SEP Revision Flashcards
Describe the cause of a molar pregnancy.
A molar pregnancy occurs due to an abnormal fertilization event leading to the growth of abnormal trophoblastic tissue.
What are the symptoms of a molar pregnancy?
Symptoms include vaginal bleeding, excessive nausea and vomiting, an enlarged uterus, and the passage of grape-like cysts.
How is a molar pregnancy typically diagnosed initially?
A molar pregnancy is initially investigated using a transvaginal ultrasound to reveal a ‘snowstorm’ pattern and by checking serum hCG levels.
What is the best diagnostic test for confirming a molar pregnancy?
The best diagnostic test is an ultrasound, which shows characteristic patterns of molar pregnancy, and histopathology following tissue examination.
Describe the key differentials between missed abortion, ectopic pregnancy, and normal pregnancy with bleeding.
Missed abortion is differentiated by ultrasound findings, ectopic pregnancy often presents with different symptoms and ultrasound findings, while normal pregnancy with bleeding may require careful monitoring and follow-up.
What is the initial treatment for removing molar tissue?
Evacuation of the uterus using suction curettage is the preferred method for removing molar tissue.
How is prophylactic chemotherapy used in the management of high-risk cases?
Prophylactic chemotherapy may be considered to prevent the development of gestational trophoblastic neoplasia (GTN) in high-risk cases.
Define the step management for molar tissue evacuation.
Step management includes performing suction curettage to remove the abnormal tissue, monitoring hCG levels weekly until undetectable, then monthly for 6 months to 1 year, advising against pregnancy during follow-up, and regular monitoring for the development of GTN or persistent trophoblastic disease.
What should be done if hCG levels plateau or rise during follow-up?
If hCG levels plateau or rise, referral to a specialist for further management, including possible chemotherapy, should be considered.
Describe the causes of immediate postoperative fever (0-48 hours)
Causes include surgical stress response, atelectasis, and reactions to medications.
What is the initial management approach for immediate postoperative fever?
Initial management involves close observation of vital signs and providing supportive care like deep breathing exercises, hydration, and pain control.
How should acute postoperative fever (Day 3-5) be managed according to RACGP guidelines?
Management involves considering causes like UTI, pneumonia, and superficial surgical site infection, and appropriate treatment based on the identified cause.
Define atelectasis in the context of postoperative fever
Atelectasis refers to the collapse of lung tissue, often triggered by anesthesia and immobility.
What should be done if the fever persists during the immediate postoperative period despite initial management?
Reassess for missed causes like infections or adverse medication reactions and consider further intervention if needed.
Describe the signs of superficial surgical site infection in the context of postoperative fever
Signs include redness, warmth, or drainage from the incision site, indicating a possible infection.
How can postoperative fever be managed in the immediate postoperative period without further intervention?
If the fever resolves spontaneously and there are no signs of infection, continued monitoring is sufficient without additional intervention.
What is the significance of urinary tract infection (UTI) in causing acute postoperative fever?
UTI is a common cause of fever on Day 3-5 post-surgery, especially in patients with indwelling catheters.
Describe the initial management steps for suspected infections postoperatively.
Perform urine culture for UTI, chest X-ray for pneumonia, and clinical examination of the surgical site.
What is the recommended action if there is a clinical suspicion of infection postoperatively?
Start empiric antibiotics and adjust therapy based on culture results.
How should antibiotic therapy be managed in postoperative infections?
Modify antibiotics based on culture and sensitivity results.
What wound care should be provided for a superficial surgical site infection?
Appropriate wound care, which may include opening the wound for drainage.
What supportive care measures are recommended for postoperative infections like pneumonia?
Continue oxygen therapy, fluids for hydration, and antipyretics to manage fever.
Where can more detailed guidelines on managing infections be found?
RACGP guidelines.
What are the potential causes of subacute postoperative fever (Day 5-8)?
Surgical site infection, deep venous thrombosis, anastomotic leak.
What imaging modalities are recommended for evaluating subacute postoperative fever causes like DVT or abscesses?
Ultrasound for DVT, CT scan for abscesses or anastomotic leaks.
What interventions may be necessary based on imaging findings in subacute postoperative fever cases?
