What are the cutoff thresholds for a prolonged corrected QT interval (QTc), and what life-threatening arrhythmia can it precipitate?

QTc is prolonged if > 450 ms in adult males or > 460 ms in adult females (severe when > 500 ms). Prolonged QTc predisposes to early afterdepolarizations that trigger Torsades de Pointes, a polymorphic ventricular tachycardia that can degenerate into ventricular fibrillation.

What is the formula for calculating Mean Arterial Pressure (MAP), and what is the minimum target in shock resuscitation?

MAP = Diastolic BP + 1/3(Systolic BP - Diastolic BP), or (2 * DBP + SBP) / 3. The minimum target in shock resuscitation is >= 65 mmHg to maintain adequate end-organ perfusion.

What are normal arterial blood gas (ABG) reference values for pH, PaCO2, PaO2, and serum bicarbonate (HCO3-)?

pH: 7.35 - 7.45 PaCO2: 35 - 45 mmHg PaO2: 80 - 100 mmHg HCO3-: 22 - 26 mEq/L

What clinical conditions cause a high anion gap metabolic acidosis (HAGMA) according to the MUDPILES mnemonic?

M: Methanol; U: Uremia; D: Diabetic ketoacidosis; P: Propylene glycol / Paraldehyde; I: Infection / Iron / Isoniazid; L: Lactic acidosis; E: Ethylene glycol; S: Salicylates.

How are anemias classified by Mean Corpuscular Volume (MCV), and what are the cutoff values?

Microcytic: MCV 100 fL (vitamin B12 or folate deficiency, liver disease, alcohol, myelodysplasia).

What are the four primary cellular adaptations to stress, and what defines metaplasia?

Hypertrophy (increase in cell size), Hyperplasia (increase in cell number), Atrophy (decrease in cell size/number), and Metaplasia (reversible replacement of one mature adult cell type by another mature cell type better able to endure stress, e.g., Barrett esophagus).

What are the clinical diagnostic criteria for orthostatic (postural) hypotension?

A sustained reduction of systolic blood pressure of >= 20 mmHg or diastolic blood pressure of >= 10 mmHg within 3 minutes of standing from a supine or seated position.

What are the three components of the Glasgow Coma Scale (GCS), their maximum scores, and the threshold indicating coma requiring intubation?

Eye opening (max 4), Verbal response (max 5), and Motor response (max 6), for a total score ranging from 3 to 15. A GCS score of <= 8 indicates severe brain injury/coma and generally warrants definitive airway protection with endotracheal intubation ('GCS <= 8, intubate').

What is the normal duration of the EKG PR interval, and what does its prolongation beyond normal limits indicate?

Normal PR interval is 120 to 200 milliseconds (3 to 5 small boxes). Prolongation > 200 ms indicates first-degree atrioventricular (AV) block, reflecting delayed conduction through the AV node.

What are the release kinetics of cardiac troponins (cTnI and cTnT) following acute myocardial infarction?

Troponins rise within 2 to 4 hours of myocardial necrosis, peak at 24 to 48 hours, and remain elevated for 7 to 14 days, providing both acute diagnostic sensitivity and late detection.

What are the standard guidelines for obtaining diagnostic blood cultures in suspected bacteremia?

Collect at least two independent sets of blood cultures (one aerobic and one anaerobic bottle per set) from separate anatomical venipuncture sites PRIOR to initiating antimicrobial therapy, with sterile skin preparation to minimize contamination.

Which coagulation pathways and anticoagulant therapies are monitored by Prothrombin Time (PT/INR) versus activated Partial Thromboplastin Time (aPTT)?

PT/INR monitors the extrinsic and common pathways (Factors VII, X, V, II, fibrinogen) and monitors Warfarin therapy. aPTT monitors the intrinsic and common pathways (Factors XII, XI, IX, VIII, X, V, II, fibrinogen) and monitors Unfractionated Heparin therapy.

What physiological states cause an elevated Blood Urea Nitrogen to Creatinine (BUN:Cr) ratio greater than 20:1?

