Cardiology
Lupus-like syndrome = SE of Procainamide (Type IA antiarrhythmic) (It inhibits Na and K channels, prolongs QRS complex and QT interval, prolongs effective refractory period (ERP)).
The most common cause of secondary hypertension are renal artery stenosis and primary hyperaldosteronism.
Beta blockers lower BP in part by reducing renin secretion from the k idneys (beta-1).
Beta blockers decrease AV conduction co nduction and therefore should be used cautiously in pts. with firstdegree heart block.
In addition to their negative inotropic effect, the more cardioselective (non-dihydropyridine) calcium channel blockers (verapamil, diltiazem) can also reduce HR by slowing impulse transmission through the AV node.
ACE inhibitors are first-line therapy for HTN in Diabetics because of t heir nephroprotective actions. SE = cough (due to bradykinin accumulation).
Beta blockers are contraindicated in Diabetics because o f hypoglycemic masking.
Thiazide diuretics can exacerbate glycemic control in diabetics, bec ause it causes hypokalemia and stimulate sympathetic nervous system via intravascular volume volume depletion.
An imbalance between myocardial oxygen supply and demand underlies the pathophysiology of angina.
Nitroglycerin’s primary mechanism of action is dilated peripheral veins, which reduces preload
and therefore myocardial oxygen demand. It also has direct effects on the coronary arteries, so it can be useful for all three forms of angina.
Digitalis (cardiac glycoside) for CHF works by increasing inotropic effect, decreasing chronotropic effect, increasing ejection fraction. I ts side effects include cholinergic effects (e.g. diarrhea, vomiting, increased PR interval), arrhythmias, and blurry yellow vision. Digitalis/digoxin toxicity is treated by stopping the medication and administering potassium, magnesium, and antidigoxin Fab fragments. Lidocaine is given for digoxin-induced arrhythmias.
Heart failure is classified by two general types: systolic (pump) and diastolic (filling) dysfunction, with considerable overlap. The initial adaptive physiologic responses (increased sympathetic activity, fluid retention, and myocardial hypertrophy) become maladaptive when prolonged, leading to progressive deterioration of cardiac function and eventual death.
When thinking about heart failure, categorize the findings accor ding to whether they suggest left-sided versus rt-sided heart failure, preserved versus reduced ejection fraction, and compensated versus decompensated cardiac output.
Aortic stenosis most commonly presents as crescendo-decrescendo systolic murmur heart loudest at the upper right sternal border and radiating to both carotid arteries. A delaye d carotid upstroke and narrowed pulse pressure are associated findings. Decreased cardiac output (in decompensated states) and increased myocardial oxygen demand are important consequences of aortic stenosis. It follows that natural history of t his condition leads to angina, syncope, heart failure, and premature death.
Defects in LDL receptor or o r internalization of LDL receptor cause Familial Hypercholesterolemia.
The metabolic syndrome is charact erized by abdominal obesity, dyslipidemia, insulin resistance, and HTN. It is a marker for increased cardiovascular risk. TX of the metabolic syndrome consists of treating each of its components with lifestyle modifications, and pharmacologic agents to control weight, improved lipid profiles, heighten insulin sensitivity, and lower BP. Cholesterollowering medications include statins (most potent for lowering LDL-C), niacin (most potent for increasing HDL-C), fibrates, and bile-sequestering resins.
In general, there is NO direct parasympathetic innervation of the vasculature. However, vasodilation of arterioles can be caused by exogenous “cholines”. These drugs act on
uninnervated M3-receptors on endothelial cells and stimulate release of nitric oxide. Nitric oxide diffuses to the adjacent smooth muscle, resulting in vasodilation and decreased peripheral resistance.
When blood pressure drops, arterial baroreceptors located w ith carotid sinus (afferent limb mediated by glossopharyngeal nerve) sense decreased vessel stretch and fire less frequently. This response increases efferent sympathetic outflow and inhibits parasympathetic outflow, which helps restore the BP by increasing HR and stimulating peripheral vasoconstriction.
The aortic arch and carotid sinuses also have chemorece ptors. Chemoreceptors work to maintain P02, PCO2, and pH.
