Internal Med & Specialtys Flashcards
osteoarthritis - CF (pain, stiffness, swelling)
Pain after activity towards the end of the day, relieved by rest.
Stiffness after activity and early morning
» LASTS <30 min
Swelling absent
osteoarthritis - management
First line: paracetamol
Second line: NSAID or COX2 (celecoxib)
Intraarticular GCS (flare up of knee OA)
Surgery (OA knee, shoulder)
Glucosamine, chondroitin, vit D, omega 3 fatty acids not recommended.
Avoid long term opioids, oral GCS, gold, antimalarias , cytotoxic
Exercise, diet, rest, heat, physiotherapy, occupational therapy, braces, orthotics, walking aids.
RA - Dx and autoantibodies for Dx
Anti-ccp (best ^^^^ specificity)
The diagnosis of RA is made on the basis of clinical presentation, in association with autoantibodies and evidence of systemic inflammation (eg elevated ESR and RCP).
The most commonly affected joints include the wrists, metacarpophalangeal joints, proximal interphalangeal joints and metatarsophalangeal joints.
The findings are generally symmetric
> The carpometacarpal and distal interphalangeal joints are not typically affected. Other large joints may also be affected by rheumatoid arthritis.
RA - extra articular manifestations
Rheumatoid nodules
Alopecia
Livedo reticularis
Chronic disease anaemia
Scleritis, episcleritis
Xerostomia
Pericarditis
RA - Pain management
NSAID or paracetamol for pain management
RA - Definitive management
- Methotrexate DMARD improves long-term outcome (consider folic acid supplementation):
methotrexate 10 mg orally, on one specified day once weekly, increasing up to 25 mg orally or subcutaneously, on one specified day once weekly
PLUS
folic acid 5 to 10 mg orally, per week (preferably not on the day methotrexate is taken).
Glucocorticosteroids for flare of RA (consider injections if large joints are involved).
Hydroxychloroquine is used in combined therapy: methotrexate + sulfasalazine + hydroxychroroquine.
Etarnacept biological DMARD is used in combination with methotrexate if monotherapy is not effective. Increased risk of infection (tuberculosis, atypical pneumonia, listeriosis).
Gout - ttx of acute attack
Avoid initiation or changing the dose of Allopurinol during an acute attack.
In acute attack Allopurinol can be safely continued.
In acute attack: NSAID or Colchicine if ulcer, systemic GCS if renal failure.
1 - a local corticosteroid injection at up to a maximum of two affected sites (see Table 12.9 for example doses)
OR
1 - NSAID orally, until symptoms abate (typically 3 to 5 days) (see Table 12.7 for dosing; the upper end of the dosing range is often required)
OR
1 - prednis(ol)one 15 to 30 mg orally, daily until symptoms abate (typically 3 to 5 days) [Note 2]
OR
2 (due to adverse effects, mostly GI) - colchicine 1 mg orally initially, then 500 micrograms 1 hour later, as a single one-day course (total dose is 1.5 mg).
Gout - when to consier GCS injections?
Consider GCS injections if one or two joints are involved (maximum 2)
Gout -when to begin Allopurinol after acute attack?
Commence Allopurinol (if needed) 6 8 weeks after an acute attack.
Gout - diagnosis
Aspiration of an affected joint, bursa or tophus is required to confirm the diagnosis of gout.
It show the presence of needle shaped negatively-birefringent uric acid crystals (monosodium urate crystals)
Serum uric concentration should be measured in all patients with suspected gout. However, the presence of hyperuricaemia alone is insufficient to diagnose gout and, in patients with acute gout, serum uric concentration may be normal. Other than the presence of tophi, individual clinical features (eg history of painful or swollen big toe, unilateral podagra) have a low diagnostic utility.
Response to colchicine does not replace aspiration in the diagnosis of gout; it can support a diagnosis of crystal arthritis, but does not distinguish between gout and acute calcium pyrophosphate crystal arthritis.
Gout - serum uric acid target
The target serum uric acid concentration is less than 0.36 mmol/L (6 mg/dL) for patients with non-tophaceous gout, and less than 0.30 mmol/L (5 mg/dL) for patients with tophaceous gout
Measure serum uric acid concentration monthly during the dose titration phase
Gout - First-line urate-lowering therapy
allopurinol 50 mg orally, daily for 4 weeks; then increase the daily dose by 50 mg every 2 to 4 weeks or by 100 mg every 4 weeks to achieve the target serum uric acid concentration, up to a maximum maintenance dose of 900 mg daily.
- If the target serum uric acid concentration cannot be achieved with allopurinol monotherapy:
probenecid 250 mg orally, twice daily for 1 week, then increase to 500 mg twice daily; then increase the daily dose by 500 mg every 4 weeks to achieve the target serum uric acid concentration, up to a maximum maintenance dose of 2 g daily in divided doses.
Gout - Flare prophylaxis when starting or increasing urate-lowering therapy
1 - colchicine 500 micrograms orally, once or twice daily. Reduce dosage in renal impairment
OR
2 - NSAID orally (see Table 12.7 for dosing; the lower end of the dosing range is usually adequate)
Gout - alternatives to colchicine
Febuxostat as an alternative urate lowering therapy .
It has the same mechanism as allopurinol (reduces the amount of uric acid made by body cells).
This would therefore be appropriate in patients with allopurinol rash or hypersensitivity to allopurinol.
»C/I in liver failure and pre-existing major cardiovascular disease
Probenecid the second line agent. Provides hyperexcretion of uric acid by blocking renal tubular reabsorption.
»C/I in urate nephrolithiasis.
Allopurinol desensitization if no alternative therapeutic options.
1febuxostat 40 mg orally, daily for 2 to 4 weeks; then increase the daily dose by 40 mg every 2 to 4 weeks to achieve the target serum uric acid concentration, up to a maximum maintenance dose of 120 mg daily
OR
2probenecid 250 mg orally, twice daily for 1 week, then increase to 500 mg twice daily; then increase the daily dose by 500 mg every 4 weeks to achieve the target serum uric acid concentration, up to a maximum maintenance dose of 2 g daily in divided doses.
Gout - indication for surgical ttx
Surgery: in destructive changes of joints
One of three surgical treatments is often recommended: tophi removal, joint fusion, or joint replacement.
SLE classification criteria:
Malar rash
Discoid rash
Photosensitivity
Arthritis (symmetrical, non erosive)
Oral ulcers (painless)
Serositis (pleurisy, pericarditis)
Proteinuria, cellular casts
Intractable headache, seizure, psychosis
Haemolytic anaemia, thrombocytopenia, leukopenia, lymphopenia
Antiphospholipid syndrome
SLE - Disease flare may be accompanied by a rise or decrease in which seromarkers?
antibodies to double-stranded DNA (dsDNA) and a reduction in C3 and C4 complement components
Azathioprine - caution for drug toxicity
hiopurine drugs are metabolised by TPMT. TPMT displays genetic polymorphism resulting in null or decreased enzyme activity (3 14% of people). These polymorphism is associated with»_space;»>increased myelosuppression risk.
Consider an alternative agent or extreme dose reduction of azathioprine for patients with los or deficient TPMT activity. Start at 30 70% of target dose for patients with intermediate enzyme activity.
Temporal arteritis - cf
Headache (new onset) throbbing pain unilateral
Scalp tenderness
Jaw claudication (pathognomonic)
Vision problems (sudden visual loss or diplopia)
Loss of pulsation of temporal artery
Malaise
The features of giant cell arteritis may be vague and nonspecific; in patients with systemic features such as weight loss, fevers, malaise and generalised pain and stiffness,
Strong association with Polymyalgia Rheumatica (50%):
Temporal arteritis - Ix and Mx
Investigation: first step: ESR/CRP. best step: biopsy of artery at least 2 cm, multiple sections (giant cells).
