with complaint of diplopia. On examination, he has right-sided ptosis. His visual acuity and visual fields are unaffected. His right eye is depressed inferiorly and laterally and he is not able to look at to the left side. The pupillary light reflex of the right eye is sluggish. The neurological examination is otherwise unremarkable.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 56-year-old man presents to the emergency department with complaint of diplopia. On examination, he has right-sided ptosis. His visual acuity and visual fields are unaffected. His right eye is depressed inferiorly and laterally and he is not able to look at to the left side. The pupillary light reflex of the right eye is sluggish. The neurological examination is otherwise unremarkable.
Which one of the following can be the most likely cause to this presentation?
Anonymous Poll
17%
a) Midbrain infarct
22%
b) Right 6 nerve palsy
34%
c) Posterior communicating artery aneurysm
17%
d) Right 4 nerve palsy
9%
e) lesion in the occipital cortex
⏳ Case-based MCQ | #Case_360 | #answer
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ C
🔎 Explanation
This patient has the classic presentation of a third cranial nerve palsy. The third cranial nerve supplies the levator muscles of the eyelid and four extraoccular muscles: (1) the medial rectus (eye adduction), (2) superior rectus (eye elevation), (3) inferior rectus (eye depression), (4) and inferior oblique (eye elevation). Additionally, the third cranial nerve constricts the pupil through its parasympathetic fibers that supply the smooth muscles of the ciliary body and the sphincter of the iris. The third nerve begins as a nucleus in the midbrain that consists of several subnuclei innervating the individual extraoccular muscles, the eyelids, and the pupils.
The etiology of the third cranial nerve palsy is vast and includes conditions such as:
• Ischemia (e.g. diabetes and midbrain infarcts)
• Compressive effects of aneurysms such as those of the posterior communicating artery, internal carotid artery and basilar artery.
• Trauma
• Infections
• Infiltrative diseases (e.g. neoplasms)
• Demyelination
• Space occupying tumors
• Meningitis
• Herniation
• Inflammatory diseases
Of the given options, only a posterior communicating aneurysm can cause a third nerve palsy that involves the pupilary reflex. Compression of the third nerve by an enlarging intracranial aneurysm is the most dreaded etiology. The most common site of an aneurysm causing a third nerve palsy is the posterior communicating artery. In the setting of an acute third nerve palsy, the aneurysm is believed to be progressively and acutely enlarging and is at imminent risk of rupture with catastrophic outcomes.
⚠ (Option A) Midbrain infarcts can cause third cranial nerve palsy. However, since the etiology is ischemic (such as in diabetes) the pupillary light reflex is expected to be unaffected most of the time. Furthermore, with a midbrain infarct, an isolated third nerve palsy as the sole presenting symptom is very unlikely and other signs and symptoms related to a midbrain infarct are expected.
⚠ (Option B) Right 6th nerve palsy presents with horizontal binocular diplopia upon looking laterally to the affected side. Furthermore, lesions of the sixth cranial nerve do not cause ptosis.
⚠ (Option D) The fourth cranial nerve palsy presents with binocular vertical diplopia. Ptosis is not a feature.
⚠ (Option E) Lesions of occipital cortex are associated with impaired vision and visual fields deficits, none of which are present here. Furthermore, ptosis is not a feature
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ C
🔎 Explanation
This patient has the classic presentation of a third cranial nerve palsy. The third cranial nerve supplies the levator muscles of the eyelid and four extraoccular muscles: (1) the medial rectus (eye adduction), (2) superior rectus (eye elevation), (3) inferior rectus (eye depression), (4) and inferior oblique (eye elevation). Additionally, the third cranial nerve constricts the pupil through its parasympathetic fibers that supply the smooth muscles of the ciliary body and the sphincter of the iris. The third nerve begins as a nucleus in the midbrain that consists of several subnuclei innervating the individual extraoccular muscles, the eyelids, and the pupils.
