Internal Medicine Flashcards

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✅ How to Calculate Serum Osmolality (Osmolarity):The most commonly used formula for calculating serum osmolality is:Seru...
15/07/2025

✅ How to Calculate Serum Osmolality (Osmolarity):

The most commonly used formula for calculating serum osmolality is:

Serum Osmolality (mOsm/kg) =
(2 × Na⁺) + (Glucose ÷ 18) + (BUN ÷ 2.8)

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📌 Units Used:

Na⁺ in mEq/L

Glucose in mg/dL

BUN in mg/dL

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🔍 Example Calculation:

If:

Na⁺ = 140 mEq/L

Glucose = 90 mg/dL

BUN = 14 mg/dL

Then:

Osmolality = (2 × 140) + (90 ÷ 18) + (14 ÷ 2.8)

Osmolality = 280 + 5 + 5

= 290 mOsm/kg

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✅ Normal Range:

275–295 mOsm/kg

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💡 Notes:

This formula estimates effective osmolality (excluding alcohols, toxins, or mannitol).

If there is a large gap between measured and calculated osmolality (>10 mOsm/kg), suspect:

Toxins like methanol, ethylene glycol, isopropanol

Mannitol, sorbitol, or other osmotically active substances

_____________________________________

The difference between osmolality and osmolarity:

✅ 1. Definition

Osmolality:
➤ Number of osmoles of solute per kilogram of solvent (water)
➤ Units: mOsm/kg H₂O

Osmolarity:
➤ Number of osmoles of solute per liter of solution
➤ Units: mOsm/L

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✅ 2. Key Practical Difference

Osmolality is more accurate in clinical settings because it’s independent of temperature and pressure.

Osmolarity can change with volume shifts due to temperature or solute effects on volume.

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✅ 3. Clinical Use

Serum osmolality is the standard measurement in medicine (used in hyponatremia, DI, SIADH).

Osmolarity is used more in laboratory and IV fluid calculations.

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✅ 4. Analogy

Think of:

Osmolality like measuring per weight (kg) — stable

Osmolarity like measuring per volume (L) — variable

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✅ In Practice

> The difference is minor in dilute solutions like plasma, so they're often used interchangeably — but technically, osmolality is preferred clinically.


🔷 I. DIABETES INSIPIDUS (DI)🚫 Misconception 1:“Patients with DI always have hypernatremia.”✅ Correction:Only if water in...
15/07/2025

🔷 I. DIABETES INSIPIDUS (DI)

🚫 Misconception 1:

“Patients with DI always have hypernatremia.”

✅ Correction:

Only if water intake is inadequate or if access to water is restricted.

Many patients maintain normal sodium by compensatory polydipsia.

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🚫 Misconception 2:

“Desmopressin helps both central and nephrogenic DI equally.”

✅ Correction:

Desmopressin works in Central DI (replaces deficient ADH).

It does not work in Nephrogenic DI, where kidneys are resistant to ADH.

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🚫 Misconception 3:

“Low urine osmolality always means Central DI.”

✅ Correction:

Low urine osmolality occurs in both Central and Nephrogenic DI.

Differentiation requires the desmopressin test.

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🚫 Misconception 4:

“All patients with polyuria have DI.”

✅ Correction:

Polyuria has multiple causes:

Primary polydipsia, uncontrolled DM, diuretics, hypercalcemia, etc.

DI is confirmed by water deprivation + desmopressin testing.

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🚫 Misconception 5:

“Thirst is always present in DI.”

✅ Correction:

Some patients (e.g., elderly, post-surgical, sedated) may have impaired thirst mechanism, leading to dangerous hypernatremia.

🧪 Crystal-Induced Arthritides – Quick Outline---🔹 1. Gout (Monosodium Urate Crystals)Pathophysiology:Due to hyperuricemi...
12/07/2025

🧪 Crystal-Induced Arthritides – Quick Outline
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🔹 1. Gout (Monosodium Urate Crystals)

Pathophysiology:
Due to hyperuricemia leading to monosodium urate crystal deposition in joints.