Treatment: High dose prednisolone (40 60 mg) orally.
Urgent! Referral to ophthalmologist.
polymyalgia rheumatica - Cf
Pain or aching is usually felt in the large muscle groups, especially around the shoulders and hips.
Patients complain of an inability to turn over in bed and of great difficulty getting out of bed. The stiffness tends to improve after a hot shower, and with activity.
Other symptoms may include:
> Stiffness, especially in the morning
and after resting
Weakness
Fatigue
Generally feeling ill
Mild fevers (occasionally)
Weight loss
A high erythrocyte sedimentation rate (ESR) is common among patients with PMR, but is not always present.
Quick recovery and disappearance of symptoms after treatment with low-dose corticosteroids.
ankylosing spondylitis - management
Physiotherapy for exercises, hydrotherapy, stretching program, postural exercises. Appropriate physiotherapy slows deterioration in spinal function.
Smoking cessation
NSAIDs are the first line treatment for patients without IBD or renal impairment
TNF-ALFA inhibitors, such as Infliximab and Adalimumab, are the first line for patients with concurrent IBD or recurrent anterior uveitis. Second line in patients with insufficient response to TWO nsaids.
Exception: etarnecept for IBD
Local GCS - isolated active sacroilitis or active enthesitis.
Sulfasalazine can be used if NSAIDs and exercise are not effective, It has little effect in spinal disease, but can be useful for an associated peripheral arthritis
ankylosing spondylitis - CF
Articular and peri-articular features
enthesitis (inflammation at the sites of tendon and ligament attachment to bone)
spondylitis (inflammation of the spine) characterised by sacroiliitis (inflammation of sacroiliac joints)
peripheral arthritis that, characteristically:
is oligoarticular
is asymmetrical
affects the lower limbs
affects large joints
dactylitis (inflammation of a whole finger or toe, ‘sausage digits’)
Possible extra-articular features:
psoriasis-like skin and nail lesions
»»conjunctivitis or acute anterior uveitis (MOST COMMON)
chronic gastrointestinal inflammation
chronic genitourinary inflammation
What vasculitis is implicated in high C-Anca levels?
Wegener’s - Granulomatosis with polyangiitis
Granulomatosis with polyangiitis - CF, Ix, Mx
Small to medium blood vessels
Cough, wheeze
Rhinitis
Sinus pain
Nasal ulcers
Epistaxis
Orbital mass
Polyarthritis
Nephrytic syndrome
C- ANCA and nd anti-proteinase-3 (PR-3) specificity.
Best for dx: Open lung biopsy
Ttx: cyclophosphamide
Most patients require intensive induction therapy. In rare cases, patients have limited disease that does not affect a major organ (eg isolated sinus disease) and treatment can be started with high-dose oral prednis(ol)one in combination with another immunomodulatory drug (eg methotrexate or mycophenolate). Once remission is achieved, a combination of prednis(ol)one and another immunomodulatory drug is usually required to maintain remission.
> TIP: Involvers SUPERIOR respiratory tract + Kidneys
Chur-Strauss Synd / Eosinophilic granulomatosis with polyangiitis - Cf, Ix, Mx
Palpalble purpura (small to medium blood vessels)
Asthma
Rhinitis
Polyneuropathy (Mononeuritis multiplex)
Nephritic syndrome
p-ANCA
Peripheral eosinophilia
GCS and cyclophosphamide
Polyarteritis nodosa - Cf, Ix, Mx
Small to medium arteries.
Arthralgia
Subcutaneous nodules
Livedo reticularis
Digital infarcts
Skin ulcers
Nephritic syndrome
> About 30% of patients with polyarteritis nodosa are positive for hepatitis B surface antigen, and these patients should be considered for antiviral therapy before starting, or stopping, immunomodulatory therapy
ANCA negative or p-ANCA
Best: muscle biopsy or angiogram
GCS and immunosuppressors
For polyarteritis nodosa without evidence of major organ or body system involvement (eg disease affecting the skin only, disease characterised by systemic symptoms only) the standard treatment is high-dose prednis(ol)one
For disease affecting a major organ or body system (eg patients with polyneuropathy, kidney or liver involvement) intravenous methylprednisolone is used instead. Cyclophosphamide is added if a visceral organ is affected or if disease is progressive despite adequate corticosteroid therapy.
Goodpasture syndrome - Cf, Ix, Mx
Haemoptysis
Cough
Dispnoea
Nephritic syndrome
Kidney biopsy
GCS immunosuppressors
> TIP: kidney involvement + LOWER respiratory tract
Atrial fibrillation + pneumonia - what to think as dx?
Eurthyroid sick syndrome
Findings in Euthyroid sick syndrome
Low TSH, T3 and T4
High rT3
It is possible that the early changes in thyroid function (low T3 and elevated reverse [rT3]) during severe illness are protective in that they prevent excessive tissue catabolism.
Thyroid function should not be assessed in seriously ill patients unless there is a strong suspicion of thyroid dysfunction, since there are many other factors in acutely or chronically ill euthyroid patients that influence thyroid function tests.
When thyroid dysfunction is suspected in critically ill patients, measurement of serum TSH alone is inadequate for the evaluation of thyroid function. In such a patient, TSH and free T4 (and often total T3) are needed to differentiate nonthyroidal illness from a thyroid disorder. However, the diagnosis may still be in doubt
Differential diagnosis of muscle weakness
Thyrotoxic myopathy or hyperthyroid myopathy.
Hyperthyroidism increases the metabolic rate and much of this energy is ineffectively used to muscle contraction. In turn, the muscles fatigue easily, and become weak and wasted.
A hyperthyroid person who has muscle weakness may or may not have other recognizable manifestation of hyperthyroidism (in this case only tachycardia is given). Myopathy can sometimes be the first presentation of the underlying hyperthyroid state.
Patient complains of low exercise tolerance, easy fatigability, difficultyof doing certain tasks. Shoulder, hand and pelvic muscles are affected and tasks like climbing stairs, getting up from a low chair or lifting arms above the shoulders become difficult. Due to the weakness, movements become clumsy and effortful.
Hyperthyroidism increases the metabolic rate and much of this energy is ineffectively used to muscle contraction. In turn, the muscles fatigue easily, and become weak and wasted.
A hyperthyroid person who has muscle weakness may or may not have other recognizable manifestation of hyperthyroidism (in this case only tachycardia is given). Myopathy can sometimes be the first presentation of the underlying hyperthyroid state.
Patient complains of low exercise tolerance, easy fatigability, difficulty of doing certain tasks. Shoulder, hand and pelvic muscles are affected and tasks like climbing stairs, getting up from a low chair or lifting arms above the shoulders become difficult. Due to the weakness, movements become clumsy and effortful.
Statin induced myositis:
from mild to severe muscle pain, usually proximal groups, muscle stiffness and weakness can occur.
Neuromuscular junction disorder:
needs to be considered although the absence of ocular symptoms (which occurs in 90% of patients with myasthenia) and lack of fluctuating symptoms would be atypical for myasthenia gravis.
Cerebellar ataxia:
characterised by difficulties maintaining normal upright posture, coordinated walking, unsteady gait, staggering, tripping. Fine motor coordination will include difficulty withhandwriting, cutting food, opening jars, buttoning clothes, typing, playing an instrument.
Inflammatory myopathy (Polymyositis, Dermatomyositis):
affects the proximal skeletal muscles with evidence of elevated CK and myositis on biopsy. Clinical manifestation includes symmetrical proximal muscle weakness and wasting. Commonly affects pelvic and shoulder girdle muscles leading to difficulties combing hair, standing up from a sitting position and climbing stairs. Tachycardia is not the sign of inflammatory myopathy.