Drainage of abscesses or revision surgery.
Describe the management approach for delayed postoperative fever after day 8.
Includes comprehensive evaluation, broad-spectrum antibiotics, surgical consultation if needed, targeted antibiotic therapy, and consideration of ICU care for severe cases.
What is the recommended management for deep abscesses causing delayed postoperative fever?
May require surgical or radiological drainage.
How should antibiotic therapy be approached in cases of delayed postoperative fever?
Continue or start antibiotics based on culture results, focusing on likely pathogens.
Define the role of anticoagulation in cases of confirmed DVT postoperatively.
Initiate anticoagulation therapy.
What additional resource can provide detailed guidance on post-surgical complications management?
RACGP guidelines.
Do you need surgical consultation for delayed postoperative fever management?
May be required for abscess drainage or correction of an anastomotic leak.
Describe the causes of delayed postoperative fever after day 8.
Include deep abscesses, anastomotic leak, and sepsis.
How should broad-spectrum antibiotics be used in cases of delayed postoperative fever?
Start empirically while awaiting specific culture results.
What imaging modality is recommended for comprehensive evaluation in cases of delayed postoperative fever?
CT scan.
Define the role of ICU care in managing delayed postoperative fever.
Consider for severe sepsis or systemic infection.
Describe post-surgery complications.
Post-surgery complications can arise due to various factors such as the type of surgery, patient’s health condition, and perioperative care.
are the symptoms of infection post-surgery?
Symptoms of infection include redness, swelling, warmth, fever, pus, or other discharge from the surgical site.
How can manifest as a post-surgery complication?
Bleeding can present as excessive bleeding from the incision site or internal bleeding leading to hypotension, tachycardia, or anemia.
Define Deep Vein Thrombosis (DVT) in the context of post-surgery complications.
DVT is characterized by pain, swelling, and redness in the limb, typically affecting the legs.
What are the signs of Pulmonary Embolism (PE) as a post-surgery complication?
Signs of PE include sudden shortness of breath, chest pain, tachypnea, and hypoxia.
Describe Atelectasis as a post-surgery complication.
Atelectasis is marked by shortness of breath, decreased oxygen saturation, fever, and decreased breath sounds.
What is Postoperative Nausea and Vomiting (PONV) and how does it manifest post-surgery?
PONV involves symptoms like nausea, vomiting, and dehydration following a surgical procedure.
How would you recognize Wound Dehiscence as a post-surgery complication?
Wound dehiscence is identified by the separation of the surgical incision, leading to exposed tissue or organs.
Describe the steps involved in the initial investigation of a post-operative patient.
Includes physical examination, blood tests (CBC), and imaging (ultrasound, chest X-ray).
What are the recommended blood tests to assess a post-operative patient for infection, anemia, or other abnormalities?
CBC (Complete Blood Count).
How can deep vein thrombosis (DVT) be assessed in a post-operative patient?
Doppler ultrasound.
Define atelectasis and how it can be diagnosed in a post-operative patient.
Atelectasis is the collapse of lung segments, diagnosed via chest X-ray.
What is the best diagnostic test for wound dehiscence in a post-operative patient?
Direct clinical examination.
Differentiate between infection and inflammation in a post-operative patient.
Infections typically present with systemic signs like fever.
Describe a key differential diagnosis between pulmonary embolism (PE) and myocardial infarction in a post-operative patient.
PE often presents with pleuritic pain and sudden onset dyspnea, while both can have chest pain.
Describe the difference between bleeding and hematoma.
Bleeding is ongoing and systemic, while a hematoma is a localized collection of blood.
What is the initial treatment for infection after obtaining cultures?
Broad-spectrum antibiotics.
How is bleeding initially treated?
Hemostasis, possible blood transfusion, and addressing the cause.
What therapy is used for DVT/PE?
Anticoagulation therapy, such as heparin.
What interventions are used for atelectasis?
Incentive spirometry, chest physiotherapy, and possibly bronchoscopy.
What medications are used for pain management?
Analgesics like paracetamol, opioids if severe.
What is the treatment for wound dehiscence if necessary?
Surgical intervention to close the wound.
Define hematoma.
A localized collection of blood.
What antibiotics are used for infections?
