1. Central cyanosis, characterized by decreased arteria oxygen saturation due to right-to-left shunting of blood or impaired pulmonary function. It includes pulmonary cyanosis and cardiac cyanosis. Pulmonary cyanosis is often seen in severe respiratory diseases, such as pneumonia, obstructive pulmonary emphysema, and primary pulmonary hypertension. Cardiac cyanosis is commonly present in congenital heart disease when the volume of a right-to-left shunt exceeds 30 per cent of the left ventricular output.
2. Peripheral cyanosis, most commonly secondary to cutaneous vasoconstriction due to a low cardiac output or exposure to cold air or water if peripheral cyanosisis localized to as extremity arterial or venous obstruction should be suspected. It also includes congestive peripheral cyanosis and ischmic peripheral cyanosis. Congestive peripheral cyanosis is often seen in right-side heart failure, constrictive pericarditis, local venous diseases. Ischmic peripheral cyanosis is often seen in severe shock.
3. Mixed cyanosis, central cyanosis and peripheral cyanosis occur in the same time, the blood is insufficiently oxygenated because the lung is congested or more deoxygenation due to slow peripheral circulatory blood flow in peripheral capillary vessels.
4. Cyanosis resulting from abnormal hemoglobin pigments in the blood.
a. Methemoglobinemia due to drugs or chemical poisoning (methemoglobin 3 gm/100 ml) such as nitrite salt, sulfa drugs or phenacetin etc.
b. Hereditary methemoglobinnemia.
c. Sulfhemoglobinemia (sulfhemoglobin 0.5 mg/100 ml).
A history of cyanosis beginning in infancy suggests a congenital cardiac malformation with a right-to-left shunt hereditary methemoglobinemia is another cause of congenital cyanosis; the diagnosis of this condition is supported by a family history of cyanosis in the absence of heart diseases. If cyanosis appears at the age of 6 months or later in childhood it may be due to the development of progression of obstruction to the right ventricular outflow in patients with ventricular septal defect. Development of cyanosis between age 5 and 15 years suggests an Eisenmenger's reaction with right-to-left shunting as a consequence of a progressive increase in pulmonary vascular resistance.
A history of cyanosis localized to the hand suggests Reynttd's phenomenon central cyanosis due to congenital heart disease or pulmonary disease characteristically worsens during exertion, whereas peripheral cyaonsis of congestive heart failure at rest may be accentrated only slightly, if at all, during exertion.
If cyanosis is caused by methemoglobinemia there is a history of contact of drugs or chemical material. Spectroscope is helpful to diagnose methemoglobinemia. If cyanosis is due to congenital heart diseases, echocardiography, right heart catherixation and angiocardiography should be performed.
Cyanosis with clubbed fingers: congenital heart disease, chronic pulmonary disease.
Acute cyanosis with conscious disturbance: medicine or chemicals poisoning, shock, acute pulmonary infection.
Chapter 9 Palpitation
Palpitation may be defined as an awareness of the beating of the heart, an awareness moat commonly brought about by a change in the heart's rhythm or rate or by an augmentation of its contractility. Palpitation is not pathognomonic of any particular group of disorders; indeed, often it signifies not a primary physical disorder but rather a psychio disturbance. Even when it occurs as a more or less prominent compliant, the diagnosis of the underlying disease is made largely on the basis of other associated symptoms and the data. Concern is al the more pronounced in patients who know or who have been told that they may have heart disease; to them palpitation may seem to be an omen of impeding disaster. Since the resulting anxiety may be associated with increased activity of the autonomic nervous system, with consequent increases of the cardiac rate and rhythm and the vigor of contraction, the patients awareness of these changes may then lead to a vicious cycle, which ultimately be responsible for this incapacitation.
Palpitation may be described by the patient in various terms, such as "fluttering", "flopping", and "skipping", and in most cases it will be obvious that the complaint is of a sensation of disturbed heartbeat. The wide variability in the sensitivity to alteration in cardiac activity among different individuals must be appreciated. Some patients seem to be unaware of the most serious and chaotic dysrrhythmias; other are seriously troubled by and occasional extrasystole. Patients with anxiety states often exhibit a lowered threshold at which disorders of rate and rhythm result in palpitation. Indeed, it is not unusual for palpitation to be the major manifestation of the emotional disorder. The awareness of the heartbeat also bends to be more common at night and during introspective moments, but is less marked during activity. Patients with organic heart disease and chronic disorders of cardiac rate, rhythm, or stroke volume tend to accommodate to these abnormalities and are often less sensitive than normal persons to such events. Persistent tachyeardia and/or atrial fibrillation may not be accompanied by continual palpitation, in contrast to a sudden, brief alteration in cardiac rate or rhythm which often causes considerable subjective discomfort. Thus, palpitation is particularly prominent when the precipitating cause for increased heart rate or contractility or arrhythmia is recent, transient, and episodic. Conversely, in emotionally well-adjusted individuals palpitation becomes progressively less disconcerting as the cause (e. g. anemia, frequent extrasytoles, complete A-V block) persists.