Typical Presentation:
Acute monoarthritis, classically affecting the first MTP joint (podagra).
Sudden, very painful, red, hot joint.

Crystals:
Negatively birefringent, needle-shaped under polarized light.

Risk Factors:
Male s*x, alcohol, thiazides, CKD, red meat, organ meats, obesity.

Diagnosis:
Synovial fluid analysis (gold standard), serum uric acid often elevated but not diagnostic during attack.

Treatment:
Acute: NSAIDs, colchicine, or corticosteroids.

Prevention:
Allopurinol or febuxostat
(after attack settles).
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🔹 2. Calcium Pyrophosphate Deposition Disease (CPPD / Pseudogout)

Pathophysiology:
CPP crystals deposit in cartilage (chondrocalcinosis) and synovium.

Typical Presentation:
Elderly patients with acute knee pain, mimicking gout or OA flare.

Often polyarticular in chronic cases.

Crystals:
Positively birefringent, rhomboid-shaped under polarized light.

Risk Factors/Associations:
Hemochromatosis, hyperparathyroidism, hypomagnesemia, hypothyroidism, aging. (+ Wilson dis)

Diagnosis:
Synovial fluid analysis, X-ray may show chondrocalcinosis (calcified cartilage).

Treatment:
Acute: NSAIDs, colchicine, intra-articular steroids.

No proven crystal-clearing long-term therapy. (Address ass dis)
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🔹 3. Basic Calcium Phosphate Deposition (Hydroxyapatite) – "Milwaukee Shoulder"

Pathophysiology:
Hydroxyapatite crystals deposit in periarticular structures.

Typical Presentation:
Older women with chronic shoulder pain, often massive rotator cuff tear.

Also affects hips, knees.

Crystals:
Not seen on routine polarized light microscopy (require special staining).

Diagnosis:
Clinically + imaging (X-ray shows periarticular calcification); aspiration rarely diagnostic.

Treatment:
NSAIDs, physical therapy; sometimes joint lavage or surgery.
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🔹 4. Calcium Oxalate Crystal Arthropathy

Pathophysiology:
Seen in chronic renal failure, especially those on long-term dialysis.

Typical Presentation:
Resembles gout or pseudogout, often polyarticular.

Crystals:
Birefringent, bipyramidal, or envelope-shaped.

Diagnosis:
Based on history (renal failure), joint aspiration rarely diagnostic.

Treatment:
Supportive: NSAIDs, low oxalate diet; optimize dialysis.
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🔹 5. Cholesterol Crystal Arthropathy

Pathophysiology:
Seen in chronic joint effusions, often in RA or OA.

Typical Presentation:
Long-standing joint swelling, low-grade pain.

Crystals:
Flat, rectangular, with notched corners; weakly birefringent.

Diagnosis:
Synovial fluid microscopy.

Treatment:
Manage underlying joint disease.
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🧠 Clinical Tip for Exams:

Gout = needle-shaped, negative birefringence.

Pseudogout = rhomboid-shaped, positive birefringence.

If shoulder pain + calcification in elderly woman → think Milwaukee shoulder (BASIC calcium phosphate).

Chondrocalcinosis + metabolic disorder → suspect CPPD.

Dialysis patient + acute arthritis → consider calcium oxalate.

100 questions with answers on DI.1. Q: What is Diabetes Insipidus?A: A disorder characterized by excessive urination and...
10/07/2025

100 questions with answers on DI.

1. Q: What is Diabetes Insipidus?
A: A disorder characterized by excessive urination and thirst due to inability to concentrate urine.

