Own Learning Flashcards
Own Learning
What are the causes of ALP rise + mnemonic
βALP RISESβ
πΉ A β Adolescence & Aging (Bone growth, Pagetβs disease)
πΉ L β Liver disease (Cholestasis, Hepatitis, PSC, PBC, Liver tumors)
πΉ P β Pregnancy (Placental ALP)
πΉ R β Renal disease (Chronic kidney disease, Renal osteodystrophy)
πΉ I β Infections & Infiltrative diseases (TB, Sarcoidosis, Liver metastases, Bone Mets)
πΉ S β Skeletal disorders (Fractures, Osteomalacia, Hyperparathyroidism)
πΉ E β Endocrine (Hyperthyroidism, Parathyroid disease)
πΉ S β Stasis of bile (Gallstones, Cholestasis, Drug-induced)
What are the causes of troponin rise + mnemonic
βTROPONINSβ
πΉ T β Thrombosis (ACS, MI)
πΉ R β Renal failure (CKD)
πΉ O β Oxygen demand-supply mismatch (Sepsis, Shock, PE)
πΉ P β Pulmonary embolism
πΉ O β Overexertion (Extreme exercise)
πΉ N β Neurogenic causes (Stroke, SAH)
πΉ I β Inflammation (Myocarditis, Pericarditis)
πΉ N β Non-cardiac surgery & Trauma
πΉ S β Stress-induced cardiomyopathy (Takotsubo)
Non-Cardiac Causes
Pulmonary Embolism (PE) β Right heart strain
Sepsis & Septic Shock β Myocardial dysfunction
Chronic Kidney Disease (CKD) β Decreased clearance
Stroke & Subarachnoid Hemorrhage (SAH) β Neurogenic myocardial injury
Extreme Exercise β Endurance athletes
Burns & Critical Illness β Systemic inflammation
Drug Toxicity β Chemotherapy, cocaine, or cardiotoxic agents
Cardiac Causes π«
Acute Coronary Syndrome (ACS) β STEMI, NSTEMI
Myocarditis β Viral, bacterial, autoimmune
Pericarditis β Severe cases can involve myocardium
Heart Failure β Acute or chronic decompensated heart failure
Atrial Fibrillation β With rapid ventricular rate
Cardiac Trauma β Contusion from accidents or post-cardiac surgery
Takotsubo Cardiomyopathy β Stress-induced
What are the causes of d-dimer rise + mnemonic
π‘ βD-DIMERβ helps recall the major causes of D-Dimer elevation:
πΉ D β DVT & PE (Thrombosis)
πΉ D β Disseminated Intravascular Coagulation (DIC)
πΉ I β Infections & Inflammation (Sepsis, COVID-19, Pneumonia, AI conditions-SLE/RA)
πΉ M β Malignancy (Cancers)
πΉ E β Emergency Situations (Trauma, Surgery, Pregnancy complications- Pre-Eclampsia/Eclampsia/Placental Abruption/Normal pregnancy (mild elevation), Aortic Dissection)
πΉ R β Renal & Liver Disease (CKD, Cirrhosis - impaired fibrinolysis product clearence)
What are the causes of bnp rise + mnemonic
BNP and NT-proBNP are biomarkers primarily released by the heart in response to ventricular wall stretch and volume overload. They are most commonly used to assess heart failure, but many other conditions can cause BNP elevation.