Thyroid function tests results in pregnancy
TSH is lower in the first trimester, TSH concentration 0.1 is normal (gestational transient thyrotoxicosis). It is self limiting (after 12 weeks) and does not require treatment.
Free T3 tends to be higher throughout pregnancy.
Free T4 is lower in the late second and third trimester.
What are the treatment options for papillary thyroid cancer based on risk?
Low risk: Hemithyroidectomy + Levothyroxine + TSH suppression 🔪💊
Criteria: Tumor <4 cm, no invasion, no vascular invasion, non-aggressive histology, complete macroscopic tumor resection, no regional lymph node metastasis 📏🚫
Intermediate risk: Total thyroidectomy + Consider RAIA (Radioactive iodine ablation) + TSH suppression 🏥🔬
High risk: Total thyroidectomy + RAIA + TSH suppression 🏥🔬🔴
Active surveillance for papillary microcarcinoma (<1 cm) with no nodal or distant metastasis. Multimorbid patients with high surgical risk ot short lige expectancy📊👀
Explain the significance of psammoma bodies in thyroid tissue.
Psammoma bodies suggest a suspicion of malignancy 🩸
Especially associated with papillary thyroid cancer 🦠
Their presence warrants further investigation 🧪
Can be a diagnostic clue for malignancy 🚨
What is the significance of transplacental passage of TRAb in Graves’ disease during pregnancy?
Transplacental passage of TRAb can lead to transient neonatal hyperthyroidism 👶🤰
Occurs in women with Graves’ disease during pregnancy 🤱
Requires careful evaluation of the neonate if TSH-receptor antibodies are high in the last trimester 📊👶
Neonatal thyrotoxicosis due to TRAb is transient and limited by maternal antibody clearance (8 - 20 weeks) ⏳
Describe the persistence of TRAb levels in treated hyperthyroidism and hypothyroidism.
TRAb levels can remain elevated despite treatment for hyperthyroidism (surgery or radioiodine) or hypothyroidism (L-Thyroxine) 📈
Monitoring TRAb levels is important in assessing treatment response 🩺💉
Elevated TRAb levels can indicate ongoing autoimmune activity 🦠
TRAb levels should be evaluated during pregnancy and postpartum for appropriate management 🤰🔬
What are the differences between bromocriptine and cabergoline in treating pituitary adenoma?
Bromocriptine is a non-selective dopamine agonist binding to D1 receptors in the gut and D2 receptors in the pituitary 🧪🧠
Cabergoline has a longer half-life and is more specific for D2 receptors 🕰️
Cabergoline is recommended as the first-line treatment for pituitary adenoma due to its superior effectiveness and tolerability 🥇
Cabergoline normalizes prolactin in up to 95% of patients, reduces tumor size in about 90%, and controls symptoms in the majority 🩺📉😃
How is treatment resistance defined in pituitary adenoma cases?
Treatment resistance is defined as less than 50% reduction in tumor size or failure to return prolactin concentration to normal with dopamine agonist therapy 📉💊❌
Occurs in 10% of patients treated with cabergoline and 25% of those treated with bromocriptine 📊
Indicates the need for alternative treatment strategies 🏥🎯
Discuss the management of patients with visual field defects, dopamine agonist resistance, and pituitary apoplexy.
Patients with persistent visual field defects, dopamine agonist resistance, and pituitary apoplexy often require transsphenoidal surgery, radiotherapy, or both 🩸🔬🪓
These interventions are crucial for managing complications and improving patient outcomes 🏥💡
Explain the diagnostic tests and findings in acromegaly.
Increased insulin-like growth factor 1 - IGF1 (somatomedin) is a hallmark of acromegaly 📈
The glucose suppression test is used to confirm the diagnosis 🩺🩹
MRI imaging typically shows enlargement of the sella turcica, a characteristic finding 📊🏥
Describe the surgical and medical options for acromegaly management.
Transsphenoidal surgery and radiation therapy are primary treatments for acromegaly 🏥🪓
Octreotide is a second-line option for refractory tumors 🩸💉
If there is prolactin co-secretion, cabergoline or bromocriptine may be added to the treatment regimen 🤝🔬
What are the common clinical features of adrenal insufficiency?
Clinical features of adrenal insufficiency include weight loss, skin pigmentation, postural hypotension, nausea, vomiting, diarrhea, and loss of appetite 🤢🏋️♀️🌡️
What is the most common cause of primary adrenal insufficiency in adults?
Explain the primary cause and its typical age of onset.
The most common cause of primary adrenal insufficiency in adults is autoimmune disease, typically occurring between 30 and 50 years of age 🧬🦠
Autoimmune conditions often coexist, with thyroid disease being the most common, along with vitiligo, type 1 diabetes, primary gonadal failure, coeliac disease, and pernicious anemia 👥🩺👨⚕️
How is rehydration typically initiated in Diabetes KetoAcidosis management?
Begin rehydration with normal saline IV at a rate of 15-20 ml/kg 🩸
If corrected sodium is >145 mmol/L, administer half saline IV to avoid overcorrection 🧪
Watch for symptoms of cerebral edema during treatment ⚠️
How is insulin administered in the treatment of DKA?
Administer short-acting insulin via IV infusion 🧬💉
Monitor glucose levels every hour and initiate glucose 5% IV when glucose falls below 15 mmol/L 📊🔬
Monitor potassium (K) levels every 2 hours and start KCl IV when K falls below 5.5 mmol/L 🧪🔍
Explain when sodium bicarbonate, antibiotics, and DVT prophylaxis are indicated in DKA management
Administer sodium bicarbonate if the pH falls below 7.0 to correct acidosis 🧪📉
Consider broad-spectrum antibiotics if there is evidence of infection 🦠🦠
Implement DVT prophylaxis measures to prevent thromboembolic events 🩺🦠
Is diabetes alone a sufficient indication for using aspirin for primary prevention of cardiovascular disease?
Diabetes alone is not a sufficient indication for using aspirin for primary prevention of cardiovascular disease 🩺🚫
Other risk factors and individual patient factors should be assessed to determine aspirin eligibility 📊👨⚕️
All adults with diabetes and clinically manifest cardiovascular disease should be treated with low-dose aspirin for secondary prevention 🩸💊
What should individuals with diabetes do regarding blood glucose levels before driving?
Monitor blood glucose concentration before driving and ensure it is above 5 mmol/L 🩺🚗
If you are driving for two hours or more, recheck your blood glucose level at least every two hours to make sure it stays above 5mmol/L.
Maintaining safe blood glucose levels is crucial for road safety 🛣️👨🚒
Always carry glucose-containing foods to manage low blood sugar episodes 🥖🍬
Inform the driving license authority about diabetes 🚗📝
IMMEDIATELY eat or drink at least 15 grams of fast acting carbohydrate and Wait 10–15 minutes and check your blood glucose level again.
What should be advised to individuals with hypoglycemia unawareness regarding driving?
Individuals with hypoglycemia unawareness should cease driving until they can demonstrate no hypoglycemia over a 6-week period and restore hypoglycemia awareness 🚫🚘
Ensures road safety and the well-being of the driver and others on the road 🛣️👀
What is hypoglycemia unawareness, and how is it characterized? Explain the risk factors and strategies for managing hypoglycemia unawareness.
