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Questions and Answers
What is the definitive treatment for AVNRT?
What is the definitive treatment for AVNRT?
Which feature is indicative of Slow-Fast AVNRT on an ECG?
Which feature is indicative of Slow-Fast AVNRT on an ECG?
Which of the following is the first-line therapy for the acute termination of AVNRT?
Which of the following is the first-line therapy for the acute termination of AVNRT?
What condition can increase the risk of gastroesophageal reflux disease (GERD)?
What condition can increase the risk of gastroesophageal reflux disease (GERD)?
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What effect does hypocalcemia have on the myocardial contractions?
What effect does hypocalcemia have on the myocardial contractions?
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What triggers transient relaxation of the lower esophageal sphincter in GERD?
What triggers transient relaxation of the lower esophageal sphincter in GERD?
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Which of the following ECG manifestations is associated with hypocalcemia?
Which of the following ECG manifestations is associated with hypocalcemia?
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How does hypernatremia primarily influence depolarization?
How does hypernatremia primarily influence depolarization?
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Which of the following is NOT a complication associated with untreated GERD?
Which of the following is NOT a complication associated with untreated GERD?
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Which ECG feature may be observed in severe cases of hyponatremia?
Which ECG feature may be observed in severe cases of hyponatremia?
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Which of these factors can contribute to the development of GERD?
Which of these factors can contribute to the development of GERD?
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What is the expected effect of hypermagnesemia on cardiac conduction?
What is the expected effect of hypermagnesemia on cardiac conduction?
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What role does delayed gastric emptying play in GERD?
What role does delayed gastric emptying play in GERD?
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What is a potential ECG manifestation of hypomagnesemia?
What is a potential ECG manifestation of hypomagnesemia?
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Which of the following best describes the effect of hyponatremia on overall cell excitability?
Which of the following best describes the effect of hyponatremia on overall cell excitability?
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How does hypernatremia affect the QRS complex?
How does hypernatremia affect the QRS complex?
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What are the components of Charcot's Triad?
What are the components of Charcot's Triad?
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Which treatment is considered emergent for jaundice caused by biliary obstruction?
Which treatment is considered emergent for jaundice caused by biliary obstruction?
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What does MRCP stand for and what is its primary use?
What does MRCP stand for and what is its primary use?
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In the liver lobule structure, what is the role of the sinusoids?
In the liver lobule structure, what is the role of the sinusoids?
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Which of the following best describes the function of hepatocytes?
Which of the following best describes the function of hepatocytes?
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Which of the following statements about the portal triad is true?
Which of the following statements about the portal triad is true?
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What additional symptoms are included in Reynold's Pentad?
What additional symptoms are included in Reynold's Pentad?
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What is the anatomical path of blood from the abdominal aorta to the hepatic vein?
What is the anatomical path of blood from the abdominal aorta to the hepatic vein?
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What ECG manifestation is commonly associated with hypokalemia?
What ECG manifestation is commonly associated with hypokalemia?
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Which type of cells has a longer refractory period due to the presence of a plateau phase?
Which type of cells has a longer refractory period due to the presence of a plateau phase?
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What mechanism is primarily activated due to decreased renal perfusion during lactate accumulation?
What mechanism is primarily activated due to decreased renal perfusion during lactate accumulation?
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What does the absolute refractory period (ARP) indicate?
What does the absolute refractory period (ARP) indicate?
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Which symptom is NOT commonly associated with lactate accumulation and metabolic acidosis?
Which symptom is NOT commonly associated with lactate accumulation and metabolic acidosis?
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During which phases are fast Na⁺ channels inactivated leading to the ARP?
During which phases are fast Na⁺ channels inactivated leading to the ARP?
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How does catecholamine release affect myocardial oxygen demand?
How does catecholamine release affect myocardial oxygen demand?
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What physiological role does the long refractory period serve in the ventricles?
What physiological role does the long refractory period serve in the ventricles?
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What characterizes the effective refractory period (ERP)?
What characterizes the effective refractory period (ERP)?
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What is the primary consequence of elevated left ventricular end-diastolic pressure (LVEDP)?
What is the primary consequence of elevated left ventricular end-diastolic pressure (LVEDP)?
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Which treatment option is typically used to support mechanical circulation?
Which treatment option is typically used to support mechanical circulation?
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What is the primary determinant of the refractory period in nodal cells?
What is the primary determinant of the refractory period in nodal cells?
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What happens to the voltage-gated Na⁺ channels during phases of an action potential?