Prerenal azotemia (enhanced proximal tubular urea reabsorption secondary to hypovolemia or decreased renal perfusion), upper gastrointestinal bleeding (digestion and absorption of blood proteins), severe catabolic states, and high-dose corticosteroid therapy.

What does a 'left shift' or bandemia on a Complete Blood Count (CBC) signify?

An increased proportion of immature neutrophil forms (bands > 10%), indicating accelerated release of granulocytes from bone marrow reserves in response to acute bacterial infection, severe sepsis, or massive tissue necrosis.

According to Sepsis-3 consensus definitions, how do sepsis and septic shock differ?

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection (SOFA score increase >= 2 points). Septic shock is a subset of sepsis with profound circulatory and metabolic abnormalities requiring vasopressors to maintain MAP >= 65 mmHg and serum lactate > 2 mmol/L despite adequate fluid resuscitation.

How do Erythrocyte Sedimentation Rate (ESR) and C-reactive Protein (CRP) differ as acute phase reactants?

ESR is an indirect measure of acute phase proteins (fibrinogen causes rouleaux formation of RBCs), rising slowly over 24-48 hours and persisting for weeks. CRP is synthesized directly by hepatocytes in response to IL-6, rising rapidly within 6 hours and clearing quickly (half-life ~19 hours) as inflammation resolves.

What is Winters' formula, and how is it used to assess respiratory compensation in metabolic acidosis?

Expected PaCO2 = 1.5 * [HCO3-] + 8 (+/- 2). If measured PaCO2 is higher than expected, a concomitant respiratory acidosis is present. If measured PaCO2 is lower than expected, a concomitant respiratory alkalosis is present.

How do coagulative necrosis and liquefactive necrosis differ in underlying pathophysiology and characteristic organ sites?

Coagulative necrosis preserves cellular outlines with protein denaturation, typical of ischemic infarction in solid organs (heart, kidney, spleen) except the brain. Liquefactive necrosis results from enzymatic digestion by neutrophils or microglia, typical of brain infarcts and bacterial/fungal abscesses.

What is the primary diagnostic utility of the plasma D-dimer assay in suspected venous thromboembolism (VTE)?

D-dimer is a fibrin degradation product with high sensitivity (>95%) and a high negative predictive value. A normal D-dimer (<500 ng/mL) safely rules out deep vein thrombosis or pulmonary embolism in low-to-intermediate risk patients, but elevated levels lack specificity.

How does an AST:ALT ratio > 2:1 differ diagnostically from an ALT > AST pattern in hepatic transaminase elevation?

AST:ALT > 2:1 with transaminases usually AST is characteristic of non-alcoholic fatty liver disease (NAFLD) and acute viral or toxin-induced hepatitis.

What three pathophysiologic factors constitute Virchow's triad of thrombosis?

1. Endothelial injury/dysfunction (e.g., atherosclerosis, vasculitis, sheer stress); 2. Stasis or turbulent blood flow (e.g., immobilization, atrial fibrillation); 3. Hypercoagulability (e.g., Factor V Leiden, malignancy, oral contraceptives, antiphospholipid syndrome).

What physiological stimulus triggers B-type Natriuretic Peptide (BNP) release, and what is its role in acute dyspnea evaluation?

BNP is synthesized and released by ventricular cardiomyocytes in response to increased ventricular wall tension and volume overload. Plasma BNP < 100 pg/mL (or NT-proBNP < 300 pg/mL) has a strong negative predictive value for ruling out acute congestive heart failure in dyspneic patients.

What defines pulse pressure, and what are common clinical causes of widened versus narrowed pulse pressure?

Pulse pressure = Systolic BP - Diastolic BP. Widened pulse pressure (>40-60 mmHg) occurs in aortic regurgitation, septic shock, thyrotoxicosis, and fever. Narrowed pulse pressure (<25 mmHg) occurs in cardiogenic shock, hypovolemia, aortic stenosis, and cardiac tamponade.

What microscopic urinalysis findings distinguish glomerulonephritis from acute pyelonephritis or acute interstitial nephritis?

Glomerulonephritis is characterized by dysmorphic red blood cells (acanthocytes) and red blood cell (RBC) casts. Acute pyelonephritis and acute interstitial nephritis are characterized by white blood cell (WBC) casts.