Under ordinary circumstances the rhythmic heartbeats is imperceptible to the healthy individual of average or placid temperament. Palpitation may be experienced by normal persons who have engaged in strenuous physical effort or have been aroused emotionally. This type of palpitation is physiologic and represents the normal awareness of an overactive heart-i.e. a heart that is beating at a rapid rate and with an increased contractility. Since palpitation due to overactivity of the heart may occur also in certain pathologic states, e. g., high fever, severe anemia, or thyrotoxicoxix, it is commonly assumed that it is the overactivity person that is responsible fore the symptom. However, overactivity of the heart is generally associated with several other alterations in cardiac function including acceleration of heart rate, more rapid development of intraventricular pressure during isometric contraction, increased intensity of the heart sounds, especially of the first sound, a short duration of systole, and a greater ejection velocity.
When palpitation is heavy and regular, it is usually caused by an augmented stroke volume, and it should raise the question of aortic or mitral regurgitation, ventricular septaldefect, or of a variety of hyperkinetic circulatory states (anemia, arteriovenous fistula, thyrotoxicosis, and the so-called idiopathic hyperkinetic heart syndrome.) It may also occur immediately after the onset of cardiac slowing, as with the sudden development of heart block, or upon the conversion of sinus rhythm from atrial fibrillation. But unusual movements of the heart within the thorax are also frequently the mechanism of palpitation. Thus, the ectopic beat and/or the compensatory pause may be appreciated, since both are associated with alteration in cardiac function.
Important causes of palpitation:
1. Disorders of the mechanism of the heartbeat.
1) Extrasystole: In most cases the dianosis will be suggested by the patient history. The premature contraction and postpremature patient may say that he feels if "the heart turns over". The pause following the premature contraction may be felt as an actual cessation of the heartbeat, in contrast with the complete unawarness of pauses of similar duration when atrial fibrillation with a slow ventricular rate occurs. The patient's apprehensions seem to magnify the duration of the interval and sometimes may make him wonder if the heart will ever resume its beat. The first ventricular contraction succeeding the pause may be felt as an unusually vigorous beat and will be described as "ourding" or "thudding".
Usually the identification of the extrasystole as the cause of palpitation is a simple matter. When extrasystoles are numerous, clinical differentiation from atrial fibril action can be made by any procedure that will bring about a definite increase in the ventricular rate; at increasingly rapid heart rate, the extrasystoles usually diminish in frequency and then disappear, whereas the irregularity of atrial fibrillation increases. A-V block with dropped beats, is the only other common arrhythmia with which the premature contraction is likely to be confused; but simple ausculatation will reveal the difference.
2) Ectopic tachycardias: These conditions are common and medically important causes of palpitation Ventricular tachycardia, one of the most serious arrhythmia, rarely is manifested as palpitation; this may be related to the abnormal sequence, and hence impaired coordination and vigor, of ventricular contraction. If the patient is seen between attacks, the diagnosis, of ectopic tachycardia and its type will have to depend upon the history, but of course the precise diagnosis can be made only when an ECF and observations on the effect of carotid sinus pressure are made during the episode. Monitoring of the ECG with a portable tape recording system and asking the patient to record the time of onset and cessation of the palpitations are extremely helpful in determining their cause. The mode of onset and offset gives the most important lead in distinguishing sinus from one of the various forms of ectopio tachycardias; sinus taohycardia commences and ceases over the course of minutes or seconds, but not instantaneously as is characteristic of ectopic rhythm.
2. Organic or functional disturbance origination outside the circulatory system:
1) Thyrotoxicosis: In its fully developed form, thyrotoxicosis will usually be evident and offers little difficulty in the may of diagnosis except in the elderly, in whom so-called apathenichyperthyroidism may be present. Thyrotoxicosis is particularly likely to be over-looked in the presence of myocardial failure.
2) Anemia: when mild, anemia may cause palpitation during exertion; when severe, palpitation may be present at rest. Appropriate studies of the blood will clarify the situation.
3) Palpitation may be present in acute infections, particularly in the early stages.