Mnemonic for BNP Elevation: βBNP RISESβ
π‘ βBNP RISESβ helps recall the major causes of BNP elevation:
πΉ B β Breathlessness Conditions (COPD, ARDS, Pulmonary Hypertension)
πΉ N β Nephropathy (Renal Failure, CKD, ESRD)
πΉ P β Pulmonary Embolism & Hypertension
πΉ R β Right & Left Heart Failure
πΉ I β Ischemia (MI, ACS, Myocarditis)
πΉ S β Sepsis & Shock
πΉ E β Endocrine & Liver Disease (Cirrhosis, Hyperaldosteronism) (Volume overload due to portal hypertension)
πΉ S β Stiff Heart (Valvular Disease, Pericardial Disease)
Mnemonic for False Low BNP: βFLOPβ
π‘ βFLOPβ helps remember the causes of falsely low BNP:
πΉ F β Fat (Obesity - (Increased clearance, BNP sequestration in fat tissue)
πΉ L β Limited Heart Stretch (Pericardial Constriction (Heart stretch is limited, reducing BNP release)
πΉ O β Overactive Clearance (Neprilysin Inhibitors)
πΉ P β Pulmonary Edema (Acute onset before BNP rises)
What are the causes of HBA1c false rise or decrease + mnemonic
Causes of False High HbA1c (Overestimation) β¬οΈ
Decreased Red Blood Cell (RBC) Turnover
Iron Deficiency Anemia (Older RBCs accumulate more glucose)
Vitamin B12 or Folate Deficiency (Megaloblastic anemia)
Asplenia/Splenectomy (Prolonged RBC lifespan)
Altered Hemoglobin Variants (Some interfere with HbA1c assays)
HbF (Fetal Hemoglobin) Persistence
HbSC, HbE, or Other Hemoglobinopathies
Uremia & CKD
Carbamylated hemoglobin interferes with some HbA1c tests
Causes of False Low HbA1c (Underestimation) β¬οΈ
Increased RBC Turnover (Shorter Lifespan)
Hemolytic Anemia
Acute or Chronic Blood Loss
Splenomegaly (Increased RBC destruction)
Conditions Leading to Increased Erythropoiesis
Recent Blood Transfusion
Erythropoietin (EPO) Therapy
Reticulocytosis (e.g., Post-Hemorrhage Recovery)
Hemoglobin Variants
Certain hemoglobinopathies can artificially lower HbA1c measurements
Mnemonic for False High HbA1c: βSUGARβ π¬
π‘ βSUGARβ helps recall the major causes of falsely high HbA1c:
πΉ S β Splenectomy (Prolonged RBC lifespan)
πΉ U β Uremia (CKD, Carbamylated Hemoglobin)
πΉ G β Genetic Hemoglobin Variants (HbF, HbSC, etc.)
πΉ A β Anemia (Iron, B12, or Folate Deficiency)
πΉ R β RBC Aging (Decreased Turnover)
Mnemonic for False Low HbA1c: βFASTβ πββοΈ
π‘ βFASTβ helps remember causes of falsely low HbA1c:
πΉ F β Frequent RBC Turnover (Hemolysis, Reticulocytosis)
πΉ A β Acute Blood Loss & Anemia (Recent transfusion, EPO therapy)
πΉ S β Splenomegaly (Increased RBC destruction)
πΉ T β Thalassemia & Other Hemoglobinopathies
What are the LBBB ECG Changes?
Left Bundle Branch Block (LBBB) ECG Changes
LBBB occurs when electrical conduction through the left bundle branch is delayed or blocked, causing abnormal depolarization of the left ventricle. This leads to characteristic ECG findings.
Key ECG Features of LBBB
π‘ Mnemonic: βWiLLiaMβ helps recall the LBBB pattern.
1οΈβ£ Wide QRS complex (β₯120 ms)
Due to delayed ventricular depolarization.
2οΈβ£ βWβ in V1, βMβ in V6 (WiLLiaM Pattern)
V1: Deep, broad S wave (resembles a βWβ)
V6: Tall, broad, notched R wave (resembles an βMβ)
3οΈβ£ Absence of Q waves in lateral leads (I, aVL, V5, V6)
Normal left ventricular activation is disrupted.
4οΈβ£ Delayed intrinsicoid deflection (>60ms) in V5-V6
Time from QRS onset to peak R wave is prolonged.
5οΈβ£ Discordant ST-T changes
ST depression & T-wave inversion in lateral leads (I, aVL, V5, V6)
ST elevation in leads with deep S waves (V1-V3)
Mnemonic for LBBB Features: βLBBB WIIDEβ
πΉ L β Lateral Lead Delayed Intrinsicoid Deflection (V5-V6)
πΉ B β Broad QRS β₯120 ms
πΉ B β Bizarre ST-T Changes (Discordance)
πΉ B β Bunny Ear R-wave (Notched R in V6)
πΉ W β WiLLiaM Pattern (W in V1, M in V6)
πΉ I β I (Lead I) & aVL: No Q waves
πΉ D β Deep S-wave in V1-V3
πΉ E β Elevated ST segment in leads with deep S waves
What are the RBBB ECG Changes?