Hypoglycemia unawareness occurs when adrenergic (autonomic) symptoms’ threshold closely aligns with or falls below the threshold for neuroglycopenic symptoms 🧠💔
This results in the absence of characteristic adrenergic symptoms, and confusion or loss of consciousness becomes the initial sign of hypoglycemia 🚫🤷
It’s more common in patients with type 1 diabetes, particularly those with over 10 years of disease duration, but can also affect type 2 diabetes patients, especially those treated with insulin or sulfonylureas 🩸📈
It can develop after repeated episodes of short-duration hypoglycemia, impairing adrenergic responses to subsequent episodes 🔄📉
Individualized glycated hemoglobin (HbA1c) targets may be needed to minimize the risk of hypoglycemia 🎯📊
Hypoglycemia unawareness and defective counter-regulatory hormone responses can potentially be reversed through strict avoidance of hypoglycemia for 2 days to 3 months 🔄⚖️
What are some long-term diabetes-related complications that may impact driving?
In addition to hypos, long-term diabetes-related complications can affect the ability to drive safely 🚗🩸
Regular eye check-ups every 12 months or as recommended by the doctor are crucial, and the doctor may clear the individual for driving for 18–24 months 🩺👁️
Similarly, regular foot check-ups every 12 months or as recommended by the doctor are essential 🦶
Seek advice from a doctor or podiatrist promptly if there are any issues, such as numbness, pain in the feet or legs, or difficulty feeling the pedals while driving 🩺🦶🚙
What is primary aldosteronism, and what are its key features?
Primary aldosteronism, also known as Conn’s syndrome, is characterized by the presence of aldosterone-producing adenoma, leading to sodium and water retention with hypertension 🩸💧
It often results in low potassium levels, causing muscle weakness, cramps, paresthesia, polyuria, and polydipsia 🏋️♂️🚰
What are the common causes or conditions associated with secondary aldosteronism?
Secondary aldosteronism can be caused by conditions such as congestive heart failure (CHF), cirrhosis, renal artery stenosis, and nephrotic syndrome 🩺🤕
Unlike primary aldosteronism, secondary aldosteronism is not driven by an aldosterone-producing adenoma 🔄
How can primary and secondary aldosteronism be distinguished?
Explain the diagnostic criteria involving renin and aldosterone levels.
To differentiate between primary and secondary aldosteronism, both renin levels and aldosterone levels should be checked 📊🩸
In primary aldosteronism, renin levels are typically low (reference range: <1 ng/mL/h), while in secondary aldosteronism, renin levels are often high (reference range: varies by laboratory) 📉📈
How can diabetes insipidus be diagnosed, and what key factors are involved?
Diabetes insipidus is diagnosed by assessing plasma and urine osmolality 🩸🧪
It results from a deficiency of antidiuretic hormone (ADH), leading to increased sodium levels but normal potassium levels 🧠📈📉
Diabetes insipidus is characterized by excessive thirst (polydipsia) and excessive urination (polyuria) with very dilute urine 🚰🚽
Reference values:
Normal plasma osmolality: Approximately 275-295 mOsm/kg
Normal urine osmolality (concentrated urine): >800 mOsm/kg
There are different forms of diabetes insipidus, including central (neurogenic) and nephrogenic, each with distinct causes and mechanisms 🧬🧪
Provide the reference values for total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides
Lipid Profile Reference Values:
Total Cholesterol:
mmol/L:
Desirable: <5.2 mmol/L
Borderline high: 5.2-6.1 mmol/L
High: ≥6.2 mmol/L
mg/dL:
Desirable: <200 mg/dL
Borderline high: 200-239 mg/dL
High: ≥240 mg/dL
LDL Cholesterol:
mmol/L:
Optimal: <2.6 mmol/L
Near optimal: 2.6-3.3 mmol/L
Borderline high: 3.4-4.1 mmol/L
High: 4.2-4.9 mmol/L
Very high: ≥5.0 mmol/L
mg/dL:
Optimal: <100 mg/dL
Near optimal: 100-129 mg/dL
Borderline high: 130-159 mg/dL
High: 160-189 mg/dL
Very high: ≥190 mg/dL
HDL Cholesterol:
mmol/L:
Low: <1.0 mmol/L
High (desirable): ≥1.6 mmol/L
mg/dL:
Low: <40 mg/dL (for men), <50 mg/dL (for women)
High (desirable): ≥60 mg/dL
Triglycerides:
mmol/L:
Normal: <1.7 mmol/L
Borderline high: 1.7-2.2 mmol/L
High: 2.3-5.6 mmol/L
Very high: ≥5.7 mmol/L
mg/dL:
Normal: <150 mg/dL
Borderline high: 150-199 mg/dL
High: 200-499 mg/dL
Very high: ≥500 mg/dL
Provide the reference values for glucose profile tests
Glucose Profile Reference Values:
Fasting Glucose:
mmol/L:
Normal: <5.6 mmol/L
Prediabetes (impaired fasting glucose): 5.6-6.9 mmol/L
Diabetes: ≥7.0 mmol/L
mg/dL:
Normal: <100 mg/dL
Prediabetes (impaired fasting glucose): 100-125 mg/dL
Diabetes: ≥126 mg/dL
HbA1c:
mmol/mol:
Normal: <39 mmol/mol
Prediabetes: 39-47 mmol/mol
Diabetes: ≥48 mmol/mol
%:
Normal: <5.7%
Prediabetes: 5.7-6.4%
Diabetes: ≥6.5%
These reference values are important for assessing lipid profiles and glucose control in individuals and may vary slightly depending on the laboratory and region.
What are the primary drug options for managing hyperlipidemia in diabetes?
Statins are the drug of choice in treating hyperlipidemia in diabetes 🩸💊
They decrease the risk of coronary events and effectively lower LDL cholesterol levels 📉❤️
Statins may have less effect on triglyceride levels, but the reduction can often bring patients closer to their lipid goals 📊🚫
Niacin can lower triglycerides, raise HDL cholesterol, and lower LDL cholesterol, but it may increase insulin resistance 🔄📈📉
Niacin is sometimes used in combination with statins or alone in patients with statin side-effects 🛠️👥
Fibric acid derivatives primarily lower triglycerides and raise HDL cholesterol, with minimal effects on LDL cholesterol 📊❤️📉
Please let me know if you would like to create more flashcards or if you have any other specific topics or details you’d like to include in the card series.
Explain Metformin’s class, mechanism of action, side effects, and considerations for use.
Metformin, belonging to the biguanide class, is the first-choice glucose-lowering medication for most patients with type 2 diabetes 🩸💊
It increases insulin sensitivity in peripheral tissues, predominantly muscle, and reduces hepatic glucose output 🫁🔽
Metformin is effective only in the presence of insulin and primarily decreases hepatic glucose output 🍽️📤
It increases insulin-mediated glucose utilization in peripheral tissues and has an antilipolytic effect, lowering serum free fatty acid concentrations 🍖🍬
Metformin also increases intestinal glucose utilization via non-oxidative metabolism 🍽️🫀
It does not cause hypoglycemia but may lead to lactic acidosis due to the accumulation of lactate 🩸🧪
Lactic acidosis may occur because Metformin inhibits gluconeogenesis by blocking pyruvate carboxylase, the first step of gluconeogenesis 🧪🔒
Common side effects include gastrointestinal symptoms like metallic taste, anorexia, nausea, abdominal discomfort, and soft bowel movements or diarrhea 🤢💩
These side effects are usually mild, transient, and reversible with dose reduction or discontinuation 🔄❌
Metformin is not metabolized and is entirely cleared by renal excretion, requiring dose adjustment in patients with stable renal impairment 🚽📉
What is Papillary Carcinoma of the Thyroid, and what are its distinguishing features?