2. Q: What are the two main types of DI?
A: Central (neurogenic) and nephrogenic DI.

3. Q: What causes central DI?
A: Deficiency of antidiuretic hormone (ADH) secretion from the posterior pituitary.

4. Q: What causes nephrogenic DI?
A: Kidneys resistant to ADH action.

5. Q: What is the classic symptom of DI?
A: Polyuria (large volumes of dilute urine) and polydipsia.

6. Q: How much urine output is typical in DI?
A: More than 3 liters per day.

7. Q: What serum sodium level is commonly seen in DI?
A: Often normal or elevated (hypernatremia).

8. Q: What happens to urine osmolality in DI?
A: It is low due to inability to concentrate urine.

9. Q: What is the key diagnostic test for DI?
A: Water deprivation test followed by desmopressin administration.

10. Q: How does urine osmolality change in central DI after desmopressin?
A: It increases significantly (>50%).

11. Q: How does urine osmolality change in nephrogenic DI after desmopressin?
A: It shows little or no increase.

12. Q: Name a common cause of central DI.
A: Head trauma, neurosurgery, tumors, idiopathic.

13. Q: Name a common cause of nephrogenic DI.
A: Lithium toxicity, hypercalcemia, hypokalemia, chronic kidney disease.

14. Q: What is the treatment for central DI?
A: Desmopressin (DDAVP).

15. Q: What is the first step in treating nephrogenic DI?
A: Correct underlying cause, thiazide diuretics, low salt diet.

16. Q: What distinguishes primary polydipsia from DI?
A: In primary polydipsia, urine osmolality increases with water deprivation.

17. Q: What is the pathophysiology of central DI?
A: Lack of ADH secretion.

18. Q: What is the pathophysiology of nephrogenic DI?
A: ADH secretion normal, but renal tubules insensitive.

19. Q: What electrolyte disturbance can be seen in DI?
A: Hypernatremia due to free water loss.

20. Q: Can DI cause dehydration?
A: Yes, if water intake is inadequate.

21. Q: What is the effect of lithium on kidneys?
A: Causes nephrogenic DI by reducing renal response to ADH.

22. Q: What test differentiates between central and nephrogenic DI?
A: Desmopressin challenge test.

23. Q: What does a water deprivation test involve?
A: Withholding fluids under supervision while monitoring weight, urine, and serum.

24. Q: Why is the water deprivation test risky?
A: Can cause severe dehydration and hypernatremia.

25. Q: How do you manage DI during pregnancy?
A: Use desmopressin as it is safe.

26. Q: What role does vasopressin play?
A: It is ADH, regulates water reabsorption in kidneys.

27. Q: How does desmopressin work?
A: It is a synthetic ADH analog that acts on renal V2 receptors.

28. Q: What are symptoms of untreated DI?
A: Severe dehydration, weakness, confusion, hypotension.

29. Q: What imaging can help diagnose central DI causes?
A: MRI of the brain and pituitary.

30. Q: What is the “bright spot” in MRI related to?
A: Normal posterior pituitary bright spot, absent in central DI.

31. Q: What is gestational DI?
A: DI occurring during pregnancy due to increased metabolism of ADH.

32. Q: Can nephrogenic DI be inherited?
A: Yes, congenital nephrogenic DI is X-linked or autosomal.

33. Q: What electrolyte abnormalities cause nephrogenic DI?
A: Hypercalcemia and hypokalemia.

34. Q: How do thiazide diuretics help nephrogenic DI?
A: They reduce urine output by causing mild volume depletion and increased proximal reabsorption.

35. Q: What is the role of NSAIDs in nephrogenic DI?
A: They reduce urine output by inhibiting prostaglandins.

36. Q: What is the usual urine specific gravity in DI?
A: Low (295 mOsm/kg).

100. Q: What is the usual prognosis of DI?
A: Good if diagnosed early and treated appropriately.

Suggest a certain topic/disease that you need it to be simplified on our page.Waiting for your comments and suggestions.
09/07/2025

Suggest a certain topic/disease that you need it to be simplified on our page.
Waiting for your comments and suggestions.

🫀 Atrial Fibrillation Q: What is the most common sustained arrhythmia?A: Atrial fibrillation.Q: What are the hallmark EC...
09/07/2025

🫀 Atrial Fibrillation

Q: What is the most common sustained arrhythmia?
A: Atrial fibrillation.