What happens to the voltage-gated Na⁺ channels during phases of an action potential?
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What effect does high blood osmolarity have on antidiuretic hormone (ADH) release?
What effect does high blood osmolarity have on antidiuretic hormone (ADH) release?
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Which hemodynamic parameter is expected to be LOW in the context of lactate accumulation?
Which hemodynamic parameter is expected to be LOW in the context of lactate accumulation?
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What is a potential sequela of high myocardial oxygen demand coupled with low oxygen delivery?
What is a potential sequela of high myocardial oxygen demand coupled with low oxygen delivery?
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What is the primary function of Kupffer cells in the liver?
What is the primary function of Kupffer cells in the liver?
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Which zone of the liver lobule is most resistant to ischemia?
Which zone of the liver lobule is most resistant to ischemia?
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What is the role of stellate cells in the liver?
What is the role of stellate cells in the liver?
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What metabolic activities are primarily associated with Zone 3 (Centrilobular Zone)?
What metabolic activities are primarily associated with Zone 3 (Centrilobular Zone)?
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Which liver condition is characterized by chronic damage leading to fibrosis?
Which liver condition is characterized by chronic damage leading to fibrosis?
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Which statement regarding the Space of Disse is correct?
Which statement regarding the Space of Disse is correct?
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Which zone of the liver lobule is the least oxygenated and most vulnerable to damage?
Which zone of the liver lobule is the least oxygenated and most vulnerable to damage?
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What is a hallmark of lobular injury in hepatic diseases?
What is a hallmark of lobular injury in hepatic diseases?
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What condition is characterized by the obstruction of bile flow due to gallstones in the common bile duct?
What condition is characterized by the obstruction of bile flow due to gallstones in the common bile duct?
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Which symptom is typically associated with cholangitis due to biliary obstruction?
Which symptom is typically associated with cholangitis due to biliary obstruction?
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What is the primary purpose of performing an MRCP in the diagnosis of gallstone disease?
What is the primary purpose of performing an MRCP in the diagnosis of gallstone disease?
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Which laboratory finding is most indicative of cholestasis due to biliary obstruction?
Which laboratory finding is most indicative of cholestasis due to biliary obstruction?
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What complication can occur if choledocholithiasis is left untreated?
What complication can occur if choledocholithiasis is left untreated?
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What effect does hyperkalemia have on the duration of the action potential?
What effect does hyperkalemia have on the duration of the action potential?
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What is an ECG manifestation associated with hypokalemia?
What is an ECG manifestation associated with hypokalemia?
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How does hypercalcemia primarily affect the refractory period of cardiac myocytes?
How does hypercalcemia primarily affect the refractory period of cardiac myocytes?
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What clinical risk is associated with prolonged QT interval as a result of hypokalemia?
What clinical risk is associated with prolonged QT interval as a result of hypokalemia?
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What happens to the resting membrane potential (RMP) during hyperkalemia?
What happens to the resting membrane potential (RMP) during hyperkalemia?
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What is a significant effect of hypocalcemia on the myocardial contraction process?
What is a significant effect of hypocalcemia on the myocardial contraction process?
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How does the T wave manifest on an ECG during hyperkalemia?
How does the T wave manifest on an ECG during hyperkalemia?
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What effect does calcium-induced calcium release have on myocardial contractility during hypercalcemia?
What effect does calcium-induced calcium release have on myocardial contractility during hypercalcemia?
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What is a consequence of H. pylori infection on the stomach lining?
What is a consequence of H. pylori infection on the stomach lining?
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What is the primary effect of chronic NSAID use on the stomach?
What is the primary effect of chronic NSAID use on the stomach?
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How does smoking affect the gastric mucosa?
How does smoking affect the gastric mucosa?
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What leads to duodenal ulcer formation in the context of H. pylori infection?
What leads to duodenal ulcer formation in the context of H. pylori infection?
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What effect does damage to the acid-producing cells have in the stomach?
What effect does damage to the acid-producing cells have in the stomach?
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What role does urease play in H. pylori infection?
What role does urease play in H. pylori infection?
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Which of the following leads to hypochlorhydria in diffuse gastritis?
Which of the following leads to hypochlorhydria in diffuse gastritis?
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What is a common effect of NSAIDs on the gastric mucosal lining?
What is a common effect of NSAIDs on the gastric mucosal lining?
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Which phase of the myocyte action potential is characterized by rapid depolarization due to sodium influx?
Which phase of the myocyte action potential is characterized by rapid depolarization due to sodium influx?