What are the four systemic inflammatory response syndrome (SIRS) criteria, and how many are required for a positive screen?

At least 2 of the following 4 criteria: 1) Body temperature > 38.0°C (100.4°F) or 90 bpm; 3) Respiratory rate > 20 breaths/min or PaCO2 12,000/mcL, 10% immature bands.

How do the causes of unconjugated (indirect) hyperbilirubinemia differ from conjugated (direct) hyperbilirubinemia?

Unconjugated hyperbilirubinemia results from excess bilirubin production (hemolysis, ineffective erythropoiesis) or impaired hepatic conjugation (Gilbert syndrome, Crigler-Najjar syndrome). Conjugated hyperbilirubinemia results from biliary tract obstruction (choledocholithiasis, cholangiocarcinoma, pancreatic head mass) or hepatocellular dysfunction (cirrhosis, Dubin-Johnson syndrome).

How do hypovolemic, cardiogenic, and septic (distributive) shock differ in CVP/PCWP, cardiac output, and systemic vascular resistance (SVR)?

Hypovolemic shock: decreased PCWP/CVP, decreased Cardiac Output, increased SVR. Cardiogenic shock: elevated PCWP/CVP, decreased Cardiac Output, increased SVR. Septic/Distributive shock: low/normal PCWP/CVP, elevated Cardiac Output (early hyperdynamic), decreased SVR.

How are serum osmolality and urine osmolality used in the differential diagnosis of hyponatremia?

Serum osmolality distinguishes isotonic/pseudohyponatremia (hyperlipidemia/hyperproteinemia), hypertonic (hyperglycemia), and true hypotonic hyponatremia ( 100 mOsm/kg).

What is the Fractional Excretion of Sodium (FeNa), and what values differentiate prerenal azotemia from intrinsic acute tubular necrosis (ATN)?

FeNa = (Urine Na * Serum Cr) / (Serum Na * Urine Cr) * 100. FeNa 2% indicates acute tubular necrosis (damaged tubular epithelium incapable of concentrating urine and conserving sodium).

What is the formula for the serum anion gap, and what is its normal physiological reference range?

Anion Gap = [Na+] - ([Cl-] + [HCO3-]). The normal reference range is approximately 8 to 12 mEq/L (primarily accounted for by negative charges on unmeasured plasma proteins, especially albumin).

How does the alveolar-arterial (A-a) oxygen gradient distinguish different etiologies of hypoxemia?

Normal A-a gradient (<10-15 mmHg) hypoxemia is caused by hypoventilation (CNS depression, neuromuscular disease) or low inspired oxygen tension (high altitude). Elevated A-a gradient hypoxemia is caused by V/Q mismatch (pulmonary embolism, COPD, pneumonia), right-to-left shunt, or diffusion impairment (interstitial fibrosis).

What is the normal EKG QRS duration, and what conditions cause widening >= 120 milliseconds?

Normal QRS duration is = 120 ms indicates ventricular conduction delay, such as bundle branch blocks (LBBB, RBBB), ventricular ectopic pacemakers (ventricular tachycardia, PVCs), hyperkalemia, or Wolff-Parkinson-White pre-excitation.

Endocrinologie — Débutant (A1/A2) 3: Clinical Foundations, Pathophysiology, Vital Signs & Core Diagnostics

[Français] Endocrinologie: Core clinical foundations including vital sign interpretation, shock states, cellular adaptation, systemic inflammation, hematology, metabolic panels, and fundamental diagnostic tests.