Q: What are the hallmark ECG findings in AF?
A: Irregularly irregular rhythm, absent P waves, and fibrillatory baseline.

Q: What is the most common cause of AF in the elderly?
A: Hypertension.

Q: Name a common reversible cause of AF.
A: Hyperthyroidism.

Q: What is paroxysmal AF?
A: AF that terminates spontaneously or with intervention within 7 days.

Q: What is persistent AF?
A: AF lasting more than 7 days or requiring intervention to terminate.

Q: What is permanent AF?
A: AF accepted by patient and physician; rhythm control not pursued.

Q: What score assesses stroke risk in AF?
A: CHA₂DS₂-VASc score.

Q: What score assesses bleeding risk in anticoagulated AF patients?
A: HAS-BLED score.

Q: What is the target INR in AF patients on warfarin?
A: 2.0–3.0.

Q: Which anticoagulants are preferred in non-valvular AF?
A: DOACs (e.g., apixaban, rivaroxaban, dabigatran, edoxaban).

Q: What is the first-line treatment for rate control in AF?
A: Beta-blockers or rate-limiting calcium channel blockers.

Q: Which AF patients should undergo rhythm control?
A: Symptomatic, younger patients, or those with first presentation.

Q: Name a drug used for rhythm control in structurally normal hearts.
A: Flecainide.

Q: What antiarrhythmic is safe in structural heart disease?
A: Amiodarone.

Q: When is electrical cardioversion preferred?
A: Hemodynamic instability or failed pharmacologic cardioversion.

Q: How long must AF be present before anticoagulation is required before cardioversion?
A: >48 hours.

Q: How long should anticoagulation continue after cardioversion?
A: At least 4 weeks.

Q: What investigation should be done before cardioversion in AF >48h?
A: TOE (transesophageal echocardiography) to exclude thrombus.

Q: What is the most feared complication of AF?
A: Stroke.

Q: What heart sound is lost in AF?
A: Atrial kick (S4).

Q: What is the pulse deficit in AF?
A: Difference between apical and radial pulse rates.

Q: What is lone AF?
A: AF without structural heart disease or risk factors.

Q: What is the typical ventricular rate in untreated AF?
A: 110–180 bpm.

Q: What does "irregularly irregular" mean on ECG?
A: No pattern in RR intervals — diagnostic of AF.

Q: Which electrolyte imbalances can precipitate AF?
A: Hypokalemia and hypomagnesemia.

Q: What is the risk of stroke per year in AF without anticoagulation (average)?
A: About 5%.

Q: What imaging is used to evaluate structural causes of AF?
A: Transthoracic echocardiography (TTE).

Q: What is the effect of digoxin on AV node conduction?
A: It slows conduction.

Q: What is the role of digoxin in AF management?
A: Rate control, especially in sedentary or heart failure patients.

Q: What is the preferred rate control strategy in patients with heart failure and AF?
A: Beta-blockers (e.g., bisoprolol) and/or digoxin.

Q: Name two rate-limiting calcium channel blockers used in AF.
A: Verapamil and diltiazem.

Q: What is the initial management of hemodynamically unstable AF?
A: Immediate DC cardioversion.

Q: What are the components of CHA₂DS₂-VASc?
A: CHF, HTN, Age ≥75 (2), DM, Stroke/TIA (2), Vascular disease, Age 65–74, S*x (female).

Q: What CHA₂DS₂-VASc score mandates anticoagulation in men?
A: ≥2.

Q: What CHA₂DS₂-VASc score mandates anticoagulation in women?
A: ≥3.

Q: What anticoagulants should be avoided in mechanical heart valves?
A: DOACs.

Q: Which surgical procedure can prevent recurrent AF?
A: Maze procedure.

Q: What is the mechanism of flecainide?
A: Class IC sodium channel blocker.

Q: When is flecainide contraindicated?
A: Structural heart disease or ischemic heart disease.