Right Bundle Branch Block (RBBB) ECG Changes
RBBB occurs when electrical conduction through the right bundle branch is delayed or blocked, causing abnormal depolarization of the right ventricle. This leads to characteristic ECG findings.
Key ECG Features of RBBB
π‘ Mnemonic: βMaRRoWβ helps recall the RBBB pattern.
1οΈβ£ Wide QRS complex (β₯120 ms)
Due to delayed right ventricular depolarization.
2οΈβ£ βMβ in V1, βWβ in V6 (MaRRoW Pattern)
V1: rSRβ pattern (M-shaped R wave)
V6: Wide S wave (resembles a βWβ)
3οΈβ£ Slurred S waves in lateral leads (I, aVL, V5, V6)
Late right ventricular depolarization.
4οΈβ£ Normal or slightly deviated axis
Unlike LBBB, which may show left axis deviation.
5οΈβ£ Discordant ST-T changes
ST depression & T-wave inversion in V1-V3 (secondary to delayed conduction).
Mnemonic for RBBB Features: βRBBB WIIIIDEβ
πΉ R β Rabbit Ear R-wave (rSRβ in V1-V2)
πΉ B β Broad QRS β₯120 ms
πΉ B β Bizarre ST-T Changes (Discordance in V1-V3)
πΉ B β Big S-wave in V6 & Lead I
πΉ W β MaRRoW Pattern (M in V1, W in V6)
πΉ I β Incomplete RBBB if QRS <120 ms
πΉ I β Inferolateral Slurred S-wave (V5-V6, I, aVL)
πΉ D β Delayed Right Ventricular Activation
πΉ E β Electrolyte/Ischemia-Related ST Changes
What are the Hypokalemia ECG Changes? + causes
Key ECG Features of Hypokalemia
π‘ Mnemonic: βLITTLE Uβ helps remember key changes.
1οΈβ£ L β Long QT interval (due to prolonged repolarization)
2οΈβ£ I β Increased P-wave amplitude & PR prolongation
3οΈβ£ T β T-wave flattening or inversion
4οΈβ£ T β Tachyarrhythmias (e.g., Ventricular tachycardia, Torsades de Pointes)
5οΈβ£ L β Low ST segment (ST depression)
6οΈβ£ E β Ectopic beats (PACs, PVCs, AF, VT, VF risk)
7οΈβ£ U β U-waves (prominent, best seen in V2-V3)
Mnemonic for Hypokalemia ECG: β6 Lowsβ
π‘ βLOW ST-U-T-P-Qβ reminds you of the key features:
πΉ L β Low Potassium (<3.5 mmol/L)
πΉ O β Outward ST Depression
πΉ W β Weak (Flat) T Waves
πΉ S β Small or Absent T Waves
πΉ T β Tachyarrhythmias (VT, VF, Torsades)
πΉ U β U-waves (Prominent in V2-V3, after T-wave)
πΉ P β Prolonged PR Interval
πΉ Q β QT Prolongation (Can predispose to Torsades de Pointes)
Clinical Significance
β
Mild (3.0-3.5 mmol/L) β T-wave flattening, U-waves.
β
Moderate (2.5-3.0 mmol/L) β ST depression, prolonged PR, PVCs.
β
Severe (<2.5 mmol/L) β Risk of Torsades, VF, sudden cardiac arrest.