HTN, age, smoking, dyslipidemia, family history, and elevated C-reactive protein (CRP) and homocysteinuria are risk factors for coronary artery disease.
Insulin stimulates lipoprotein lipase protein synthesis. If this enzyme is low as in Type 1 diabetes, then TG accumulate in the circulation and can develop atherosclerosis.
Pulmonary:
Histamine (Gq-H1) = bronchoconstriction leading to respiratory symptoms.
The predominant mechanism of respiratory suppression of the barbiturates, benzos, opioids, and general anesthetics is to make the medullary respiratory center less responsive to increase in paCo2.
Asthma: Wheezing, cough (that is worse late at night or early morning), chest tightness, and dyspnea. Symptoms are often triggered or worsened by exercise, cold air, or inhaled noxious particles. A history of prolonged upper respiratory tract infections is also characteristic of asthma. Pathology includes smooth muscle hypertrophy secondary to recurrent bronchoconstriction and mucosal edema (with a relative eosinophilia) secondary to chronic subacute inflammatory process. Curshmann’s spirals and Charcot -Leyden crystals are found in
the mucus of asthmatics.
Diagnosis of Asthma: Disproportionate decrease in the FEV1/FVC ratio in response to Methachoine.
Management of Asthma: Steroids, beta-2 agonists, mast ce ll stabilizers, anticholinergics, leukotriene receptor antagonists, 5 -lipoxygenase inhibitors, and theophylline.
Asthmatics who also suffer from rhinitis and nasal polyps may develop fatal bronchospasm from ingesting aspirin, ibuprofen, and naproxen. Avoid t hem.
Hypersensitivity Pneumonitis: wheezing and dyspnea; often triggered or worsened by variety of antigens (including occupational exposures). Diffuse infiltrates on chest x-ray. Biopsy may show noncaseating granulomas or mononuclear cell infiltrates. Reversible if offending agent removed; otherwise progresses to pulmonary fibrosis.
Allergic bronchopulmonary aspergillosis caused by aspergillus (and could be another fungi) typically occurs in asthmatics and manifests with dyspnea, fever, eosinophilia, and infiltrates on x-ray. TX are corticosteroids.
Progressive dyspnea and other overlapping symptoms are seen in emphysema and chronic bronchitis (because they are both COPD).
Emphysema: Hyperresonance of the chest, decreased breath sounds bilaterally, prolonged expiratory phase, PURSED LIP breathing, FEV1/FVC < 75%, increased anteroposterior diameter (“barrel chest”), and flattening of the diaphragm. Pathology is that the lung parenchyma g ets
destroyed from the pathologic activation of proteases. The destruction of alveolar elastin re sults in permanent abnormal enlargement of the air spaces distal to the terminal bronchiole. This is accompanies by destruction of the alveolar walls, but without obvious fibrosis. TX includes short acting beta2-agonist such as albuterol for acute symptoms, ipratropium, and glucocorticoids for long-term.
Chronic bronchitis: Productive cough, cyanosis, crackles, and wheezing. Productive cough for 3 months in at least 2 consecutive years. FEV1/F VC < 75%. Pts. are often hypoxemic and hypocapnic. Pathology includes hypertrophy of submucosal glands and goblet cells, resulting in mucus hypersecretion. TX is bronchodilators and corticosteroids.
Asbestosis: Exertional dyspnea; with advanced disease, dyspnea at rest, dry cough, chest pain, and recurrent resp. tract infections. Look for history of exposure. Ferruginous bodies (or asbestos bodies) which are fibers of asbestos lined by hemosiderin deposits. These are yellow to brown rod-shaped bodies stain positively with Pr ussian blue.
Methemoglobinemia – is another potential cause of cyanosis. In co nditions such as pyruvate kinase def. or G6PD def. or following exposure to oxidizing agent such as benzocaine, the mechanisms that defend against oxidative stress with the RBCs are overwhelmed, and the ferrous Fe2+ of the heme is oxidized to ferric Fe3+. This converts hemoglobin to methemoglobin, which is unable to bind oxygen.