Papillary Carcinoma of the Thyroid is a type of thyroid cancer characterized by papillary structures within follicles with epithelial cells having nuclei with cleared centers, often referred to as “orphan Annie eyes” 👁️🔍
This type of thyroid cancer accounts for 60% to 70% of all thyroid cancers and tends to be more frequent in younger patients but can be more aggressive in the elderly 👴👵
It typically presents as a single dominant nodule in the thyroid gland, and this nodule is “cold” on thyroid scan, meaning it does not take up radioactive iodine 📡🚫
Papillary Carcinoma of the Thyroid has a relatively better prognosis compared to other types of thyroid cancers, especially in smaller lesions that can be treated with thyroid lobectomy alone 📈✅
Larger or more diffusely spreading lesions may require complete thyroidectomy, sometimes followed by the ablation of any residual thyroid tissue using large doses of Iodine 131 (radioactive iodine) 🩺🔬
Distinguishing from other thyroid conditions:
Follicular Carcinoma of the Thyroid lacks the papillary structures and orphan Annie nuclei seen in papillary carcinoma and can be challenging to differentiate from normal thyroid tissue 🤔
Graves Disease is characterized by hyperthyroid symptoms and a symmetric, diffusely enlarged goiter, not a single dominant nodule 🌀😓
Hashimoto Disease results in a diffuse goiter with an intense lymphocytic infiltrate and follicle destruction on biopsy, often leading to hypothyroidism symptoms 🛡️😥
Nontoxic Goiter may present with a smooth or multinodular goiter but typically lacks a single dominant nodule and has a wide range of follicle sizes on biopsy, with patients usually being clinically euthyroid 🦋🩸
If you’d like to create more flashcards or have specific topics or details to include in the card series, please let me know.
User
i need it to be a little more concise (WITHOUT LOOSING CONTENT) or be split in two
ChatGPT
Certainly, I can make it more concise while retaining the key content. Here’s a more concise version:
Papillary Carcinoma of the Thyroid
Papillary Carcinoma of the Thyroid is the most common type of thyroid cancer.
It is characterized by papillary structures within follicles with unique “orphan Annie eyes” nuclei.
Accounts for 60-70% of thyroid cancers.
Common in younger patients but can be more aggressive in the elderly.
Typically presents as a single dominant “cold” nodule on thyroid scan.
Better prognosis, especially in smaller lesions treated with thyroid lobectomy.
Larger lesions may require complete thyroidectomy and radioactive iodine ablation.
Distinguishing from other thyroid conditions:
Follicular Carcinoma lacks papillary structures and is challenging to differentiate from normal thyroid tissue.
Graves Disease shows hyperthyroid symptoms and a diffusely enlarged goiter.
Hashimoto Disease results in a goiter with lymphocytic infiltrate and hypothyroidism.
Nontoxic Goiter is typically euthyroid without a single dominant nodule.
If you’d like to split it into two flashcards or have any specific adjustments, please let me know
What laboratory tests are involved in evaluating hypertension?
Hypertension is defined as a sustained blood pressure ≥130 mm Hg systolic or ≥80 mm Hg diastolic.
Initial evaluation should identify complications (e.g., chronic kidney disease) and comorbid conditions (e.g., hyperlipidemia).
Laboratory tests include:
Renal function tests (serum electrolytes, creatinine, urinalysis).
Endocrine tests (fasting glucose or hemoglobin A1c, lipid profile, TSH).
What other tests and considerations are important in the evaluation of hypertension?
Tests for hypertension also include:
Cardiac tests (ECG, optional echocardiography).
Other tests (complete blood count, optional uric acid).
Screening for diabetes with fasting blood glucose or hemoglobin A1c is advised for patients age >40 years every 3 years.
Consider screening at younger ages (18 years above) for those with additional risk factors.
ECG may be recommended to identify signs of left ventricular hypertrophy.
Further assessment with echocardiography is specific but may have low yield in young patients with mild hypertension and normal ECG.
Testing for sleep apnea is indicated for symptomatic patients and may be considered for those with refractory hypertension.
What is Osteosarcoma, and what are its key features?
Osteosarcoma 🦴 is the most common primary bone tumor in children and young adults.
It primarily affects boys aged 13 to 16. 👦👦
Commonly occurs at the metaphyses of long bones (e.g., distal femur, proximal tibia, proximal humerus). 🦴🔍
Constitutional symptoms like fever, weight loss, and malaise are usually absent. 🚫🤒📉
On physical examination, a tender soft-tissue mass is a significant finding. 🩺💡
Characteristic X-ray findings include a spiculated “sunburst” pattern and periosteal elevation known as the Codman triangle. 🌞🔍
Elevated alkaline phosphatase and lactate dehydrogenase levels result from turnover of damaged osteocytes; high levels may correlate with an adverse prognosis. 📈🩸
Increased erythrocyte sedimentation rate (ESR) serves as a nonspecific marker of inflammation. 📈🩺
Differential diagnosis: Distinguish from Ewing sarcoma, which is the second most common primary bone malignancy. Ewing sarcoma may have systemic symptoms and shows an “onion skin” appearance on X-ray. 🧅🔍
Osteoid Osteoma 🦴 appears as a sclerotic, cortical lesion on imaging with a central nidus of lucency.
It typically causes pain that worsens at night and is unrelated to activity. 🌙🩺
Pain is quickly relieved by nonsteroidal anti-inflammatory medications. 💊📉
What is the diagnosis, treatment, and management of Primary Adrenal Insufficiency (PAI), and how does it manifest?
Primary Adrenal Insufficiency (PAI), also known as Addison’s disease, results from autoimmune destruction of the bilateral adrenal cortex.
PAI presents with the following clinical features:
Mineralocorticoid deficiency leads to renal salt wasting, hypotension, weight loss, hyponatremia, hyperkalemia, and dietary salt craving. 🌊🧂
Glucocorticoid deficiency causes fatigue, anorexia, and various psychiatric manifestations (e.g., irritability, depressed mood), contributing to hypotension. 😴🍽️🧠
Androgen deficiency results in loss of libido and suppression of secondary sexual characteristics, typically seen in women due to continued androgen production in men. 🚻🔻
In patients with suspected AI, salt craving and hyperpigmentation are specific to PAI and help differentiate it from secondary AI. 🧂🌞
The diagnosis of PAI is confirmed through stimulation testing with cosyntropin, a synthetic form of ACTH. Low cortisol production following cosyntropin administration is diagnostic of PAI. 🩺🔬
Please review this card, and if it aligns with your expectations, we can continue creating more cards or make adjustments as needed.
What are the clinical features and diagnostic tests for Cushing’s syndrome in women?
Clinical Features of Cushing’s Syndrome in Women:
Anxiety 😰
Tremulousness 🤯
Weight gain 🏋️♀️
Severe fatigue 😴
Menstrual irregularities 🩸
Hypertension 🩺
Hyperglycemia 📈
Thin, easily-bruising skin 🏥
Purplish pink striae may be present on buttocks, thighs, abdomen, and breast 🪡
Proximal muscle weakness 💪
Diagnosis of Cushing’s Syndrome:
Screening: Overnight dexamethasone (1 mg) challenge test is performed.
High-Dose Suppression Test: Patients with unsuppressed cortisol levels undergo a high-dose dexamethasone suppression test.
Definitive Diagnosis: If high-dose dexamethasone fails to suppress serum cortisol levels, a 24-hour urine cortisol level measurement is the most definitive diagnostic test. 🩺🔍
What are the causes and manifestations of hypoglycemia, including its neurogenic and neuroglycopenic symptoms?
Causes of Hypoglycemia:
Excessive insulin secretion in relation to glucose levels, often seen in patients taking exogenous insulin.
Vulnerability to exercise-induced hypoglycemia in insulin-treated patients due to continued insulin release despite falling glucose levels.