Level: basic
Languages: fr → fr
Cards: 32
Markdown: Endocrinologie — Débutant (A1/A2) 3: Clinical Foundations, Pathophysiology, Vital Signs & Core Diagnostics (.md)

Flashcards (32)

#	Front (Term / Question)	Back (Definition / Answer)
1	What are the cutoff thresholds for a prolonged corrected QT interval (QTc), and what life-threatening arrhythmia can it precipitate?	QTc is prolonged if > 450 ms in adult males or > 460 ms in adult females (severe when > 500 ms). Prolonged QTc predisposes to early afterdepolarizations that trigger Torsades de Pointes, a polymorphic ventricular tachycardia that can degenerate into ventricular fibrillation.
2	What is the formula for calculating Mean Arterial Pressure (MAP), and what is the minimum target in shock resuscitation?	MAP = Diastolic BP + 1/3(Systolic BP - Diastolic BP), or (2 * DBP + SBP) / 3. The minimum target in shock resuscitation is >= 65 mmHg to maintain adequate end-organ perfusion.
3	What are normal arterial blood gas (ABG) reference values for pH, PaCO2, PaO2, and serum bicarbonate (HCO3-)?	pH: 7.35 - 7.45 PaCO2: 35 - 45 mmHg PaO2: 80 - 100 mmHg HCO3-: 22 - 26 mEq/L
4	What clinical conditions cause a high anion gap metabolic acidosis (HAGMA) according to the MUDPILES mnemonic?	M: Methanol; U: Uremia; D: Diabetic ketoacidosis; P: Propylene glycol / Paraldehyde; I: Infection / Iron / Isoniazid; L: Lactic acidosis; E: Ethylene glycol; S: Salicylates.
5	How are anemias classified by Mean Corpuscular Volume (MCV), and what are the cutoff values?	Microcytic: MCV < 80 fL (iron deficiency, thalassemia, anemia of chronic disease, lead poisoning, sideroblastic anemia); Normocytic: MCV 80-100 fL (acute blood loss, hemolysis, mixed causes, renal failure); Macrocytic: MCV > 100 fL (vitamin B12 or folate deficiency, liver disease, alcohol, myelodysplasia).
6	What are the four primary cellular adaptations to stress, and what defines metaplasia?	Hypertrophy (increase in cell size), Hyperplasia (increase in cell number), Atrophy (decrease in cell size/number), and Metaplasia (reversible replacement of one mature adult cell type by another mature cell type better able to endure stress, e.g., Barrett esophagus).
7	What are the clinical diagnostic criteria for orthostatic (postural) hypotension?	A sustained reduction of systolic blood pressure of >= 20 mmHg or diastolic blood pressure of >= 10 mmHg within 3 minutes of standing from a supine or seated position.
8	What are the three components of the Glasgow Coma Scale (GCS), their maximum scores, and the threshold indicating coma requiring intubation?	Eye opening (max 4), Verbal response (max 5), and Motor response (max 6), for a total score ranging from 3 to 15. A GCS score of <= 8 indicates severe brain injury/coma and generally warrants definitive airway protection with endotracheal intubation ('GCS <= 8, intubate').
9	What is the normal duration of the EKG PR interval, and what does its prolongation beyond normal limits indicate?	Normal PR interval is 120 to 200 milliseconds (3 to 5 small boxes). Prolongation > 200 ms indicates first-degree atrioventricular (AV) block, reflecting delayed conduction through the AV node.
10	What are the release kinetics of cardiac troponins (cTnI and cTnT) following acute myocardial infarction?	Troponins rise within 2 to 4 hours of myocardial necrosis, peak at 24 to 48 hours, and remain elevated for 7 to 14 days, providing both acute diagnostic sensitivity and late detection.
11	What are the standard guidelines for obtaining diagnostic blood cultures in suspected bacteremia?	Collect at least two independent sets of blood cultures (one aerobic and one anaerobic bottle per set) from separate anatomical venipuncture sites PRIOR to initiating antimicrobial therapy, with sterile skin preparation to minimize contamination.
12	Which coagulation pathways and anticoagulant therapies are monitored by Prothrombin Time (PT/INR) versus activated Partial Thromboplastin Time (aPTT)?	PT/INR monitors the extrinsic and common pathways (Factors VII, X, V, II, fibrinogen) and monitors Warfarin therapy. aPTT monitors the intrinsic and common pathways (Factors XII, XI, IX, VIII, X, V, II, fibrinogen) and monitors Unfractionated Heparin therapy.