IV cefazolin or piperacillin-tazobactam.
What antiemetics are used for nausea?
Ondansetron, metoclopramide.
Describe Restless Leg Syndrome (RLS)
It is a neurological disorder characterized by an uncontrollable urge to move the legs, often due to discomfort, and commonly associated with conditions like iron deficiency or chronic kidney disease.
Do individuals with RLS experience uncomfortable sensations in their legs?
Yes, they often experience sensations like tingling or burning in their legs.
Define the initial investigation for RLS
It involves a clinical diagnosis based on symptom criteria, including the urge to move legs, worsening at rest, and relief with movement, along with checking iron levels.
How can RLS be diagnosed if the symptoms are unclear?
A sleep study (Polysomnography) may be conducted to rule out other sleep disorders.
Describe the role of ferritin levels in diagnosing RLS
Ferritin levels are checked to assess iron deficiency, which is often linked to RLS, with levels below 50 µg/L commonly associated with the condition.
Describe the difference between peripheral neuropathy and nocturnal leg cramps in terms of symptom relief with movement.
Peripheral neuropathy symptoms are not typically relieved by movement, while nocturnal leg cramps are usually not associated with the urge to move the legs.
What are the initial treatment options for Restless Legs Syndrome (RLS) if ferritin levels are low?
Iron supplementation.
List some lifestyle modifications recommended for managing Restless Legs Syndrome (RLS).
Regular exercise, good sleep hygiene, avoiding caffeine or alcohol before bedtime.
What are the first-line pharmacological treatments for moderate to severe Restless Legs Syndrome (RLS)?
Dopamine agonists like Pramipexole and Ropinirole.
When should Gabapentin or Pregabalin be considered in the management of Restless Legs Syndrome (RLS)?
For patients with painful symptoms or those who do not respond to dopamine agonists.
Why is regular monitoring important in the management of Restless Legs Syndrome (RLS)?
To adjust treatment and manage potential side effects like augmentation (worsening of symptoms).
Pain with Restless leg sybdeome
gapapentine
rest leg intermittent symptoms treatment
levodopa
Describe the purpose of transdermal estrogen patch in menopausal symptom management.
Delivers systemic estrogen to alleviate vasomotor symptoms and improve vaginal atrophy.
What advantage does the transdermal route of estrogen delivery offer over oral estrogen?
Lower risk of thromboembolism and effectiveness in reducing flushing and vaginal symptoms.
How does estradiol, whether oral or transdermal, provide relief in menopausal symptoms?
By offering systemic relief of symptoms like hot flashes and vaginal dryness.
Describe the purpose of topical estrogen in managing menopausal symptoms.
Primarily targets vaginal symptoms like dryness and dyspareunia but does not address systemic symptoms like flushing.
What is a limitation of using topical estrogen for managing menopausal symptoms?
While effective for vaginal symptoms, it is not sufficient for managing systemic menopausal symptoms like flushing.
How can the choice of estrogen therapy be adjusted based on symptom severity?
The option can be adjusted by choosing different formulations (oral vs. patch) to offer flexibility in managing both vasomotor and local symptoms.
What is the preferred management for a patient needing to address both flushing and vaginal symptoms during menopause?
A transdermal estrogen patch or estradiol would be the most suitable options to relieve vasomotor symptoms while also improving vaginal health.
What are some common symptoms of menopause?
Common symptoms of menopause include hot flashes, night sweats, vaginal dryness, mood changes sleep disturbances, irregular periods, and decreased libido.
What is the initial investigation for menopause?
The initial investigation for menopause includes assessing symptoms, menstrual history, and general health.
How is menopause diagnosed?
Menopause can be diagnosed through clinical symptoms, age, and hormonal levels, with the FSH test being a key diagnostic tool.
What are the key differentials for menopause?
Thyroid disorders such as hyperthyroidism or hypothyroidism can mimic menopausal symptoms.
Describe the overlap between depression/anxiety and mood changes during menopause.
Depression/anxiety may overlap with mood changes experienced during menopause.
Define Premature Ovarian Insufficiency.
Premature Ovarian Insufficiency refers to menopause-like symptoms occurring before the age of 40.
What are the initial treatment options for menopausal symptoms?