4) Hypoglycemia: Palpitation is often a prominent feature of the condition and appears to be related to release of catecholaminels. The diagnosis is confirmed by appropriate blood sugar estimations, by reproduction of the symptom when hsulin is administered, and by prompt relief of symptoms on the administration of glucose.
5) Drugs: The relationship between the development of palpitation and the use tobacco, tea, alcohol epinephrine, ephedrine, aminophylline, atroping, or thyroid extract is obvious.
6) Tumors of the adrenal medulla (pheochromecytoma).
Palpitation as a manifestation of the anxiety state
Chapter 10 Gastrointestinal Hemorrhage
Gastrointestinal bleeding may be obvious efflux of blood from the gastrointestinal tract (gloss blood) or no external manifestation (occult blood).
Chapter 12 Nausea and Vomiting Nausea and Vomiting are common clinical symptoms. Nausea is a sensation of upper abdominal discomfort and having an urge to vomit. It goes with the symptom of vagus exciting, such as paleness, sweatiness, salivation, low blood pressure and bradycardia. Nausea is a prelude of vomiting, but sometimes vomiting occurs without nausea or nausea occurs without vomiting. Vomiting is forcing the contents of the stomach and small intestine up through the esophagus and out of the mouth. They are complex reflex caused by multiplicate reasons.
【Causes】According to the pathogenisis, the causes of nausea and vomiting can be devided into several sorts as follows:
irritation of pharynx: smoking, severe cough, nasopharyngitis and so on.
Gastroduodenal diseases: acute and chronic gastroenteritis, peptic ulcer, acute gastric dilatation, pyloric obstruction, duodenal stasis and so on.
Intestinal diseases: acute appendicitis, intestinal obstruction, acute necrotizing enterocolitis, abdominal type of allergic purpura and so on.
Hepatic, biliary and pancreatic diseases: acute hepatitis, liver chirrosis, hepatic congestion, acute and chronic cholecystitis, pancreatitis and so on.
Diseases of peritoneum and mesentery: such as acute peritonitis.
Systemic diseases: nephrolithiasis, acute pyelonephritis, acute inflammation of pelvic cavity, rupture of ectopic pregnancy and so on. Myocardial infarction, heart failure, diseases of labyrinth, glaucoma and inappropriate refraction also can lead to nausea and vomiting.
Encephalic inflammation, all kinds of cephalitis and meningitis.
Cerebral vascular disease such as cerebral hemorrage, cerebral infarction, cerebral thrombosis, hypertentional encephalopathy and migraine.
Skull and intracranial injury: brain contusion or intracranial hematoma.
Epilepsies, especially status epilepticus.
Systemic diseases: hydrocephalus and elevated intracranial cavity pressure (ICP) caused by uremia, hepatic encephalopathy, diabetic ketoacidosis (DKA) and hypoglycemia.
Drugs: such as antibiotics, many chemotherapy drugs, digitalis and morphia, these drugs stimulate vomiting center and lead to vomiting.
Neuropathic vomiting：gastrointestinal neurosis and anorexia nervosa.
【Pathogenesis】Vomiting is a complicated reflex including three stages: nausea, vomiturition and vomiting. In the stage of nausea, tensility and peristalsis of stomach decrease, while tensility of duodenum increases with or without reflux of duodenal fluid. In the stage of vomiturition, upper part of stomach relax with transient contraction of gastric antrum. In the stage of vomiting, the abdominal muscles tighten against a relaxed stomach with an open sphincter. The contents of the stomach are propelled up and out. Vomiting is different from countercurrent regurgitation, in which the contents of the stomach reflow up through the esophagus and out of the mouth without nausea and contraction of diaphragm.
The center of vomiting is located in the medulla consist of two parts with different function. One is neural reflex center----vomiting center, which located in the lateral medullary reticular formation in the medulla. The other is chemoreceptor trigger zone at the base of the fourth ventricle of the brain. Vomiting center receives afferent impulsion from digestive tract, pallium, inner ear vestibule, coronary artery and chemoreceptor trigger zone, and administrates the vomiting action directly. The chemoreceptor trigger zone has numerous dopamine D2 receptors, serotonin 5-HT3 receptors, opioid receptors, Acetylcholine receptors, and receptors for substance P. Stimulation of different receptors are involved in different pathways leading to vomiting.
the time of vomiting: vomiting which occurs upon waking is often induced by morning sickness, uremia, chronic alcoholism, functional dyspepsia or sinusitis. If the vomiting occurs at night, the common cause is pyloric obstruction.