Tumors at the apex of the lung are known as Pancoast tumors. They are MC seen with squamous cell carcinoma of the lung. Ipsilateral ptosis, miosis, anhydrosis (Horner’s syndrom e).
Note that in Lambert-Eaton syndrome, ptosis is Bilateral.
Another commonly seen complications of lung tumors is superior vena cava syndrome (often associated with small cell carcinoma), in which the superior vena cava is compressed by the growing tumor. This impairs venous drainage of the head and upper limbs, re sulting in swelling and purple discoloration of the arms and face.
Small Cell Cancer of the lung: Dyspnea, rapid unexplained wt loss, SIADH.
Elevated ACE are frequently associated with sarcoidosis. The hypercalcemia that dev elops in sarcoidosis is due to increased production of 1,25-dihydroxyvitamin D3 by the macrophages in granulomas. It is also associated with Bell’s palsy.
Sarcoidosis: lung, skin, anterior uveitis, polyarthritis, bilateral hilar lymphadenopathy, noncaseating granulomas. TX is glucocorticoids.
A pneumothorax can cause a mixed resp and metabolic acidosis because of both impaired ventilation, which increases CO2 levels; and increase anaerobic metabolism which increases plasma levels of acids such as lactic acidosis.
Pneumothorax – sudden onset of severe dyspnea with sharp pain in one’s side. The trachea and mediastinum WILL shift away from the side of t he pneumothorax. Hyperresonance, absence of breath sounds. Commonly associated with asthma, emphysema, Marfan’s, trauma.
Nephrology:
The causes of acute renal failure (ARF) are divided into 3 groups: prerenal, renal (intrinsic), and postrenal (obstructive).
Common causes of postrenal failure include BPH or prostate c ancer, bladder tumors, and urinary retention (due to neurogenic bladder or anticholinergic, opiate, or sympathomimetic).
The diagnosis of obstructive renal failure is made, in part, by detection of hydronephrosis (pelvicalicectasis) on renal ultrasound.
Acute tubular necrosis (ATN) is the MCC of intrinsic renal failure. ATN can be ischemic or toxic. Toxins capable of ATN include cisplatin, aminoglycosides, vancomycin, amphotericin, IV contrast agents, and myoglobin.
Ischemic ATN is distinguished from prerenal azotemia by th e presence of “muddy brown” casts in the urinary sediment and an FENa+ >2%. Prerenal azotemia, in contrast, show bland sediment, by a FENa+ <1%.
NSAIDs-induced decrease GFR
NSAIDs can cause AIN, nephrotic syndrome, and most commonly Hemodynamic renal failure from inhibition of vasodilatory prostaglandins. Pts. with advanced age, renal dysfunction, or CHF are at the highest risk for NSAID-induced acute renal failure (ARF).
MC conditions that cause eosinophilia include helminthic infections, asthma, allergy, druginduced acute interstitial nephritis (AIN), Hodgkin’s lymphoma.
AIN is classically a triad of fever, rash, and peripheral eosinophilia in a setting of ARF after introduction of a new drug. Agents are penicillins, cephalosporins, sulfonamides, NSAIDs, PPIs.
HTN is both major cause and a major complication of chronic renal failure (CRF).
CRF is characterized by normocytic anemia (due to loss of renal erythropoietin production), hyperkalemia, hypocalcemia, hyperphosphatemia, and mixed anion gap/non-anion gap metabolic acidosis.
Uremia is a clinical syndrome in renal failure that shows nausea, pruritis, malaise, seizures, confusion, bleeding pericarditis, and fluid overload.
CRF results in secondary hyperparathyroidism. Increase PTH, in turn, can cause abnormal bone formation (osteitis fibrosa cystica), whereas deficiency of activated vit d can (in adults) lead to osteomalacia. The full spectrum of bony changes resulting from high PTH, low Ca2+, and chronic acidosis is called renal osteodystrophy.
Berry aneurysm is associated with Autosomal dominant adult polycystic disease (ADPKD).
Lupus-like syndrome = SE of Procainamide (Type IA antiarrhythmic) (It inhibits Na and K channels, prolongs QRS complex and QT interval, prolongs effective refractory period (ERP)).