π©Ί Common Causes:
Mnemonic for Hypokalemia Causes: βD-I-T-C-H K+β
π‘ βDITCH K+β reminds you of the key causes of low potassium:
πΉ D β Drugs (Diuretics, Insulin, Beta-agonists, Laxatives)
πΉ I β Inadequate Intake (Starvation, Alcoholism)
πΉ T β Too Much Loss (Vomiting, Diarrhea, NG Suction)
πΉ C β Cushingβs & Hyperaldosteronism
πΉ H β Hypothermia & Alkalosis (K+ Shift into Cells)
πΉ K+ β Kidney Losses (RTA, Diuretics, Hyperaldosteronism)
What are the Hyperkalemia ECG Changes? + causes and mneumonic
Mnemonic for Hyperkalemia Causes: βMACHINEβ
π‘ βMACHINEβ helps recall the key causes:
πΉ M β Medications (ACE inhibitors, ARBs, K+-sparing diuretics, NSAIDs, Heparin)
πΉ A β Acidosis (Metabolic & Respiratory β K+ shifts out of cells)
πΉ C β Cell Lysis (Hemolysis, Rhabdomyolysis, Tumor Lysis Syndrome)
πΉ H β Hypoaldosteronism & Addisonβs Disease
πΉ I β Intake (Excessive K+ Supplements, IV K+ administration)
πΉ N β Nephron Failure (Acute & Chronic Kidney Disease)
πΉ E β Excessive Tissue Breakdown (Burns, Trauma, Crush Injury)
π‘ Mnemonic: βPeaked Tβs & Widened QRS = Risk of Arrest!β
π΄ Mild (5.5-6.5 mmol/L):
β Peaked T waves (Tall, narrow, tented) β Best seen in precordial leads (V2-V4)
π΄ Moderate (6.5-7.5 mmol/L):
β Widened QRS complex
β Flattened/Absent P waves
β Prolonged PR interval
π΄ Severe (>7.5 mmol/L):
β Sine-wave pattern (Pre-terminal)
β Ventricular tachycardia, VF, Asystole
Causes of Hyperkalemia
Hyperkalemia results from:
1οΈβ£ Decreased Excretion (Renal Failure, Medications)
2οΈβ£ Cellular Shift (Acidosis, Hemolysis)
3οΈβ£ Increased Intake (Excess Supplements, IV K+)
Mnemonic for Hyperkalemia ECG: βP-Wave Drops, T-Wave Popsβ
πΉ P β P waves disappear
πΉ W β Widened QRS complex
πΉ D β Delayed PR interval
πΉ T β Tall, Peaked T waves
πΉ S β Sine-wave pattern (Pre-terminal ECG)
Name the different blood products and their components
1οΈβ£ Packed Red Blood Cells (PRBCs) π©Έ
β Contains: Red blood cells (RBCs) with minimal plasma.
β Indication: Anemia, hemorrhage, blood loss, low hemoglobin (<7 g/dL)
β Does NOT contain: Platelets or clotting factors.
π‘ Mnemonic: βPacks of O2β
π PRBCs = Oxygen Delivery!
2οΈβ£ Fresh Frozen Plasma (FFP) βοΈ
β Contains: All clotting factors (I-XIII) & plasma proteins.
β Indication: Coagulopathy, Liver disease, DIC, Warfarin reversal, Massive transfusion
β Does NOT contain: Red blood cells or platelets.
π‘ Mnemonic: βFrozen Factors Plasmaβ
π FFP = Coagulation Factors!
3οΈβ£ Platelet Concentrate (PLT) π‘
β Contains: Platelets + small plasma volume.
β Indication: Thrombocytopenia (<10,000), Bleeding with low platelets (<50,000), DIC, Bone marrow failure
β Does NOT contain: RBCs or clotting factors.
π‘ Mnemonic: βPLT = Prevents Leaky Tissuesβ
π Platelets = Stop Bleeding!
4οΈβ£ Cryoprecipitate (Cryo) βοΈ
β Contains: Fibrinogen, Factor VIII, vWF, Factor XIII
β Indication: Low fibrinogen (<100 mg/dL), DIC, Hemophilia A, von Willebrand Disease, Uremic bleeding
β Does NOT contain: RBCs, most clotting factors.
π‘ Mnemonic: βCryo = Fibrinogen Firstβ
π Cryo = Fibrinogen & vWF Boost!
5οΈβ£ Whole Blood π₯
β Contains: RBCs, Plasma, Platelets, Clotting Factors
β Indication: Massive hemorrhage, Trauma, Military use
β Rarely used today due to increased risk of volume overload & reactions.
π‘ Mnemonic: βWhole = All Componentsβ
π Whole Blood = Trauma Use!
Mnemonic for Blood Products: βPlease Find Proper Clottingβ (PRBC, FFP, PLT, Cryo)
β
P β Packed RBCs β Oxygen delivery
β
F β Fresh Frozen Plasma β Clotting factors
β
P β Platelets β Stops bleeding
β
C β Cryoprecipitate β Fibrinogen & vWF