the relation with eating: the vomiting occurs some time after dinner is always caused by food poisoning, especially for the collective pacients. Vomiting just after dinner may be neuropathic vomiting. Lingering vomiting (deferred vomiting) is defined as the vomiting occurs more than 1h after dinner, which indicates decline of gastric tensility. Vomiting after several meals is often cuased by pyloric obstruction.
the features of vomiting: neuropathic or ICP vomiting are lack of nausea. Projectile vomiting always indicates ICP.
character of vomitus: The barmy or septic smell indicates retention of gastric juice and food. Feculent vomitus occurs with low-intestine obstructive lesions. When the vomitus contains bile it suggests the obstruction located under duodenal papilla. If the vomitus contains no bile it suggests the obstruction located upon the duodenal papilla. Vomitus with plenty of acid fluid indicates duodenal ulcer or gastrinoma. Vomitus without acid fluid is always due to cardiac stenosis. Obstruction of upper digestive tract can be determined according to the quantity of vomitus, and the amount of liquid loss can be estimated.
【Associated manifestations】The associated manifestations followed are helpful to the diagnosis of nausea and vomiting. (1)When vomiting is associated with abdominal pain and diarrhea it maybe a result of acute gastroenteritis, bacterial food poisoning, cholera, paracholera and acute toxicosis. (2) Vomiting associated with right upper abdominal pain, fever, chill or jaundice suggests cholecystitis or gallstone. (3) Projectile vomiting with headache is due to ICP or glaucoma.(4) Vomiting with vertigo and nystagmus may occur in vestibule lesion.(5) When vomiting occurs during the treatment of antibiotics and chemotherapy, it maybe due to the side effect.(6) If a woman develops vomiting which occurs upon waking and menopause, it often indicates morning sickness.
Beginning of vomiting: with or without inducement, rapid or slow initiation, association with food, history of abdominal surgery, menstrual history and so on.
Inducment: such as position, eating and stimulation of pharynx.
Associated menifestations mentioned before.
Examination and treatment: X-ray of barium meal, endoscopy, ultrasonic exam, blood sugar, BUN and so on.
Chapter 13 Jaundice
Accumulation of bilirubin in the bloodstream causes yellow pigmentation of the plasma,leading to discoloration of heavily perfused tissues. Clinically , hyperbilirubinemia appears as jaundice or icterus ,yellow pigmentation of the skin and scerae .
normal serum bilirubin concentrations range from 5 to 17 μmol/L (0.3 to 1.o mg/dl).More than 90 percent of serum bilirubin in normal individuals is in the unconjugated form . The remainder is conjugated to a polar group (primarily glucuronide ),rendering it water-soluble and thus able to be filtered and excreted by the kidney.
Approximately 90 percent of circulating bilirubin in derived from senescent red blood cells.When circulating erythrocytes reach the end of then normal life span of approximately 120 days,they are destroyed by reticuloendothelial cells . Oxidation of the heme moiety dissociated from the hemoglubin within these cells generates biliverdin ,which is than metabolize to bilirubin .Approximately 15 to 20 percent of circulating bilirubin is derived from other sources ,including (1)ineffective erythropoiesis resulting from destruction of maturing erythroid cells in the bone marrow,and , (2) the metabolism of other heme-containing proteins , most notably hepatic cytochromes, muscle myoglobin ,and widely distributed heme-containing enzymes.
Unconjugated bilirubin liberated into the plasma is bound tightly,but nonconvalently, to albumin. Certain organic anion , such as sulfonamide and salicylate , compete with bilirubin for binding sites on albumin ,permitting the released pigment to enter tisssues. Conjugated bilirubin is bound to albumin in two forms reversible and irreversible . Reversible , noncovalent binding is similar to that of unconjugated bilirubin , although the complex is less stable . When present in serum for extended periods of time (e.g. , with cholestasis ), conjugated bilirubin can form an irreversible,covalent complex with albumin referred to as delta bilirubin or biliprotein . Because of the irreversibility of binding , this complex is not excreted by the kidney .