The most common cause of secondary hypertension are renal artery stenosis and primary hyperaldosteronism.
Beta blockers lower BP in part by reducing renin secretion from the k idneys (beta-1).
Beta blockers decrease AV conduction co nduction and therefore should be used cautiously in pts. with firstdegree heart block.
In addition to their negative inotropic effect, the more cardioselective (non-dihydropyridine) calcium channel blockers (verapamil, diltiazem) can also reduce HR by slowing impulse transmission through the AV node.
ACE inhibitors are first-line therapy for HTN in Diabetics because of t heir nephroprotective actions. SE = cough (due to bradykinin accumulation).
Beta blockers are contraindicated in Diabetics because o f hypoglycemic masking.
Thiazide diuretics can exacerbate glycemic control in diabetics, bec ause it causes hypokalemia and stimulate sympathetic nervous system via intravascular volume volume depletion.
An imbalance between myocardial oxygen supply and demand underlies the pathophysiology of angina.
Nitroglycerin’s primary mechanism of action is dilated peripheral veins, which reduces preload
and therefore myocardial oxygen demand. It also has direct effects on the coronary arteries, so it can be useful for all three forms of angina.
Digitalis (cardiac glycoside) for CHF works by increasing inotropic effect, decreasing chronotropic effect, increasing ejection fraction. I ts side effects include cholinergic effects (e.g. diarrhea, vomiting, increased PR interval), arrhythmias, and blurry yellow vision. Digitalis/digoxin toxicity is treated by stopping the medication and administering potassium, magnesium, and antidigoxin Fab fragments. Lidocaine is given for digoxin-induced arrhythmias.
Heart failure is classified by two general types: systolic (pump) and diastolic (filling) dysfunction, with considerable overlap. The initial adaptive physiologic responses (increased sympathetic activity, fluid retention, and myocardial hypertrophy) become maladaptive when prolonged, leading to progressive deterioration of cardiac function and eventual death.
When thinking about heart failure, categorize the findings accor ding to whether they suggest left-sided versus rt-sided heart failure, preserved versus reduced ejection fraction, and compensated versus decompensated cardiac output.
Aortic stenosis most commonly presents as crescendo-decrescendo systolic murmur heart loudest at the upper right sternal border and radiating to both carotid arteries. A delaye d carotid upstroke and narrowed pulse pressure are associated findings. Decreased cardiac output (in decompensated states) and increased myocardial oxygen demand are important consequences of aortic stenosis. It follows that natural history of t his condition leads to angina, syncope, heart failure, and premature death.
Defects in LDL receptor or o r internalization of LDL receptor cause Familial Hypercholesterolemia.
The metabolic syndrome is charact erized by abdominal obesity, dyslipidemia, insulin resistance, and HTN. It is a marker for increased cardiovascular risk. TX of the metabolic syndrome consists of treating each of its components with lifestyle modifications, and pharmacologic agents to control weight, improved lipid profiles, heighten insulin sensitivity, and lower BP. Cholesterollowering medications include statins (most potent for lowering LDL-C), niacin (most potent for increasing HDL-C), fibrates, and bile-sequestering resins.
In general, there is NO direct parasympathetic innervation of the vasculature. However, vasodilation of arterioles can be caused by exogenous “cholines”. These drugs act on
uninnervated M3-receptors on endothelial cells and stimulate release of nitric oxide. Nitric oxide diffuses to the adjacent smooth muscle, resulting in vasodilation and decreased peripheral resistance.
When blood pressure drops, arterial baroreceptors located w ith carotid sinus (afferent limb mediated by glossopharyngeal nerve) sense decreased vessel stretch and fire less frequently. This response increases efferent sympathetic outflow and inhibits parasympathetic outflow, which helps restore the BP by increasing HR and stimulating peripheral vasoconstriction.
The aortic arch and carotid sinuses also have chemorece ptors. Chemoreceptors work to maintain P02, PCO2, and pH.
HTN, age, smoking, dyslipidemia, family history, and elevated C-reactive protein (CRP) and homocysteinuria are risk factors for coronary artery disease.