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During which phase does the calcium-induced calcium release (CIRC) occur?
During which phase does the calcium-induced calcium release (CIRC) occur?
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What is the primary ion flow during Phase 3 of the myocyte action potential?
What is the primary ion flow during Phase 3 of the myocyte action potential?
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What is maintained by the Na⁺/K⁺-ATPase during the resting membrane potential?
What is maintained by the Na⁺/K⁺-ATPase during the resting membrane potential?
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Which phase corresponds with the T wave on the ECG?
Which phase corresponds with the T wave on the ECG?
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What initiates depolarization in cardiac myocytes?
What initiates depolarization in cardiac myocytes?
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Which phase is responsible for maintaining a stable myocardium contraction duration?
Which phase is responsible for maintaining a stable myocardium contraction duration?
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At what membrane potential do voltage-gated Na⁺ channels begin to open?
At what membrane potential do voltage-gated Na⁺ channels begin to open?
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What is the primary function of Phase II reactions in drug metabolism?
What is the primary function of Phase II reactions in drug metabolism?
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Which of the following enzymes is involved in alcohol metabolism?
Which of the following enzymes is involved in alcohol metabolism?
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What is the role of Kupffer cells in the liver?
What is the role of Kupffer cells in the liver?
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What primarily determines coagulation times, specifically the Prothrombin Time (PT)?
What primarily determines coagulation times, specifically the Prothrombin Time (PT)?
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How does the liver contribute to glucose homeostasis?
How does the liver contribute to glucose homeostasis?
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Which process is NOT performed by the liver in the context of detoxification?
Which process is NOT performed by the liver in the context of detoxification?
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Which type of compounds does the liver primarily convert through Phase I reactions?
Which type of compounds does the liver primarily convert through Phase I reactions?
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What are the major polar groups that drugs are conjugated with during Phase II reactions?
What are the major polar groups that drugs are conjugated with during Phase II reactions?
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What condition is indicated by severe hepatocellular damage and may lead to mixed hyperbilirubinemia?
What condition is indicated by severe hepatocellular damage and may lead to mixed hyperbilirubinemia?
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Which symptom is NOT commonly associated with cholelithiasis?
Which symptom is NOT commonly associated with cholelithiasis?
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What is a key differentiating factor between cholecystitis and cholelithiasis?
What is a key differentiating factor between cholecystitis and cholelithiasis?
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Which are risk factors for developing cholelithiasis?
Which are risk factors for developing cholelithiasis?
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Which of the following statements about Dubin-Johnson Syndrome is true?
Which of the following statements about Dubin-Johnson Syndrome is true?
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What is a common complication associated with untreated cholecystitis?
What is a common complication associated with untreated cholecystitis?
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Which symptom is often used to diagnose cholecystitis?
Which symptom is often used to diagnose cholecystitis?
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In what condition does bile stasis occur due to gallstone obstruction?
In what condition does bile stasis occur due to gallstone obstruction?
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Study Notes
Acute MI (Different Coronary Arteries)
- Acute MI usually begins with coronary artery disease (CAD), characterized by atherosclerotic plaque formation in coronary arteries.
- Plaque consists of cholesterol, inflammatory cells, and connective tissue within arterial walls.
- Plaque rupture or erosion triggers a cascade of events:
- Activation of platelets
- Release of Tissue Factor (Factor III)
- Conversion of Factor X to Xa
- Conversion of Factor II to IIa
- Conversion of Factor I to Ia
- Formation of a thrombus (partial or complete obstruction).
- Thrombus leads to myocardial ischemia.
- Reduced or absent blood flow deprives myocardial tissue of oxygen and nutrients.
- Ischemia affects the subendocardial layer, furthest from the blood supply and with the highest oxygen demand, most susceptible to irreversible injury.
- Myocyte necrosis releases intracellular contents (troponin, CK-MB) into the bloodstream.
- Inflammatory response & leukocytes infiltrate the affected areas to remove dead cells and prolong injury.
Stable Angina, Angina Pectoris, Unstable Angina, NSTEMI, STEMI
- Stable angina: Predictable chest pain related to exertion or stress.
- Angina Pectoris: General term for angina, which is chest pain caused by reduced blood flow to the heart muscle.
- Unstable angina: Chest pain that is new, more severe, and occurs at rest or with less exertion than previously tolerated.
- NSTEMI (Non-ST-elevation myocardial infarction): Coronary artery blockage, but the blockage is not complete.