13	What physiological states cause an elevated Blood Urea Nitrogen to Creatinine (BUN:Cr) ratio greater than 20:1?	Prerenal azotemia (enhanced proximal tubular urea reabsorption secondary to hypovolemia or decreased renal perfusion), upper gastrointestinal bleeding (digestion and absorption of blood proteins), severe catabolic states, and high-dose corticosteroid therapy.
14	What does a 'left shift' or bandemia on a Complete Blood Count (CBC) signify?	An increased proportion of immature neutrophil forms (bands > 10%), indicating accelerated release of granulocytes from bone marrow reserves in response to acute bacterial infection, severe sepsis, or massive tissue necrosis.
15	According to Sepsis-3 consensus definitions, how do sepsis and septic shock differ?	Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection (SOFA score increase >= 2 points). Septic shock is a subset of sepsis with profound circulatory and metabolic abnormalities requiring vasopressors to maintain MAP >= 65 mmHg and serum lactate > 2 mmol/L despite adequate fluid resuscitation.
16	How do Erythrocyte Sedimentation Rate (ESR) and C-reactive Protein (CRP) differ as acute phase reactants?	ESR is an indirect measure of acute phase proteins (fibrinogen causes rouleaux formation of RBCs), rising slowly over 24-48 hours and persisting for weeks. CRP is synthesized directly by hepatocytes in response to IL-6, rising rapidly within 6 hours and clearing quickly (half-life ~19 hours) as inflammation resolves.
17	What is Winters' formula, and how is it used to assess respiratory compensation in metabolic acidosis?	Expected PaCO2 = 1.5 * [HCO3-] + 8 (+/- 2). If measured PaCO2 is higher than expected, a concomitant respiratory acidosis is present. If measured PaCO2 is lower than expected, a concomitant respiratory alkalosis is present.
18	How do coagulative necrosis and liquefactive necrosis differ in underlying pathophysiology and characteristic organ sites?	Coagulative necrosis preserves cellular outlines with protein denaturation, typical of ischemic infarction in solid organs (heart, kidney, spleen) except the brain. Liquefactive necrosis results from enzymatic digestion by neutrophils or microglia, typical of brain infarcts and bacterial/fungal abscesses.
19	What is the primary diagnostic utility of the plasma D-dimer assay in suspected venous thromboembolism (VTE)?	D-dimer is a fibrin degradation product with high sensitivity (>95%) and a high negative predictive value. A normal D-dimer (<500 ng/mL) safely rules out deep vein thrombosis or pulmonary embolism in low-to-intermediate risk patients, but elevated levels lack specificity.
20	How does an AST:ALT ratio > 2:1 differ diagnostically from an ALT > AST pattern in hepatic transaminase elevation?	AST:ALT > 2:1 with transaminases usually < 500 IU/L is strongly suggestive of alcoholic liver disease (due to pyridoxal-5-phosphate deficiency impairing ALT and alcohol-induced mitochondrial injury). ALT > AST is characteristic of non-alcoholic fatty liver disease (NAFLD) and acute viral or toxin-induced hepatitis.
21	What three pathophysiologic factors constitute Virchow's triad of thrombosis?	1. Endothelial injury/dysfunction (e.g., atherosclerosis, vasculitis, sheer stress); 2. Stasis or turbulent blood flow (e.g., immobilization, atrial fibrillation); 3. Hypercoagulability (e.g., Factor V Leiden, malignancy, oral contraceptives, antiphospholipid syndrome).
22	What physiological stimulus triggers B-type Natriuretic Peptide (BNP) release, and what is its role in acute dyspnea evaluation?	BNP is synthesized and released by ventricular cardiomyocytes in response to increased ventricular wall tension and volume overload. Plasma BNP < 100 pg/mL (or NT-proBNP < 300 pg/mL) has a strong negative predictive value for ruling out acute congestive heart failure in dyspneic patients.