Insulin stimulates lipoprotein lipase protein synthesis. If this enzyme is low as in Type 1 diabetes, then TG accumulate in the circulation and can develop atherosclerosis.
Pulmonary:
Histamine (Gq-H1) = bronchoconstriction leading to respiratory symptoms.
The predominant mechanism of respiratory suppression of the barbiturates, benzos, opioids, and general anesthetics is to make the medullary respiratory center less responsive to increase in paCo2.
Asthma: Wheezing, cough (that is worse late at night or early morning), chest tightness, and dyspnea. Symptoms are often triggered or worsened by exercise, cold air, or inhaled noxious particles. A history of prolonged upper respiratory tract infections is also characteristic of asthma. Pathology includes smooth muscle hypertrophy secondary to recurrent bronchoconstriction and mucosal edema (with a relative eosinophilia) secondary to chronic subacute inflammatory process. Curshmann’s spirals and Charcot -Leyden crystals are found in
the mucus of asthmatics.
Diagnosis of Asthma: Disproportionate decrease in the FEV1/FVC ratio in response to Methachoine.
Management of Asthma: Steroids, beta-2 agonists, mast ce ll stabilizers, anticholinergics, leukotriene receptor antagonists, 5 -lipoxygenase inhibitors, and theophylline.
Asthmatics who also suffer from rhinitis and nasal polyps may develop fatal bronchospasm from ingesting aspirin, ibuprofen, and naproxen. Avoid t hem.
Hypersensitivity Pneumonitis: wheezing and dyspnea; often triggered or worsened by variety of antigens (including occupational exposures). Diffuse infiltrates on chest x-ray. Biopsy may show noncaseating granulomas or mononuclear cell infiltrates. Reversible if offending agent removed; otherwise progresses to pulmonary fibrosis.
Allergic bronchopulmonary aspergillosis caused by aspergillus (and could be another fungi) typically occurs in asthmatics and manifests with dyspnea, fever, eosinophilia, and infiltrates on x-ray. TX are corticosteroids.
Progressive dyspnea and other overlapping symptoms are seen in emphysema and chronic bronchitis (because they are both COPD).
Emphysema: Hyperresonance of the chest, decreased breath sounds bilaterally, prolonged expiratory phase, PURSED LIP breathing, FEV1/FVC < 75%, increased anteroposterior diameter (“barrel chest”), and flattening of the diaphragm. Pathology is that the lung parenchyma g ets
destroyed from the pathologic activation of proteases. The destruction of alveolar elastin re sults in permanent abnormal enlargement of the air spaces distal to the terminal bronchiole. This is accompanies by destruction of the alveolar walls, but without obvious fibrosis. TX includes short acting beta2-agonist such as albuterol for acute symptoms, ipratropium, and glucocorticoids for long-term.
Chronic bronchitis: Productive cough, cyanosis, crackles, and wheezing. Productive cough for 3 months in at least 2 consecutive years. FEV1/F VC < 75%. Pts. are often hypoxemic and hypocapnic. Pathology includes hypertrophy of submucosal glands and goblet cells, resulting in mucus hypersecretion. TX is bronchodilators and corticosteroids.
Asbestosis: Exertional dyspnea; with advanced disease, dyspnea at rest, dry cough, chest pain, and recurrent resp. tract infections. Look for history of exposure. Ferruginous bodies (or asbestos bodies) which are fibers of asbestos lined by hemosiderin deposits. These are yellow to brown rod-shaped bodies stain positively with Pr ussian blue.
Methemoglobinemia – is another potential cause of cyanosis. In co nditions such as pyruvate kinase def. or G6PD def. or following exposure to oxidizing agent such as benzocaine, the mechanisms that defend against oxidative stress with the RBCs are overwhelmed, and the ferrous Fe2+ of the heme is oxidized to ferric Fe3+. This converts hemoglobin to methemoglobin, which is unable to bind oxygen.
Tumors at the apex of the lung are known as Pancoast tumors. They are MC seen with squamous cell carcinoma of the lung. Ipsilateral ptosis, miosis, anhydrosis (Horner’s syndrom e).
Note that in Lambert-Eaton syndrome, ptosis is Bilateral.