Altered skin perfusion during strenuous exertion leading to increased insulin absorption.
Delayed clearance of insulin by the kidneys in patients with chronic kidney disease.
Additional risk factors such as altered nutrition and autonomic dysfunction.
Manifestations of Hypoglycemia:
Neurogenic symptoms: Sweating, tremor, palpitations due to autonomic activation.
Neuroglycopenic symptoms: Confusion, impaired consciousness due to inadequate CNS glucose supply.
Differential Diagnosis:
Patients with diabetes and coronary artery disease may present with atypical anginal symptoms such as fatigue, dyspnea, and nausea, but mental confusion is more consistent with neuroglycopenic effects.
Pheochromocytoma presents with headache, palpitations, diaphoresis, and severe hypertension, but confusion is less typical.
Orthostatic hypotension leads to presyncope or syncope symptoms and is unlikely to cause confusion
What do T-scores indicate in osteoporosis diagnosis, and what is the most appropriate advice for preventing osteoporosis in postmenopausal women without evident bone loss?
T-score of -2.5 or less indicates osteoporosis 🦴
T-scores between -1 to -2.5 suggest osteopenia 🦴
T-score of -1 or above is considered normal bone density 🟩
For prevention, maintain a high-calcium diet with a total daily calcium intake of 1300 mg, with diet being the preferred source of calcium 🍽️💊
Encourage patients with low dietary calcium intake to increase their intake of calcium-rich foods instead of supplements 🥛🧀
Limit the dose from a supplement to 500 to 600 mg of elemental calcium daily, ideally achieved from dietary sources 🚫
Bisphosphonates are used for treatment of established osteoporosis or osteopenia, not for prevention 🚫
Calcium supplementation is used when adequate calcium intake cannot be ensured through diet 🚫
Exercise has additional benefits but is not the primary preventive measure 🏋️♀️
Exposure to sunlight is necessary for vitamin D production, which aids calcium absorption but is not the primary preventive measure ☀️
Maintain a serum 25-hydroxyvitamin D concentration above 50 nanomol/L in patients taking drug therapy for osteoporosis 🌞
How should osteoporosis treatment be monitored, and when should bone mineral density (BMD) measurements be taken?
To monitor osteoporosis treatment, use actual BMD values; T-scores and Z-scores are not appropriate 🦴
Measure BMD at the lumbar spine and hip:
2 years after starting treatment
1 to 2 years after a significant change in treatment 📊
Consider more frequent BMD measurement (but not more often than once a year) in patients with severe osteoporosis or high risk of bone loss, including those taking high-dose glucocorticoid therapy ⏳
If BMD is stable or improving, subsequent measurement is not required for at least 2 years; an interval of up to 5 years may be reasonable 📈
If BMD decreases by more than 5% or 0.05 grams/cm2 at any major site, or if a fracture occurs, consider investigation for new or unrecognised risk factors, and check adherence to therapy. A change of therapy may be appropriate. 🚑
How should osteoporosis be managed and monitored, especially in patients with fracture risk?
Measure bone mineral density (BMD) in patients with significant risk factors for fracture, and in patients 70 years and older.
Calculate absolute fracture risk using online calculators (eg Fracture Risk Assessment Tool [FRAX])
Start osteoporosis drug therapy for patients aged 70 and older with T-scores of –2.5 or less.
Consider treatment for younger patients with declining BMD or high fracture risk; seek specialist advice when needed.
Ensure sufficient calcium and vitamin D intake and advise on fracture prevention.
After a minimal-trauma fracture, assess BMD, and treat if T-score is osteopenic or osteoporotic.
For normal T-scores, investigate other causes of fracture and consider treatment based on fracture site and risk factors.
If BMD measurement isn’t possible, start drug therapy for hip or vertebral fractures, and consider follow-up BMD when available
What are the commonly used drugs for osteoporosis treatment, and what are their advantages and disadvantages?
Alendronate: Oral dosing 🩸, Low cost 💰, Can cause or exacerbate upper gastrointestinal tract irritation 😫, Absorption reduced by food, antacids, calcium, magnesium, and iron 🚫, Requires more frequent dosing than intravenous options 📅, Not recommended in severe kidney disease 🚑.
Risedronate: Oral dosing 🩸, Low cost 💰, Enteric-coated formulation available (may have a lower incidence of gastrointestinal adverse effects, and absorption less affected by food, antacids, calcium, magnesium, and iron) 🍽️, Can cause or exacerbate upper gastrointestinal tract irritation 😫, Absorption reduced by food, antacids, calcium, magnesium, and iron 🚫, Requires more frequent dosing than intravenous options 📅, Not recommended in severe kidney disease 🚑, Enteric-coated formulation only available as a weekly dose (non–enteric-coated formulation available as a monthly dose) 🗓️.
Zoledronic Acid: Intravenous administration avoids gastrointestinal adverse effects 💉, Yearly dosing can improve adherence 🗓️, Intravenous administration not acceptable to some patients 🚫, Not recommended in severe kidney disease 🚑, Can cause transient influenza-like symptoms 🤒, Can cause uveitis (uncommon) 👁️, Can cause hypocalcaemia (particularly in patients with impaired kidney function, vitamin D deficiency, or a malabsorption disorder) 🚑.
Denosumab: Subcutaneous administration avoids gastrointestinal adverse effects 💉, Dose adjustment not required in kidney disease 🚑, 6-monthly dosing can improve compliance 🗓️, Subcutaneous dosing not acceptable to some patients 🚫, Adherence to 6-monthly dosing regimen is essential to prevent loss of bone mineral density between doses 📅, Therapy must be either indefinite or replaced by a bisphosphonate if stopped 🔄, Withdrawal or interruption of treatment (dose delayed by more than 4 weeks) is associated with an increased risk of multiple spontaneous vertebral fracture 🦴, Can cause hypocalcaemia (particularly in patients with impaired kidney function, vitamin D deficiency, or a malabsorption disorder) 🚑.
What are the suitable regimens for bisphosphonate treatment in osteoporosis, and what precautions should be taken during their administration?
Alendronate: 70 mg orally, once weekly on an empty stomach 💊🍽️, Low cost 💰, Limited by upper gastrointestinal irritation 😫, Absorption affected by food, antacids, calcium, magnesium, and iron 🚫, Frequent dosing required 📅, Caution in severe kidney disease 🚑.
Risedronate: 35 mg orally, once weekly on an empty stomach 💊🍽️, Low cost 💰, Enteric-coated formulation available for reduced gastrointestinal adverse effects 🍽️, Can cause or exacerbate upper gastrointestinal tract irritation 😫, Absorption affected by food, antacids, calcium, magnesium, and iron 🚫, Frequent dosing required 📅, Caution in severe kidney disease 🚑, Monthly dosing option available 🗓️.
Zoledronic Acid: 5 mg intravenous infusion once a year 💉, Avoids gastrointestinal adverse effects 💊🍽️, Improves adherence with yearly dosing 📅, Risk of transient influenza-like symptoms 🤒, Risk of uveitis (uncommon) 👁️, Risk of hypocalcaemia, especially with risk factors 🚑.
Denosumab: 60 mg subcutaneously every 6 months 💉🗓️, Increases BMD and reduces fractures 🦴, Need for patient adherence to 6-month regimen 🔄, Considerations upon therapy cessation leading to rapid bone turnover and loss of BMD 📈🦴, Risk of hypocalcaemia, especially with risk factors 🚑, Requires calcium and vitamin D sufficiency 🍽️🌞, Discussion with patients on the importance of adherence and therapy continuation or replacement 🗣️.
What are the effects of glucocorticoids on bone mineral density (BMD), and how can glucocorticoid-induced osteoporosis be prevented and managed?