The etiology of the third cranial nerve palsy is vast and includes conditions such as:
• Ischemia (e.g. diabetes and midbrain infarcts)
• Compressive effects of aneurysms such as those of the posterior communicating artery, internal carotid artery and basilar artery.
• Trauma
• Infections
• Infiltrative diseases (e.g. neoplasms)
• Demyelination
• Space occupying tumors
• Meningitis
• Herniation
• Inflammatory diseases
Of the given options, only a posterior communicating aneurysm can cause a third nerve palsy that involves the pupilary reflex. Compression of the third nerve by an enlarging intracranial aneurysm is the most dreaded etiology. The most common site of an aneurysm causing a third nerve palsy is the posterior communicating artery. In the setting of an acute third nerve palsy, the aneurysm is believed to be progressively and acutely enlarging and is at imminent risk of rupture with catastrophic outcomes.
⚠ (Option A) Midbrain infarcts can cause third cranial nerve palsy. However, since the etiology is ischemic (such as in diabetes) the pupillary light reflex is expected to be unaffected most of the time. Furthermore, with a midbrain infarct, an isolated third nerve palsy as the sole presenting symptom is very unlikely and other signs and symptoms related to a midbrain infarct are expected.
⚠ (Option B) Right 6th nerve palsy presents with horizontal binocular diplopia upon looking laterally to the affected side. Furthermore, lesions of the sixth cranial nerve do not cause ptosis.
⚠ (Option D) The fourth cranial nerve palsy presents with binocular vertical diplopia. Ptosis is not a feature.
⚠ (Option E) Lesions of occipital cortex are associated with impaired vision and visual fields deficits, none of which are present here. Furthermore, ptosis is not a feature
👍3
⏳ Case-based MCQ | #Case_361
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 72-year-old woman has been on routine dialysis sessions for the past 6 months due to end-stage renal disease. At the beginning of each session, she is found to have a high blood pressure (BP). During the session the BP normalizes, but goes up again after the session.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 72-year-old woman has been on routine dialysis sessions for the past 6 months due to end-stage renal disease. At the beginning of each session, she is found to have a high blood pressure (BP). During the session the BP normalizes, but goes up again after the session.
Which one of the following would be the most appropriate management option for this patient?
Anonymous Poll
23%
a) Addition of hypertensive medications
31%
b) Addition of furosemide, daily
31%
c) Increasing the dialysis time
9%
d) Sedation before dialysis
7%
e) Decreasing the dialysis time
⏳ Case-based MCQ | #Case_361 | #answer
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
✅ C
🔎 Explanation
Although hypotension during hemodialysis is a frequent complication, some patients (5-15%) develop paradoxical hypertension in the later stages of dialysis or when the patients
comes off the dialysis machine, a time at which most of the excess fluid has already been removed. The pathogenesis is unclear; however, the following mechanisms have been hypothesized as the cause:
1. Renin-angiotensin system activation because of ultrafiltration (UF) induced hypovolemia
2. Sympathetic overactivity
3. Intradialytic Ca++ / k+ variations
4. Blood viscosity/hemoconcentration-induced vasoconstriction caused by erythropoietin treatment
5. Fluid overload
6. Increased cardiac output
7. Endothelin-driven vasoconstriction
8. Antihypertensive drug removal by dialysis treatment
The optimal therapy for this problem is not known. While antihypertensive medications such as angiotensin converting enzyme inhibitors (ACE inhibitors) and alpha-blockers have been used before (or during) dialysis, they have not been predictably effective. Carvedilol, which blocks endothelin-1 release, appears to be effective.
Although there are no validated universal guidelines regarding management of such patients, fluid removal has been accepted as the first-line treatment for intradialytic hypertension (IDH). Theoretically, increasing the time of the dialysis session and ultrafiltration (UF) rate would be efficient; however, this decision faces many difficulties such as patient refusal or the unit limitations. This treatment should be done with caution to avoid hazardous blood pressure drop that may occur in the elderly or patients with severe comorbidity.
The dry weight of patients should be gradually reduced by increasing the dialysis time and the UF rate. In addition, patients should be advised to decrease their daily salt and water intake in between their dialysis sessions.