Another commonly seen complications of lung tumors is superior vena cava syndrome (often associated with small cell carcinoma), in which the superior vena cava is compressed by the growing tumor. This impairs venous drainage of the head and upper limbs, re sulting in swelling and purple discoloration of the arms and face.
Small Cell Cancer of the lung: Dyspnea, rapid unexplained wt loss, SIADH.
Elevated ACE are frequently associated with sarcoidosis. The hypercalcemia that dev elops in sarcoidosis is due to increased production of 1,25-dihydroxyvitamin D3 by the macrophages in granulomas. It is also associated with Bell’s palsy.
Sarcoidosis: lung, skin, anterior uveitis, polyarthritis, bilateral hilar lymphadenopathy, noncaseating granulomas. TX is glucocorticoids.
A pneumothorax can cause a mixed resp and metabolic acidosis because of both impaired ventilation, which increases CO2 levels; and increase anaerobic metabolism which increases plasma levels of acids such as lactic acidosis.
Pneumothorax – sudden onset of severe dyspnea with sharp pain in one’s side. The trachea and mediastinum WILL shift away from the side of t he pneumothorax. Hyperresonance, absence of breath sounds. Commonly associated with asthma, emphysema, Marfan’s, trauma.
Nephrology:
The causes of acute renal failure (ARF) are divided into 3 groups: prerenal, renal (intrinsic), and postrenal (obstructive).
Common causes of postrenal failure include BPH or prostate c ancer, bladder tumors, and urinary retention (due to neurogenic bladder or anticholinergic, opiate, or sympathomimetic).
The diagnosis of obstructive renal failure is made, in part, by detection of hydronephrosis (pelvicalicectasis) on renal ultrasound.
Acute tubular necrosis (ATN) is the MCC of intrinsic renal failure. ATN can be ischemic or toxic. Toxins capable of ATN include cisplatin, aminoglycosides, vancomycin, amphotericin, IV contrast agents, and myoglobin.
Ischemic ATN is distinguished from prerenal azotemia by th e presence of “muddy brown” casts in the urinary sediment and an FENa+ >2%. Prerenal azotemia, in contrast, show bland sediment, by a FENa+ <1%.
NSAIDs-induced decrease GFR
NSAIDs can cause AIN, nephrotic syndrome, and most commonly Hemodynamic renal failure from inhibition of vasodilatory prostaglandins. Pts. with advanced age, renal dysfunction, or CHF are at the highest risk for NSAID-induced acute renal failure (ARF).
MC conditions that cause eosinophilia include helminthic infections, asthma, allergy, druginduced acute interstitial nephritis (AIN), Hodgkin’s lymphoma.
AIN is classically a triad of fever, rash, and peripheral eosinophilia in a setting of ARF after introduction of a new drug. Agents are penicillins, cephalosporins, sulfonamides, NSAIDs, PPIs.
HTN is both major cause and a major complication of chronic renal failure (CRF).
CRF is characterized by normocytic anemia (due to loss of renal erythropoietin production), hyperkalemia, hypocalcemia, hyperphosphatemia, and mixed anion gap/non-anion gap metabolic acidosis.
Uremia is a clinical syndrome in renal failure that shows nausea, pruritis, malaise, seizures, confusion, bleeding pericarditis, and fluid overload.
CRF results in secondary hyperparathyroidism. Increase PTH, in turn, can cause abnormal bone formation (osteitis fibrosa cystica), whereas deficiency of activated vit d can (in adults) lead to osteomalacia. The full spectrum of bony changes resulting from high PTH, low Ca2+, and chronic acidosis is called renal osteodystrophy.
Berry aneurysm is associated with Autosomal dominant adult polycystic disease (ADPKD).
Subjects
Usmle Step 1 Notes Free Download For Mac
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* Up-to-date: Updated annually by Kaplan's all-star faculty
* Integrated: Packed with clinical correlations and bridges between disciplines
* Learner-efficient: Organized in outline format with high-yield summary boxes
* Trusted: Used by thousands of students each year to succeed on USMLE Step 1
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Kaplan Usmle Step 1 Lecture Notes Anatomy Free Download