- STEMI (ST-elevation myocardial infarction): Complete coronary artery blockage, leading to irreversible myocardial damage & necrosis.
Cardiac Shock
- Pump failure caused by:
- MI (most common)
- HF
- Myocarditis
- Valve dysfunction
- Reduced cardiac output → hypotension.
- Impaired coronary artery perfusion → worsening ischemia.
- Reduced organ perfusion → tissue hypoperfusion leads to ischemia and anaerobic metabolism
- Metabolic acidosis: lactate buildup.
- Kidney injury, altered mental status (brain), and impaired liver metabolism (jaundice)
- Systemic Hypoperfusion triggers circulatory failure and possible sepsis.
Cardiogenic Shock Compensation Mechanisms
- Sympathetic nervous system activation
- Increased heart rate
- Vasoconstriction
- Increased blood pressure
- Renin-angiotensin-aldosterone system (RAAS) activation
- Maintaining blood pressure by retaining sodium & water.
Pulmonary Edema (Associated with Hypertensive Crisis)
- Elevated LVEDP (Left Ventricular End Diastolic Pressure)
- Increased capillary hydrostatic pressure
- Reduced oncotic pressure
- Impaired lymphatic drainage
Starling Forces
- Movement of fluid between capillaries and surrounding tissues.
- Relationship between capillary hydrostatic pressure (Pc), interstitial hydrostatic pressure (Pi), capillary oncotic pressure (πc), and interstitial oncotic pressure (πi)
- Net filtration pressure (NFP) = (Pc - Pi) - (πc - πi).
- Increased pressure → more fluid, leading to edema.
Cardiogenic Shock Treatment
- Restore hemodynamic stability (fluids, vasopressors)
- Treat underlying cause
- Support (monitoring vital functions & managing complications).
Cardiac Tamponade
- Obstructive shock caused by fluid accumulation in the pericardial sac
- Pericardial effusion compresses the heart → reduced cardiac output (reduced CO).
- Symptoms include dyspnea, hypotension, and muffled heart sounds.
- Echocardiogram → pericardial effusion, diastolic collapse of the right heart chambers
Cardiac Tamponade Treatment
- Pericardiocentesis → remove the accumulated fluid form the pericardial sac
- Consider inotropes and in cases of worsening, mechanical support (if needed)
Relationship between CO, SVR, and BP
- MAP = CO x SVR (mean arterial pressure = cardiac output x systemic vascular resistance)
- Increased CO: raises BP if SVR remains constant.
- Decreased CO: lowers BP if SVR doesn't compensate.
Frank-Starling Law
- Relationship between preload, contractility and stroke volume • Increasing preload (stretching of cardiac fibres) → proportionally increases stroke volume up to an optimum point.
- At high preload, overstretched fibers do not respond effectively → reduced contractility → reduced stroke volume.
Left Ventricular Hypertrophy (LVH), Concentric vs. Eccentric (FORMATIVE)
- Concentric: Increased wall thickness with a relatively smaller chamber size triggered by pressure overload. (e.g. hypertension or aortic stenosis)
- Eccentric: Increased wall size and chamber enlargement with normal or even decreased wall thickness triggered by volume overload as a compensation. (e.g., valvular regurgitation and high-output states).
- Both lead to impaired relaxation and filling
- Clinical presentation depends on the predominant mechanism
Aortic Stenosis
- Narrowing of the aortic valve → increased afterload.
- Reduced stroke volume and cardiac output
- Blood pressure increases due to increased afterload and reduced stroke volume
- EKG findings consistent with these effects
Mitral Stenosis
- Narrowing of the mitral valve → reduced preload.
- Reduced stroke volume and ventricular filling → reduced cardiac output
Cardiac Action Potential
- Phase 0: Rapid depolarization mediated largely by fast sodium channels (voltage-gated sodium channels) resulting in rising action potentials
- Phase 1: Early repolarization, rapid potassium efflux through these voltage-gated channels resulting in early phase of repolarization
- Phase 2 Plateau phase, the slow calcium influx balances potassium efflux, contributing to prolonged contraction required for effective ejection of blood from the heart
- Phase 3: Rapid repolarization, voltage gated potassium channels open further, triggering the efflux of potassium ions
- Phase 4: Resting membrane potential, maintained by sodium-potassium ATPase, responsible for returning the cells to a resting potential after each contraction
Nodal Action Potential
- Phase 4: the slow spontaneous depolarization period, characterized by a slow influx of sodium and calcium ions, which gradually raise the membrane potential towards the threshold potential
- Phase 0: depolarization from the influx of fast sodium and calcium ions, eventually initiating the firing of an action potential
- Phase 1: very brief and small repolarization, triggered by the closure of sodium channels and the opening of the potassium channels, which causes slight drop in membrane potential
- Phase 2: plateau phase, occurs because calcium influx (through L-type calcium channels) balances potassium efflux
- Phase 3: rapid repolarization, which is due to the closing of the calcium channels and a major efflux of potassium.