Q: What’s the “pill-in-the-pocket” approach in AF?
A: Single-dose oral flecainide or propafenone at AF onset in selected patients.

Q: What class of drug is amiodarone?
A: Class III antiarrhythmic (mainly K+ channel blocker, but broad spectrum).

Q: What organ systems require monitoring in patients on amiodarone?
A: Thyroid, lungs, liver, eyes.

Q: What is the long-term complication of amiodarone in the lungs?
A: Pulmonary fibrosis.

Q: What thyroid dysfunction is associated with amiodarone?
A: Both hypothyroidism and thyrotoxicosis.

Q: What are two common symptoms of AF?
A: Palpitations and fatigue.

Q: What’s the main goal of rate control?
A: To prevent tachycardia-induced cardiomyopathy.

Q: What’s the first-line treatment for AF in a hyperthyroid patient?
A: Beta-blocker (propranolol) + treat hyperthyroidism.

Q: When should rhythm control be considered over rate control?
A: Younger patients, paroxysmal AF, or symptomatic patients.

Q: What is the significance of left atrial enlargement in AF?
A: Predicts poor response to rhythm control.

Q: What is the main risk of rapid ventricular response in AF?
A: Tachycardia-induced cardiomyopathy.

Q: Can alcohol trigger AF?
A: Yes — known as "holiday heart syndrome."

Q: What is atrial flutter?
A: A macro-reentrant atrial rhythm with sawtooth flutter waves.

Q: Can atrial flutter progress to AF?
A: Yes.

Q: What is the typical atrial rate in AF?
A: 300–600 bpm.

Q: What is the effect of AV node on ventricular rate in AF?
A: It filters impulses, leading to a slower, irregular ventricular response.

Q: What condition must be ruled out before giving a calcium channel blocker in AF?
A: Pre-excitation (e.g., WPW syndrome).

Q: Why are beta-blockers contraindicated in WPW with AF?
A: They may enhance conduction through accessory pathways, risking VF.

Q: What is the preferred treatment for WPW with AF?
A: Procainamide or DC cardioversion.

Q: What is the role of catheter ablation in AF?
A: Pulmonary vein isolation for rhythm control in symptomatic patients.

Q: When is catheter ablation considered first-line in AF?
A: Symptomatic paroxysmal AF with preserved LV function.

Q: Can obesity contribute to AF?
A: Yes — via increased atrial pressure and inflammation.

Q: What is the most common valvular cause of AF worldwide?
A: Rheumatic mitral stenosis.

Q: What is the main difference between valvular and non-valvular AF in terms of anticoagulation?
A: DOACs are contraindicated in valvular AF (use warfarin instead).

Q: What class of drug is sotalol?
A: Class III antiarrhythmic with beta-blocking properties.

Q: What ECG abnormality must be monitored with sotalol?
A: QT prolongation.

Q: What is silent AF?
A: Asymptomatic AF discovered on ECG or device monitoring.

Q: What is AF burden?
A: The proportion of time a patient is in AF (important for prognosis).

Q: What scoring system helps decide between rate and rhythm control?
A: No universally accepted scoring — decision is individualized.

Q: Is cardioversion more successful in paroxysmal or permanent AF?
A: Paroxysmal AF.

Q: What’s the role of TOE before cardioversion?
A: To exclude left atrial thrombus.

Q: What does a "chaotic" baseline on ECG suggest?
A: Atrial fibrillation.

Q: What drugs can cause AF?
A: Theophylline, adenosine, alcohol, sympathomimetics.

Q: What is the term for AF with no identifiable cause?
A: Idiopathic or lone AF.

Q: What class of antiarrhythmics are propafenone and flecainide?
A: Class IC.

Q: What should always accompany Class IC drugs in AF?
A: AV node blocker (e.g., beta-blocker) to prevent 1:1 atrial flutter.

Q: How is stroke risk different in AF with heart failure?
A: It is higher.

Q: Why is AF common in mitral stenosis?
A: Due to left atrial enlargement.