Initial treatment options include lifestyle modifications, non-hormonal options, and medications.
How can lifestyle modifications help manage menopausal symptoms?
Lifestyle modifications such as regular exercise, healthy diet, and maintaining a cool sleeping environment can help manage symptoms.
What are some non-hormonal options for symptom relief during menopause?
Non-hormonal options include vaginal lubricants for dryness and SSRIs for mood disturbances and hot flashes.
What is Hormone Replacement Therapy (HRT) used for in menopausal treatment?
Hormone Replacement Therapy (HRT) is used for relief of moderate to severe menopausal symptoms.
What is the purpose of Step Management in menopausal treatment?
Step Management involves assessing symptoms, discussing lifestyle changes, considering HRT, and exploring non-hormonal therapies.
How should menopausal symptoms be monitored in the long term?
Menopausal symptoms should be regularly monitored for osteoporosis and cardiovascular health risks.
Do hypertensive encephalopathy commonly cause intracerebral hemorrhage or diffuse brain edema?
Hypertensive encephalopathy is more commonly associated with diffuse brain edema rather than intracerebral hemorrhage.
Describe the neurological symptoms associated with hypertensive encephalopathy.
Hypertensive encephalopathy typically leads to diffuse neurological symptoms like confusion, headache, and visual disturbances.
Define cerebral amyloid angiopathy.
Cerebral amyloid angiopathy involves the deposition of amyloid in the small and medium-sized blood vessels of the brain, leading to hemorrhages.
How does cocaine use relate to the likelihood of cerebral amyloid angiopathy?
Cocaine use is unlikely to be related to cerebral amyloid angiopathy.
Describe arteriovenous malformation (AVM) in relation to hemorrhagic strokes.
AVMs can cause hemorrhagic strokes, including subarachnoid hemorrhage.
Do AVMs typically result from acute drug use like cocaine?
AVMs are congenital and not typically precipitated by acute drug use like cocaine.
Describe the relationship between cocaine use and the risk of aneurysm rupture according to the RACGP perspective.
Cocaine use can lead to a sudden increase in blood pressure, making it more likely to cause an aneurysm to rupture than trigger an AVM hemorrhage.
Do coagulopathies due to chronic liver disease commonly lead to subarachnoid hemorrhage (SAH)?
No, coagulopathies associated with chronic liver disease are less likely to cause SAH, especially in a young patient with no history of liver disease but a known history of cocaine use.
Define the most likely cause of SAH in a patient with a history of cocaine use according to the RACGP perspective.
The most likely cause of SAH in a patient with a history of cocaine use is a ruptured aneurysm, as cocaine use can lead to sudden and severe increases in blood pressure, precipitating an aneurysm rupture.
How does cocaine use affect the risk of aneurysm rupture in the context of acute use?
Cocaine use, due to its potent effects on blood pressure, increases the risk of aneurysm rupture, making it the most likely cause of SAH in the context of acute cocaine use.
Do young individuals with a history of cocaine use have a higher risk of intracerebral hemorrhage compared to the general population?
Yes, young individuals with a history of cocaine use have a higher risk of intracerebral hemorrhage due to cocaine-induced vasoconstriction and hypertension.
Define hypertensive encephalopathy and its relationship to intracerebral hemorrhage in the context of cocaine use.
Hypertensive encephalopathy is characterized by severe hypertension and can lead to intracerebral hemorrhage, particularly in individuals with a history of cocaine use.
How does cocaine-induced vasoconstriction contribute to the development of intracerebral hemorrhage?
Cocaine-induced vasoconstriction can lead to acute elevations in blood pressure, increasing the risk of intracerebral hemorrhage, especially in young individuals with a history of cocaine use.
Explain why hypertensive encephalopathy is the most likely cause of intracerebral hemorrhage in a young female with a history of recent cocaine use presenting with a seizure.
The acute hypertensive crisis induced by cocaine, leading to hypertensive encephalopathy, is the most direct and likely cause of intracerebral hemorrhage in this scenario, given the association between cocaine use and elevated blood pressure.
Describe the relationship between cocaine use and subarachnoid hemorrhage (SAH).
Cocaine use can lead to the rupture of pre-existing cerebral aneurysms, resulting in SAH due to the intense and sudden increase in blood pressure.