23	What defines pulse pressure, and what are common clinical causes of widened versus narrowed pulse pressure?	Pulse pressure = Systolic BP - Diastolic BP. Widened pulse pressure (>40-60 mmHg) occurs in aortic regurgitation, septic shock, thyrotoxicosis, and fever. Narrowed pulse pressure (<25 mmHg) occurs in cardiogenic shock, hypovolemia, aortic stenosis, and cardiac tamponade.
24	What microscopic urinalysis findings distinguish glomerulonephritis from acute pyelonephritis or acute interstitial nephritis?	Glomerulonephritis is characterized by dysmorphic red blood cells (acanthocytes) and red blood cell (RBC) casts. Acute pyelonephritis and acute interstitial nephritis are characterized by white blood cell (WBC) casts.
25	What are the four systemic inflammatory response syndrome (SIRS) criteria, and how many are required for a positive screen?	At least 2 of the following 4 criteria: 1) Body temperature > 38.0°C (100.4°F) or < 36.0°C (96.8°F); 2) Heart rate > 90 bpm; 3) Respiratory rate > 20 breaths/min or PaCO2 < 32 mmHg; 4) WBC > 12,000/mcL, < 4,000/mcL, or > 10% immature bands.
26	How do the causes of unconjugated (indirect) hyperbilirubinemia differ from conjugated (direct) hyperbilirubinemia?	Unconjugated hyperbilirubinemia results from excess bilirubin production (hemolysis, ineffective erythropoiesis) or impaired hepatic conjugation (Gilbert syndrome, Crigler-Najjar syndrome). Conjugated hyperbilirubinemia results from biliary tract obstruction (choledocholithiasis, cholangiocarcinoma, pancreatic head mass) or hepatocellular dysfunction (cirrhosis, Dubin-Johnson syndrome).
27	How do hypovolemic, cardiogenic, and septic (distributive) shock differ in CVP/PCWP, cardiac output, and systemic vascular resistance (SVR)?	Hypovolemic shock: decreased PCWP/CVP, decreased Cardiac Output, increased SVR. Cardiogenic shock: elevated PCWP/CVP, decreased Cardiac Output, increased SVR. Septic/Distributive shock: low/normal PCWP/CVP, elevated Cardiac Output (early hyperdynamic), decreased SVR.
28	How are serum osmolality and urine osmolality used in the differential diagnosis of hyponatremia?	Serum osmolality distinguishes isotonic/pseudohyponatremia (hyperlipidemia/hyperproteinemia), hypertonic (hyperglycemia), and true hypotonic hyponatremia (<280 mOsm/kg). Urine osmolality in hypotonic hyponatremia distinguishes primary polydipsia (<100 mOsm/kg) from states of impaired water excretion with elevated ADH (>100 mOsm/kg).
29	What is the Fractional Excretion of Sodium (FeNa), and what values differentiate prerenal azotemia from intrinsic acute tubular necrosis (ATN)?	FeNa = (Urine Na * Serum Cr) / (Serum Na * Urine Cr) * 100. FeNa < 1% indicates prerenal azotemia (intact tubular reabsorption preserving sodium). FeNa > 2% indicates acute tubular necrosis (damaged tubular epithelium incapable of concentrating urine and conserving sodium).
30	What is the formula for the serum anion gap, and what is its normal physiological reference range?	Anion Gap = [Na+] - ([Cl-] + [HCO3-]). The normal reference range is approximately 8 to 12 mEq/L (primarily accounted for by negative charges on unmeasured plasma proteins, especially albumin).
31	How does the alveolar-arterial (A-a) oxygen gradient distinguish different etiologies of hypoxemia?	Normal A-a gradient (<10-15 mmHg) hypoxemia is caused by hypoventilation (CNS depression, neuromuscular disease) or low inspired oxygen tension (high altitude). Elevated A-a gradient hypoxemia is caused by V/Q mismatch (pulmonary embolism, COPD, pneumonia), right-to-left shunt, or diffusion impairment (interstitial fibrosis).
32	What is the normal EKG QRS duration, and what conditions cause widening >= 120 milliseconds?	Normal QRS duration is < 120 milliseconds (< 3 small boxes). Widening >= 120 ms indicates ventricular conduction delay, such as bundle branch blocks (LBBB, RBBB), ventricular ectopic pacemakers (ventricular tachycardia, PVCs), hyperkalemia, or Wolff-Parkinson-White pre-excitation.