Q: Is aspirin adequate for stroke prevention in AF?
A: No — anticoagulation is superior.

Q: What is the most appropriate initial test in suspected new-onset AF?
A: 12-lead ECG.

Q: What lab test is essential in all new AF cases?
A: TFTs (thyroid function tests).

Q: What imaging is helpful in evaluating thromboembolic risk in AF?
A: TTE and TOE.

Q: What is the goal resting heart rate in AF (rate control)?
A:

100 Questions & Answers on IHD...Etiology & Risk Factors1. Q: What is the MCC of IHD?A: Atherosclerosis.2. Q: Name a mod...
02/07/2025

100 Questions & Answers on IHD.
..

Etiology & Risk Factors

1. Q: What is the MCC of IHD?
A: Atherosclerosis.

2. Q: Name a modifiable RF for IHD.
A: HTN.

3. Q: Which lipoprotein is most atherogenic?
A: LDL cholesterol.

4. Q: Name one non-modifiable risk factor for IHD.
A: Age.

5. Q: Which diabetes type increases IHD risk more?
A: Type 2 diabetes mellitus.

6. Q: What syndrome combines obesity, insulin resistance, and HTN?
A: Metabolic syndrome.

7. Q: Which gender has higher premenopausal protection from IHD?
A: Females.

8. Q: Which marker indicates inflammation and IHD risk?
A: High-sensitivity CRP.

9. Q: What is the role of lipoprotein(a) in IHD?
A: It increases atherosclerotic risk.

10. Q: How does smoking affect IHD risk?
A: It significantly increases risk.
_____________________________________
Pathophysiology

11. Q: What is myocardial ischemia?
A: Inadequate blood supply to the myocardium.

12. Q: What are the primary coronary arteries?
A: LAD, LCX, and RCA.

13. Q: What is coronary artery dominance?
A: The artery that gives rise to the PDA. (Heart dominance is described by the coronary artery branch giving off the posterior descending artery and supplying the inferior wall, characterized as left, right, or codominant)

14. Q: Which is the most commonly affected artery in MI?
A: Left anterior descending (LAD).

15. Q: What causes stable angina?
A: Fixed atherosclerotic plaque.

16. Q: What is the cause of UA?
A: Ruptured plaque with thrombosis.

17. Q: What is myocardial infarction?
A: Myocardial necrosis due to prolonged ischemia.

18. Q: Which enzyme is most specific for MI?
A: Troponin I/T.

19. Q: What is a supply-demand mismatch in IHD?
A: Ischemia due to increased demand or decreased supply.

20. Q: What is coronary vasospasm?
A: Transient narrowing of coronary arteries.

Clinical Presentation

21. Q: Classic symptom of stable angina?
A: Exertional chest pain.

22. Q: How long does stable angina pain typically last?
A: Less than 20 minutes.

23. Q: How is UA different?
A: Occurs at rest or with minimal exertion.

24. Q: What is typical anginal pain location?
A: Retrosternal, may radiate to left arm or jaw.

25. Q: What is angina equivalent?
A: Dyspnea or fatigue instead of chest pain.

26. Q: What is Levine’s sign?
A: Clenched fist over chest indicating angina.

27. Q: Most common symptom in women with IHD?
A: Fatigue.

28. Q: What ECG finding suggests ischemia?
A: ST depression or T-wave inversion.

29. Q: What ECG change indicates acute MI?
A: ST elevation.

30. Q: What is silent ischemia?
A: Ischemia without symptoms.
_____________________________________
Diagnostics

31. Q: First-line test for suspected stable angina?
A: Exercise stress ECG.

32. Q: What test is used when ECG is non-diagnostic?
A: Stress echo or nuclear imaging.

33. Q: Gold standard for diagnosing coronary artery disease?
A: Coronary angiography.

34. Q: What imaging identifies coronary calcification?
A: Coronary CT calcium score.

35. Q: What does a positive stress test indicate?
A: Ischemia with exertion.

36. Q: What is a normal troponin level?
A:

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