Do hypertensive crises caused by cocaine use directly lead to subarachnoid hemorrhage (SAH)?
No, hypertensive crises caused by cocaine use can contribute to the rupture of pre-existing cerebral aneurysms, which then leads to SAH.
Define subarachnoid hemorrhage (SAH).
SAH is bleeding into the subarachnoid space between the arachnoid membrane and the pia mater surrounding the brain.
How does cocaine’s vasoconstrictive properties contribute to the formation and rupture of aneurysms?
Cocaine’s vasoconstrictive properties can increase blood pressure, leading to the rupture of pre-existing cerebral aneurysms.
Describe the most likely cause of subarachnoid hemorrhage (SAH) in a young female with a history of cocaine use presenting with a seizure.
The most likely cause is a ruptured aneurysm due to the sudden increase in blood pressure associated with cocaine use.
Describe the cause of gout.
Gout is caused by hyperuricemia, which is elevated levels of uric acid in the blood leading to the formation of urate crystals that accumulate in joints.
List some risk factors for developing gout.
Genetics, diet high in purines (e.g., red meat, shellfish), obesity, certain medications (e.g., diuretics), and alcohol consumption are risk factors for gout.
What are the symptoms of gout?
Symptoms of gout include acute joint pain, swelling and redness in the affected joint, tophi formation, and limited joint mobility during acute attacks.
How is gout diagnosed initially?
Gout is initially diagnosed by checking serum uric acid levels, performing joint aspiration for urate crystal detection, and using X-rays to visualize joint damage or tophi in chronic cases.
Describe the best diagnostic test for confirming gout.
Joint Aspiration and Synovial Fluid Analysis: Identifies needle-shaped urate crystals.
What are the key differentials to consider when diagnosing gout?
Pseudogout (caused by calcium pyrophosphate crystals), Septic Arthritis, Rheumatoid Arthritis.
How can NSAIDs be used in the treatment of gout?
First-line treatment to reduce pain and inflammation, best started at the onset of an acute gout attack for quick relief.
Define Colchicine and its role in managing gout flares.
Colchicine is used to manage acute flares, especially if NSAIDs are contraindicated or ineffective. Best when taken within 24 hours of an attack onset.
What is the role of corticosteroids in treating gout?
Effective for individuals who cannot take NSAIDs or colchicine due to contraindications or intolerance.
Describe the use of oral or intra-articular steroids like Prednisone or Triamcinolone in gout management.
They are used for acute attacks, especially in patients with multiple comorbidities.
What is the purpose of using Allopurinol in gout management?
It is a xanthine oxidase inhibitor used to lower uric acid levels for long-term management.
How should Allopurinol be initiated in gout patients?
It should be started after an acute attack has resolved and is recommended for patients with recurrent or chronic gout.
Define Febuxostat and its role in gout treatment.
Febuxostat is an alternative xanthine oxidase inhibitor to Allopurinol, used for long-term uric acid reduction, especially in patients with refractory hyperuricemia.
When is Probenecid considered in gout management?
It is considered in patients with under-excretion of uric acid and normal renal function, either added to Allopurinol or used alone if Allopurinol is not tolerated.
Describe the cause of Hereditary Spherocytosis.
It is caused by genetic mutations, most commonly autosomal dominant mutations affecting RBC membrane proteins like ankyrin, spectrin, and band 3.
What are the symptoms of Hereditary Spherocytosis?
Symptoms include hemolytic anemia (fatigue, pallor, shortness of breath), jaundice (due to increased bilirubin from hemolysis), splenomegaly (enlarged spleen), and gallstones (from chronic hemolysis).
How is Hereditary Spherocytosis diagnosed initially?
It is diagnosed initially through a CBC showing anemia with high MCHC and a peripheral smear revealing spherocytes (small, round RBCs without central pallor).
Define the best diagnostic tests for Hereditary Spherocytosis.
The best diagnostic tests are the Osmotic Fragility Test, showing increased RBC fragility in hypotonic solutions, and the EMA Binding Test, confirming HS by reduced band 3 protein.
Describe the key differentials for Hereditary Spherocytosis.