Effects of Glucocorticoids on BMD: Reduce bone formation, increase bone resorption, affect osteoblast function, hinder intestinal calcium absorption, cause osteocyte dysfunction, lead to hypercalciuria, and suppress gonadal function 🦴📉.
Fracture Risk with Glucocorticoids: Increased fracture risk regardless of BMD, higher risk compared to non-users with similar BMD 🦴📈.
Factors Affecting Bone Loss: Highest bone loss rate in the initial 3 to 6 months, dose and duration-dependent bone loss, prednis(ol)one dose ≥ 7.5 mg/day or equivalent associated with highest risk, increased risk even with low doses (≥ 2.5 mg/day) 📆.
Prevention and Management: Assess fracture risk, measure BMD, ensure sufficient calcium and vitamin D intake, optimize other fracture risk factors, advise on minimal-trauma fracture prevention 📊🍽️🌞.
Treatment Options: Bisphosphonates (first-line), Denosumab, Teriparatide (strict eligibility criteria), Estrogen therapy (for postmenopausal women) 💊🦴.
Monitoring: Consider BMD measurement every 12 to 24 months initially, with less frequent monitoring if stable and acceptable results 📏🔄.
What is transient osteoporosis of pregnancy, and how does it manifest?
Definition: Rare demineralizing condition, primarily affecting the hip, but can impact other joints. Mechanism unknown 🤰🦴.
Distinguishing Factors: Differentiate from physiological bone mass loss during pregnancy and lactation. Presents in the third trimester with severe atraumatic anterolateral groin pain, anterior thigh radiation, acute or insidious onset 🚼🤕.
Bone Mineral Density: Hip BMD significantly reduced compared to lumbar spine 📏.
Resolution: Self-limiting, typically resolves 2 to 6 months postpartum 🔄.
Management: Requires specialist assessment and management 👩⚕️.
What are common symptoms associated with thyroid dysfunction (hyper AND hypo)?
Decreased Libido
Psychosis
What treatment options are available for osteoporosis in patients with Anorexia nervosa?
Treatment with calcium (1200-1600mg daily) and vitamin D is recommended for all patients with AN. 🥛🌞
Calcium and vitamin D can’t restore bone density but can prevent further bone loss. 🛡️🦴
Alendronate and other bisphosphonates are first-line treatments for postmenopausal women with established osteoporosis but are not routinely recommended for premenopausal women due to teratogenicity and insufficient safety data. ⚠️💊
Estrogen therapy is secondary to weight gain as the most effective treatment. 🩺💪
Weight-bearing exercises have equivocal results and are less effective for athletes. 🏋️♀️❌
Androgens have shown no benefit in AN-related osteoporosis. 🚫🦴
How does hypothyroidism differ from subclinical hypothyroidism in terms of thyroid function tests?
Hypothyroidism is characterized by elevated TSH levels and decreased T3 and T4 levels. 📉🩸
Subclinical hypothyroidism involves elevated TSH beyond the normal limit but normal T3 and T4 values. 📈
What is the difference between subclinical and overt hyperthyroidism, and why is it important to consider symptoms in diagnosis? What are the common causes of subclinical hyperthyroidism?
Laboratory findings consistent with hyperthyroidism include subnormal TSH with elevated serum T4, T3, or both. 🩸🔬
Subclinical hyperthyroidism is characterized by subnormal TSH with normal T3 and T4 levels. 🔬🩸
Symptoms are essential in diagnosis, as patients with subclinical hyperthyroidism may still exhibit hyperthyroid symptoms despite normal T3 and T4 levels. 💡👩⚕️Graves disease is the most common cause of both subclinical and overt hyperthyroidism. 👁️🗨️💼
Toxic nodules can also be a cause but are less common than Graves disease. 📊
How to differentiate primary hyperparathyroidism from malignancy in hypercalcemia cases?
Primary hyperparathyroidism and malignancy are common hypercalcemia causes. ⚕️
Malignancy often results in higher calcium levels and more symptoms than primary hyperparathyroidism. 📈
In atypical presentations, measuring intact PTH can distinguish between them. 🩺
Intact PTH is usually low in malignancy and elevated in primary hyperparathyroidism. 📉📈
Rarely, concomitant conditions like PTH-secreting tumors can complicate diagnosis. ⚠️
What are the key characteristics and diagnostic markers of primary hyperparathyroidism?
Common cause of hypercalcemia with elevated intact PTH levels. 🩺🔬
Symptoms include bone pain, kidney stones, and GI issues. 🦴🤕
Diagnosis: Serum calcium, intact PTH, imaging (e.g., ultrasound). 📈🩺📸
Treatment when indicated: Parathyroidectomy. 🏥🔪
What are the key characteristics and diagnostic markers of hypercalcemia of malignancy?
Often presents with severe hypercalcemia and pronounced symptoms. 🩺🤯
Symptoms: Fatigue, confusion, constipation, muscle weakness. 🚽🤕
Diagnosis: Undetectable/low intact PTH, imaging, tumor markers. 📉🩺📸
Management: Address underlying malignancy, hydration, bisphosphonates. 💧🩺🩹
What is the most important initial step in the management of diabetic-related foot ulcers (DRFU)?
The most important initial step in DRFU management is debridement of the ulcer. 🩹
Debridement allows for a thorough assessment of the wound, wound bed, and actual wound size. It can convert a chronic wound into an acute one with accelerated healing. 🩺📈
What should be done after debridement in the management of Diabetic-Related Foot Ulcers
After debridement, swabs should be taken for bacteriological assessment and culture. 🧫🔬
This should be performed before starting antibiotics. 🚫💊
Empirical antibiotic treatment should be guided by the characteristics of the ulcer. 📊
Antibiotic therapy should be initiated if indicated based on the ulcer’s characteristics. 🦠🩺
What is the recommended empirical antibiotic therapy for mild diabetic foot infection, and when is it used?
For acute, mild diabetic foot infection without recent antibiotic use and low risk of MRSA:
Use dicloxacillin 500 mg orally, 6-hourly. OR
Use flucloxacillin 500 mg orally, 6-hourly. OR
For delayed nonsevere hypersensitivity to penicillins, consider cefalexin 500 mg orally, 6-hourly. OR
For immediate or delayed severe hypersensitivity to penicillins or increased MRSA risk, consider clindamycin 450 mg orally, 8-hourly. OR
Use trimethoprim+sulfamethoxazole 160+800 mg orally, 12-hourly for MRSA risk. 💊
Modify therapy based on culture and susceptibility results. Duration: Typically 1 to 2 weeks. ⏳
What is the recommended empirical antibiotic therapy for moderate diabetic foot infection?
For moderate infection, use initial intravenous therapy. For oral therapy, it is suitable if there’s osteomyelitis without systemic inflammatory response syndrome.
For patients at low MRSA risk, use amoxicillin+clavulanate 1+0.2 g intravenously, 8-hourly (or 6-hourly for bone infection). 🦴💊
For nonsevere hypersensitivity to penicillins, consider cefazolin 2 g intravenously, 8-hourly PLUS metronidazole 500 mg intravenously, 12-hourly. 🩺🦠
For severe hypersensitivity to penicillins or MRSA risk, use trimethoprim+sulfamethoxazole plus metronidazole. Consider ciprofloxacin plus clindamycin or lincomycin for severe cases. 💉
Switch to oral therapy after improvement. Modify therapy based on culture and susceptibility results. Duration varies, seek expert advice for deeper tissue involvement. ⚕️
What is the recommended empirical antibiotic therapy for severe diabetic foot infection?