⚠ (Options A and B) Addition of anti-hypertensive or other medications ACE inhibitors or angiotensin receptor blockers (ARBs), beta blockers, endothelin-1 receptor blockers, furosemide, etc has been associated with conflicting results. In some patients, hypertensive crises may occur. These hypertensive crises are not persistent and usually the blood pressure level quickly decreases spontaneously; however, addition of antihypertensive medications might be indicated. There is no comment regarding a ypertensive crisis in this patient to necessitate addition of antihypertensives. Furosemide is not the first-line option for management of hypertension crisis if it occurs.
⚠ (Option D) Sedation before dialysis has no role in management of IDH or post-dialytic hypertension.
⚠ (Option E) Decreasing the dialysis time results in insufficient excess fluid removal and hypertension due to volume overload
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✅ C
🔎 Explanation
Although hypotension during hemodialysis is a frequent complication, some patients (5-15%) develop paradoxical hypertension in the later stages of dialysis or when the patients
comes off the dialysis machine, a time at which most of the excess fluid has already been removed. The pathogenesis is unclear; however, the following mechanisms have been hypothesized as the cause:
1. Renin-angiotensin system activation because of ultrafiltration (UF) induced hypovolemia
2. Sympathetic overactivity
3. Intradialytic Ca++ / k+ variations
4. Blood viscosity/hemoconcentration-induced vasoconstriction caused by erythropoietin treatment
5. Fluid overload
6. Increased cardiac output
7. Endothelin-driven vasoconstriction
8. Antihypertensive drug removal by dialysis treatment
The optimal therapy for this problem is not known. While antihypertensive medications such as angiotensin converting enzyme inhibitors (ACE inhibitors) and alpha-blockers have been used before (or during) dialysis, they have not been predictably effective. Carvedilol, which blocks endothelin-1 release, appears to be effective.
Although there are no validated universal guidelines regarding management of such patients, fluid removal has been accepted as the first-line treatment for intradialytic hypertension (IDH). Theoretically, increasing the time of the dialysis session and ultrafiltration (UF) rate would be efficient; however, this decision faces many difficulties such as patient refusal or the unit limitations. This treatment should be done with caution to avoid hazardous blood pressure drop that may occur in the elderly or patients with severe comorbidity.
The dry weight of patients should be gradually reduced by increasing the dialysis time and the UF rate. In addition, patients should be advised to decrease their daily salt and water intake in between their dialysis sessions.
⚠ (Options A and B) Addition of anti-hypertensive or other medications ACE inhibitors or angiotensin receptor blockers (ARBs), beta blockers, endothelin-1 receptor blockers, furosemide, etc has been associated with conflicting results. In some patients, hypertensive crises may occur. These hypertensive crises are not persistent and usually the blood pressure level quickly decreases spontaneously; however, addition of antihypertensive medications might be indicated. There is no comment regarding a ypertensive crisis in this patient to necessitate addition of antihypertensives. Furosemide is not the first-line option for management of hypertension crisis if it occurs.
⚠ (Option D) Sedation before dialysis has no role in management of IDH or post-dialytic hypertension.
⚠ (Option E) Decreasing the dialysis time results in insufficient excess fluid removal and hypertension due to volume overload
⏳ Case-based MCQ | #Case_362
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A 66-year-old man presents with Intermittent right upper quadrant pain. An ultrasound, performed for revealing the cause gallstones, reveals a lesion In the liver. Triple phase CT scan Is performed for more evaluation showing a 35 mm subcortical lesion with early prominent dense enhancement, which spreads through the lesion In the late portal venous phase.
〰〰〰〰〰〰〰〰〰〰〰〰〰〰
A 66-year-old man presents with Intermittent right upper quadrant pain. An ultrasound, performed for revealing the cause gallstones, reveals a lesion In the liver. Triple phase CT scan Is performed for more evaluation showing a 35 mm subcortical lesion with early prominent dense enhancement, which spreads through the lesion In the late portal venous phase.