Key differentials include autoimmune hemolytic anemia (differentiated by a positive Coombs test) and other hemolytic anemias like G6PD deficiency.
What is the initial treatment for Hereditary Spherocytosis?
Initial treatment includes folic acid supplementation (1 mg daily) to support RBC production and blood transfusions for severe anemia or aplastic crises.
How is Hereditary Spherocytosis managed step by step?
Management involves diagnosis based on clinical findings, lab tests, and possibly genetic testing, supportive care with folic acid and regular monitoring, splenectomy consideration for severe cases to reduce hemolysis, and post-splenectomy care with prophylactic antibiotics and vaccinations.
What should be monitored regularly in patients with Hereditary Spherocytosis?
Regular follow-up is needed to monitor for complications like gallstones.
Do patients with Hereditary Spherocytosis require blood transfusions?
Yes, blood transfusions may be necessary for severe anemia or aplastic crises in patients with Hereditary Spherocytosis.
Describe G6PD Deficiency.
It is an X-linked recessive genetic disorder caused by a deficiency in the enzyme glucose-6-phosphate dehydrogenase, crucial for protecting red blood cells from oxidative damage.
Do episodes of hemolytic anemia occur in G6PD Deficiency?
Yes, triggered by certain medications, foods (like fava beans), or infections.
Define the best diagnostic test for G6PD Deficiency.
initial blood smear Shows bite cells and Heinz bodies.- Quantitative G6PD enzyme assay to confirm the deficiency.
How does G6PD Deficiency differ from Autoimmune Hemolytic Anemia?
G6PD Deficiency has a negative Coombs test, while Autoimmune Hemolytic Anemia has a positive Coombs test.
Describe the initial treatment for G6PD Deficiency.
Avoidance of known triggers, supportive care during hemolytic episodes, including hydration, and possibly blood transfusions if severe.
What is the management approach for G6PD Deficiency?
Educate patients on avoiding triggers, regular monitoring during infections, and provide genetic counseling for families.
Where are the likely primary sites for metastasis to the inguinal lymph nodes?
Anus and rectum (especially distal).
What are the primary sites for metastasis to the lungs?
Mediastinal nodes, brain, bones.
Where is the primary site for metastasis to the testicles?
Retroperitoneal lymph nodes.
What is the primary site for metastasis to the stomach?
Supraclavicular nodes (Virchow’s node), liver.
Describe the cause of Polyarteritis Nodosa (PAN)
PAN is a rare, systemic necrotizing vasculitis that affects medium-sized muscular arteries, leading to inflammation and damage to the arterial walls.
What are some symptoms of Polyarteritis Nodosa (PAN) related to the skin?
Symptoms include livedo reticularis, subcutaneous nodules, and ulcers.
How does Polyarteritis Nodosa (PAN) affect the renal system?
It can lead to hypertension and renal insufficiency due to renal artery involvement.
Define Mononeuritis multiplex in the context of Polyarteritis Nodosa (PAN)
It involves asymmetrical peripheral neuropathy.
What initial investigations are commonly done for suspected Polyarteritis Nodosa (PAN)?
Blood tests showing elevated ESR/CRP, leukocytosis, and anemia, hepatitis B and C serology, and urinalysis for proteinuria or hematuria.
Describe the role of tissue biopsy in diagnosing the condition.
Confirms the diagnosis by showing necrotizing vasculitis in the affected tissues.
What is the purpose of angiography in this context?
Identifies aneurysms and stenoses in medium-sized arteries, particularly in the kidneys, liver, and mesenteric arteries.
Differentiate Microscopic Polyangiitis from the condition described.
Involves small vessels and is often associated with ANCA positivity.
How does Granulomatosis with Polyangiitis differ from the condition discussed?
Primarily affects small vessels and often has granulomatous inflammation.
Explain the involvement of Systemic Lupus Erythematosus (SLE) in this scenario.
Can present with similar systemic features but typically involves autoantibodies like ANA.
What is the initial treatment approach for the condition?
The overall aim of therapy is to control disease activity. Mild activity can be managed with non-steroidal anti-inflammatory drugs (NSAIDs) or low-dose steroids, but more severe manifestations require prompt treatment with moderate-to-high doses of steroids to minimise organ damage. Steroid-sparing immunosuppressive medications should be considered early to prevent steroid-related morbidities.