For severe diabetic foot infection, use piperacillin+tazobactam 4+0.5 g intravenously, 6-hourly. 🌡️
For penicillin hypersensitivity, consider ciprofloxacin 400 mg intravenously, 8-hourly PLUS clindamycin or lincomycin. 💉
Consider vancomycin for severe or life-threatening MRSA risk. Modify therapy based on culture and susceptibility results. 🩺🔬
Switch to oral therapy after improvement. Duration varies; typically 3 weeks for severe cases. Seek expert advice for deeper tissue involvement. ⏳⚕️
Who is eligible for teriparatide treatment for osteoporosis?
Teriparatide is a synthetic parathyroid hormone that primarily stimulates osteoblasts (bone-forming cells) and induces new osteoblast formation. 💉🦴
It is a costly medication, and its effectiveness typically requires at least 18 months of continuous use. ⏳
Teriparatide is reimbursed by the PBS (Pharmaceutical Benefits Scheme) for patients with severe osteoporosis and a very high risk of fractures who meet one of the following criteria:
BMD T-score of ≤ -3.0. OR
2 OR MORE minimal trauma fractures. OR
At least ONE SYMPTOMATIC fracture after at least 12 months of continuous therapy with an anti-resorptive agent in adequate doses. 📊🩺
BMD (Bone Mineral Density) begins to decline approximately 12 months after the cessation of teriparatide therapy. ⏳🦴
Therefore, it is generally recommended to continue therapy with an anti-resorptive agent, typically a bisphosphonate, after teriparatide treatment. 🩺💊
What are the commonly prescribed anti-resorptive agents for osteoporosis? Bisphosphonates available in Australia
Bisphosphonates are the most commonly prescribed anti-resorptive agents for osteoporosis. 🦴💊
In Australia, the following bisphosphonates are available:
Alendronate (10mg/day or 70mg/week, orally). 🟠
Risedronate (5mg/day or 35mg/week, orally). 🟢
Zoledronic acid (administered intravenously). 🔵
Bisphosphonates should be used for at least 12 months before their efficacy in the treatment of osteoporosis is assessed. ⏳🦴
When can hormone therapy be considered for osteoporosis, and what are the options?
Hormone therapy, including estrogen and tibolone, can be considered in postmenopausal women younger than 60 years, especially those with other indications for hormone therapy (e.g., menopausal symptoms). 🌸
SERMs also have a preventive effect on breast cancer, making them suitable for postmenopausal women with a family or personal history of breast cancer who are concerned about vertebral fracture due to osteoporosis. 🩺🌼
While there is excellent evidence (Grade A) that raloxifene reduces the risk of vertebral fractures, there is limited evidence supporting its effect on non-vertebral fractures. Jane, who also has osteoporosis in her femur, may not be the ideal candidate for raloxifene as a first-line oConsider hormone therapy (estrogen, tibolone) for postmenopausal women under 60, especially with other indications like menopausal symptoms. 🌸
Raloxifene (a SERM) is an option for young postmenopausal women with spinal osteoporosis, particularly those at risk of breast cancer. It’s reimbursed by PBS for postmenopausal osteoporosis. 🦴💊
SERMs also reduce breast cancer risk, making them suitable for those with a family or personal history of breast cancer concerned about vertebral fractures due to osteoporosis. 🩺🌼
Raloxifene primarily prevents vertebral fractures (Grade A evidence), with limited data on non-vertebral fractures.
Pheochromocytoma and its symptoms and Dx
Pheochromocytoma is a rare adrenal tumor causing excess catecholamines (epinephrine, norepinephrine) production. 🫁
Symptoms include palpitations, flushing, sweating, headache, tremor, and anxiety due to catecholamine excess. 🌬️😰
Severe hypertension is common, but up to 15% of patients may have normal blood pressure. ⚡🩺
Diagnosis relies on tests like plasma metanephrine (high sensitivity, lower specificity) and 24-hour urinary metanephrines (high sensitivity, high specificity). 🩸🚽
Test selection depends on risk factors, with plasma metanephrines for high-risk patients and 24-hour urinary collection for others. 📝📉
Pheochromocytoma Diferential Diagnosis
Similar symptoms can occur in thyrotoxicosis, hypoglycemia, anxiety/panic attacks, hyperthyroidism, adrenal issues, familial dysautonomia, and brain lesions. 🌡️🧠
Certain tumors like neuroblastomas and related tumors may also mimic pheochromocytomas. 🫀🔍
Diferential dx of hyperparathyroidism according to calcium levels, PTH and calcium excretion
PTH high, Calcium low, Calcium excretion low - Secondary
PTH high, Ca high, Excretion high, Low Phosphate - Terciary
PTH low, Ca high, Exc high - Ectopic bone mtx
PTH normal, High ca, low excretion - Genetic (familial benign Hypocalciuric hypercalcaemia)
Whats Conn syndrome?
Primary aldosteronism
What are the characteristics of primary aldosteronism (Conn’s syndrome)?
🩺 Primary aldosteronism is often caused by an aldosterone-producing adenoma.
🌊 It results in increased sodium and water retention, leading to hypertension.
🉑 It also causes low potassium levels, leading to symptoms like muscle weakness, cramps, paraesthesia, polyuria (excessive urination), and polydipsia (excessive thirst).
What are the common causes of secondary aldosteronism?
💔 Congestive Heart Failure (CHF)
🩸 Cirrhosis (liver disease)
🩺 Renal artery stenosis (narrowing of the renal artery)
📉 Nephrotic syndrome (kidney disorder)
What key factors help differentiate between primary and secondary aldosteronism?
🩸 In primary aldosteronism, renin levels are low.
🩸 In secondary aldosteronism, renin levels are high
How is diabetes insipidus diagnosed, and what are its characteristics?
🩺 To diagnose diabetes insipidus, plasma and urine osmolality are checked.
🌡️ Diabetes insipidus results from deficient antidiuretic hormone (ADH), leading to increased sodium levels but normal potassium levels.
🩸 It is characterized by excessive urination and increased thirst.
How do you choose among different respiratory devices for oxygen therapy?
The choice of respiratory device depends on the desired fraction of inspired oxygen (FiO2) 💨
Standard nasal cannulae provide FiO2 of 0.24 to 0.35 at 1 to 4 liters per minute of oxygen flow 🩸
Venturi masks offer FiO2 ranging from 0.24 to 0.60 ⚙️
Simple face masks deliver FiO2 of 0.35 to 0.60 at 5 to 10 liters per minute of oxygen flow 😷
100% non-rebreather reservoir masks provide FiO2 greater than 0.60 at 15 liters per minute 🌬️
High-flow nasal cannulae provide FiO2 from 0.21 to 0.80 and generate continuous positive airway pressure (CPAP) 🚀
High-flow nasal cannula therapy is used in various clinical situations but should be applied with expertise or consultation with a specialist center, especially in children 🧒👶
What are the indications for acute oxygen therapy?
Oxygen therapy is not generally indicated unless the patient is hypoxaemic ❗️
Indications include SpO2 less than 92% or SpO2 less than 88% in patients at risk of hypercapnia 📈
Oxygen therapy is also recommended in critical conditions like cardiac arrest, shock, and major trauma ⚡
Choose the oxygen delivery system based on desired FiO2 💨
Monitor acute oxygen therapy with pulse oximetry and consider arterial blood gas analysis in patients at risk of hypercapnia 📊
What are the health risks associated with asbestos exposure?
Asbestos exposure is linked to an increased risk of bronchogenic carcinoma, mesothelioma, gastrointestinal cancers, and asbestosis among workers. ☠️
Adequate screening for asbestos-related diseases is currently unavailable. 🚫
Even minimal or accidental asbestos exposure can lead to significant disease, warranting evaluation. ⚠️