- Phase 4: resting membrane potential, occurs rapidly from the movement of potassium to the outside of the cell.
Refractory Period (Nodal)
- ARP (absolute refractory period): period before the cell can be excited by a stimulus
- ERP (effective refractory period): period where the cell may respond to a stimulus by depolarizing minimally and not for propagation of the action potential
- RRP (relative refractory period): period following the ARP where the cells respond to stronger than normal stimuli by initiating an action potential.
Prolonged QT Interval (ECG Manifestations)
- Hypercalcemia: Short QT interval, faster repolarization.
- Hypocalcemia: Prolonged QT interval, slower repolarization.
- Hypokalemia: Flattened T waves, prolonged QT interval, slower repolarization.
- Hyperkalemia: Peaked T waves, shortened QT interval, rapid repolarization.
Liver-related Coagulation Deficiencies
- Prolonged PT (prothrombin time) and INR (international normalized ratio)
- Decreased production of clotting factors
- Liver dysfunction → impaired synthesis of coagulation factors → prolonged clot formation (hemorrhage potential)
- Vitamin K deficiency could occur in patients with cholestasis (obstruction of the bile ducts) → impairment in Vitamin K absorption.
- DIC (disseminated intravascular coagulation) - a serious and sometimes life-threatening condition
Liver Function Tests Elevated ALT, AST, ALP (and GGT) & Bilirubin
- ALT (alanine aminotransferase, a measure of hepatocellular injury)
- AST (aspartate aminotransferase, a measure of hepatocellular injury)
- ALP (alkaline phosphatase, indicates cholestatic processes, as commonly found in the bile ducts.)
- GGT (gamma-glutamyl transpeptidase) → enzyme found in the bile ducts so high values suggest cholestasis
- Bilirubin (elevated levels suggest the liver is not excreting it efficiently → jaundice potential)
Portal Hypertension
- Increased resistance to blood flow in the liver → elevated pressure in the portal vein. Common causes are cirrhosis, portal vein thrombosis.
- Complications include ascites, varices (enlarged veins), and hepatic encephalopathy
Varices
- Dilated, and weakened veins. Common sites are esophagus and stomach.
- Due to portal hypertension Risk of bleeding → hematemesis, melena.
- Endoscopy (gold standard for detection and grading)
- Medical management: non-selective Beta blockers; endoscopic variceal ligation (EVL)
Medications that interfere with Liver Function
- Many medications, including NSAIDs (nonsteroidal anti-inflammatory drugs), other medications → can strain the liver if administered too often or in high doses.
Hyperbilirubinemia
- Jaundice: yellowing of skin, sclera & mucous membranes due to elevated bilirubin levels
- Pre-hepatic: RBC lysis → unconjugated bilirubin
- Hepatic: Impaired bilirubin conjugation → Mixed (unconjugated & conjugated) bilirubin
- Post-hepatic: Obstruction of bile ducts → conjugated bilirubin
Cholangitis/Cholecystitis
- Cholangitis: Inflammation of the common bile duct. Often caused by gallstones obstructing the duct, infection in the bile ducts.
- Cholecystitis: Inflammation of the gallbladder, likely from gallstones obstructing the cystic duct.
Nerve Conduction (general)
- Action potentials travel along the sarcolemma and into the T-tubules via myofibrils leading to the release of Ca++ initiating contraction
- Depolarization → opening of voltage-gated channels → Na+ inflow → K+ outflow
Cholinergic Crisis/ Myasthenia Crisis
- Cholinergic crisis due to excessive acetylcholine at the neuromuscular junction, leading to muscle weakness, fasciculations, and excessive sweating.
- Myasthenia Crisis → muscle weakness due to insufficient acetylcholine at the neuromuscular junction → caused by medications/ disease processes impacting acetylcholine receptors at the NMJ.
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Description
Test your knowledge on the treatment of AVNRT and its associated ECG features. This quiz covers conditions like GERD, hypocalcemia, and various electrolyte imbalances affecting cardiac function. Challenge yourself with scenarios and questions based on clinical practices.