Hydroxychloroquine is an effective treatment in SLE, especially for arthritis and rash. Furthermore, it has a protective effect in reducing damage accrual in the long term, and confers a survival benefit in SLE patients. Hydroxychloroquine is well tolerated and, when dosed appropriately, ocular toxicity is very rare.27
What are the key medications used in the treatment of this condition?
Prednisone and Cyclophosphamide.
How is Prednisone typically administered in the treatment plan?
hydroxyused. Used initially at high doses (e.g., 1 mg/kg/day) to control inflammation. Not work then methotrexate
When is Cyclophosphamide specifically used in the treatment regimen?
For more severe cases or as a steroid-sparing agent.
lupus nephritis
Describe the step management for PAN treatment.
The step management includes confirming diagnosis, initiating corticosteroids, considering immunosuppressants, addressing associated infections, monitoring for complications, tapering steroids, and regular follow-up.
What is the role of antiviral therapy in PAN associated with hepatitis B?
Antiviral therapy is necessary alongside immunosuppressive therapy.
How is the diagnosis of PAN confirmed?
Through biopsy and angiography after clinical suspicion.Biopsy of clinically uninvolved tissue is often useless because the disease is focal; biopsy should target sites suggested by clinical evaluation. Samples of subcutaneous tissue, sural nerve, and muscle, if thought to be involved, are preferred to samples from the kidneys or liver; kidney and liver biopsies may be falsely negative because of sampling error and may cause bleeding from unsuspected microaneurysms. Unlike in granulomatosis with polyangiitis (GPA), biopsy is unlikely to show marked parenchymal inflammation.
What is the initial treatment for controlling acute symptoms in PAN?
Initiating high-dose prednisone.
What should be done in severe cases of PAN or when unresponsive to steroids?
Consider adding immunosuppressants like cyclophosphamide.
Define the follow-up protocol for PAN patients.
Regular monitoring of renal function, blood pressure, potential side effects of therapy, and imaging studies to monitor aneurysms and stenoses.
Do you taper steroids in PAN treatment? If so, when?
Yes, steroids are gradually tapered once the disease is under control to minimize side effects.
Describe the cause of cervical spondylosis.
Age-related degeneration involving wear and tear of cervical discs and osteophyte formation.
What are the symptoms of cervical spondylosis?
Neck pain, radiculopathy (pain radiating to arms/hands), myelopathy (weakness, gait disturbance, loss of fine motor skills), headaches (occipital headaches, radiating forward).
What is the initial investigation for cervical spondylosis?
Physical exam to check for tenderness, range of motion, and neurological signs; X-ray to show disc space narrowing and osteophytes.
How is cervical spondylosis diagnosed?
Best diagnostic test is MRI to evaluate discs, spinal cord, and nerve roots.
What are the key differentials for cervical spondylosis?
Herniated disc, rheumatoid arthritis, spinal tumors, differing based on onset, systemic symptoms, and progressive deficits.
What is the initial treatment approach for cervical spondylosis?
Conservative management including physical therapy, NSAIDs, and lifestyle modifications; temporary collar use for pain relief.
What medications are commonly used in treating cervical spondylosis?
NSAIDs for pain/inflammation (e.g., Ibuprofen), muscle relaxants (e.g., Cyclobenzaprine), Gabapentin/Pregabalin for neuropathic pain.
What are the steps in managing cervical spondylosis?
Physical therapy for strengthening, pain management with NSAIDs, lifestyle adjustments (ergonomics, posture), surgical consultation if severe symptoms persist.
How should follow-up be conducted for cervical spondylosis patients?
Regular monitoring for symptom progression or new neurological signs.
Describe a cervical rib.
An extra rib arising from the cervical spine, usually at C7.
What is the cause of a cervical rib?
It is a congenital anomaly.
What symptoms can a cervical rib cause?
Thoracic Outlet Syndrome, vascular symptoms like coldness or cyanosis of the hand.
What is the initial investigation for a suspected cervical rib?
Physical exam including Adson’s test, neurological and vascular assessment, and X-ray.
How is a cervical rib typically diagnosed?
Primarily through X-ray to confirm its presence and assess its size.