Hepatic metabolism of Bilirubin: The liver has a central role in the metabolism of the bile pigments . This process can be devided into three distinct phases: (1) hepatic uptake: unconjugated bilirubin bound to albumin is presented to the liver cells. The uptake and subsequent hepatocyte storage of bilirubin involve binding of bilirubin to cytoplasmic anion-binding proteins,especially ligandin (glutathione-s-tansferase B),that prevent efflux of bilirubin back into the plasma; (2) conjugation: unconjugated bilirubin is water-insoluble unless complexed to an amphipathic molecule such as albumin . Since albumin is absent from bile,bilirubin must converted to a water-soluble derivative before biliary excretion. The process is accomplished predominantly by conjugation of bilirubin to glucuronic acid , generating bilirubin glucuronide . The conjugation reaction occurs in the endoplasmic riticulum of hepatocytes and is catalyzed by bilirubin glucuronozyl transeferase ; (3) Excretion: In normal circumstances, only conjugated bilirubin can be excreted into bile . Impaired excretion lends to decreased bilirubin concentrations in the bile and concomitant efflux of conjugated bilirubin through the sinusoidal menbrane of the hepatocyte into the blood stream .
Intestinal phase of Bilirubin Metabolism: after secretion into the bile,conjugated bilirubin is transported through the biliary ducts into the duodenum .Conjugated bilirubin is not reabsorbed by the intestinal mucosa . It is either excreted unchanged in the stool or metabolized by ileal and colonic bacteria to urobilinogen and related products. Urobilinogen can be reabsorbed from the small intestinel and colon and enters the portal circulation .Some of the portal Urobilinogen is taken up by the liver and reexcreted into the bile,and the remainder by passes the liver and is excreted by the kidney . Under normal conditions,the daily urinary excretion of urobilinogen does not exceed 4 mg.When the hepatic uptake and excretion of urobilinogen is impaired (e.g.in hepatocellular disease)or the production of bilirubin is greatly increased (e.g.with hemolysis),daily urinary urobilinogen excretion may increase significantly .In contrast,cholestasis or extrahepatic biliary obstruction interferes which the intestinal phage of bilirubin metabolism and leads to markedly decreased production and urinary excretion of urobilinogen,measurement of urinary urobilinogen can thus be a useful tool in distinquishing possible cause of hyperbilirubinemia .
Renal Excretion of Bilirubin : The urine normally contains no detectable bilirubin by usual clinical assays. Unconjugated bilirubin ,being tightly bound into albumin,is not filtered by the renal glomeruli. Because there is no tubular secretory process for bilirubin,unconjugated bilirubin is not excreted in urine. In contrast ,conjugated bilirubin is a polar molecule less tightly bound to albumin,and is filtered by the renal glomeruli and appears in the urine.The presence of bilirubin in the urine is evidence of conjugated hyperbilirubinemia and can be a useful differentiating point early in the evaluation of jaundice .
【Classification of Jaundice 】
1.Overproduction of bilirubin: An increaced amount of hemoglobin released from senescent or hemolyzed blood cells leads to increased bilirubin production. Erythrocyte destruction leading to hyperbilirubinemia most commonly results from intravascular hemolysis.(e.g.autoimmune ,microangiopathic ,or hemoglobinopathy_associated),or reabption of a large hematoma . Excess bilirubin production is reflected in increased serum bilirubin levels of up to 51 to 68
μmol/L (3 to 4 mg/dl),with a predominance of unconjugated bilirubin.
2.Impaired hepatic uptake of bilirubin: The uptake of bilirubin by hepatocytes requires dissociation of the nonpolar pigment molecule from albumin,transport across the cell menbrane,and binding to ligandin .In rare cases of drug_induced jaundice and possibly in some Gilbert's Syndrome ,there may be disruption of this phase of bilirubin.
3.Impaired glucuronide conjugation : Deficiency in glucuronide transferase activity can occur as a result of both acquired and genetic defects. In the fetus and neonatal,glucurononocyl transferas activity is normally low. Although transiet,together with increased neonatal intestinal absorption of unconjugated bilirubin,contribute to the development of neonatal jaundice that occurs between the second and fifth days of life. The significant of inherited deficiencies of glucucoronosyl transferase depends on the level of residual enzyme activity. Gilbert' Syndrome associated with mild decrease in activity,produces mild ,asymptomatic ,unconjugated hyperbilirubinemia. Moderately decreased activity occurs in Crigger_Najjar Syndrome typeII,this enzyme is totally absent in Crigger_Najjar Syndrom typeI,an autosomal recessive disorder associated with kernicterus and childhood mortality from central nervous system dysfunction. Acquired defects in glucuronosyl transferase activity may be induced by drugs (i.e.direct enzyme inhibition),or be associated with liver disease generally.
Jaundice with prodominantly conjugated bilirubiemia:
Pathogenesis: 1.it is due to intra_and_extrahepatic Obstruction of bile ducts.
2.Intrahepatic Jaundice: Hepatitis,PBS,Drugs.
3.Extrahepatic Biliary obstruction: stones,stricture inflammation,tumors(Ampulla of vater)