(临床诊断学) 仁济临床医学院诊断学教研室 An Introduction to Clinical Diagnostics


Etiology and pathogenesis



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Etiology and pathogenesis

Any stimulus to intercostal nerve, nerves from heart, lung, diaphragm, bronchus or esophagus, aorta will cause chest pain. Common causes are listed as follows:


  1. Diseases of chest wall: such as Herpes zoster, costal chondritis, chest wall tumors.

  2. Cardiac and blood vessel causes: myocardial ischemia (angina pectoris, myocardial infarction, aortic stenosis),myocarditis, pericarditis

  3. Respiratory diseases: pleuritis, pneumonia or lung cancer

  4. Mediastinal disease: mediastinitis

  5. Others: esophageal reflux

Clinical manifestations



  1. Localization: herpes zoster cause blister along the intercostal nerve, chondritis with local tenderness and elevation of bone.

  2. Quality: intercostal neuralgia with prickling pain and local tenderness; angina with precordial distress.

  3. Factors related to chest pain: angina usually induced after effort or mental stress and relieved by nitroglycerine.

  4. Associated symptoms: bronchitis with cough, lung cancer with bloody sputum.

Diagnostic points

Detailed history: onset, quality, localization, provocating factors and associated symptomns. P. E: especially neck lymph nodes and chest examination. Laboratory and instrumental check up: especially sputum and chest X-ray film.
Abdominal pain
Abdominal pain is one of the most frequent complaints for which patients seek medical attention. It may be classified into acute and chronic.
Acute abdominal pain
Etiology and pathogenesis:


  1. Parietal peritoneal inflammation: bacterial contamination (e.g., perforated appendix) and chemical irritation (e.g., perforated ulcer, pancreatitis).
  2. Acute inflammation of abdominal organs: gastritis, enteritis.


  3. Mechanical obstruction of hollow viscera: obstruction of the small or large intestine.

  4. Vascular disturbances: embolism, vascular rupture, torsion of the organs.

  5. Referred pain: pneumonia, coronary occlusion.

  6. Abdominal well: trauma

  7. Metabolic and toxic causes: allergic factors etc.

Clinical manifestations



  1. Localization: usually with tenderness over the diseased organ

  2. Quality and severity: perforation with severe dull pain over upper abdomen. Renal colic with severe pain over back radiating to lower abdomen.

  3. Provocation and relief: acute gastritis and enteritis are induced by eating unfresh or raw foods, and ameliorated after vomiting or discharge.

  4. Associated manifestations: jaundice favors liver, gallbladder or pancreatic disease. Hematuria is usually due to renal stone.

Diagnostic points:

The history should be emphasized on the onset, location, quality and possible etiologic factor of the abdominal pain. Detailed physical examination of chest and abdomen is important. Echo and X-ray examination, gastroscopy and intestinal fibroscopy are sometimes needed. If the diagnosis remained indefinite, laparotomy is indicated.
Chronic abdominal pain
Etiology and pathogenesis:


  1. Chronic inflammation of abdominal organs: reflux esophagitis, chronic ulcerative colitis.

  2. Peptic ulcer

  3. Distention of visceral surfaces: hepatic or renal capsules.

  4. Metabolic and toxic causes: uremia

  5. Infiltration of tumor

  6. Neurogenic: irritable colon, neurosis.

Clinical manifestations:


  1. Past history: Acute inflammation of abdominal organs may cause adhesion and chronic inflammation of the organs.


  2. Localization: Pain is usually consistent with the diseased organ.

  3. Quality: Duodenal ulcer is related to hunger, liver cancer is with persistent pain.

  4. Pain and position of the body: Ptosis of stomach or kidney shows pain when standing for long time.

  5. Associated symptoms: When associated with fever, they are usually due to chronic infection, lymphoma or malignant tumor of abdominal organ. When associated with vomiting, diseases of esophagus, stomach, billary tree may be indicated.

Diagnostic points:



Same as in acute abdominal pain.
Chapter 3 Edema


  1. Definition

Edema is defined as a clinically apparent increase in the interstitial fluid volume. Depending on its cause and mechanism, edema may be localized or have a generalized distribution. Ascites and hydrothorax refer to accumulation of excess fluid in the peritoneal and pleural cavities, respectively, and are considered to be special forms of edema.


  1. Pathogenesis

The hydrostatic pressure within the vascular system and the colloid oncotic pressure in the interstitial fluid tend to promote a movement of fluid from the vascular to the extravascular space. In contrast, the colloid oncotic pressure contributed by the plasma proteins and the hydrostatic pressure within the interstitial fluid ,referred to as the tissue tension, promote the movement of fluid into the vascular compartment. As a consequence of these forces there is a large movement of water and diffusible solutes from the vascular space at the arterial end of the microcirculation and back into the vascular compartment at the venous end. These forces are usually balanced so that a steady state exsits in the sizes of the intravascular and interstitial compartments,and yet a large exchange between them is permitted. However,should any one of the hydrostatic or oncotic forces be altered significantly, a net movement of fluid between the two components of the extracellular space will occur. The development of edema then depends on.



  1. Etiology and Clinical Appearances

  1. Generalized Edema

  1. Cardiogenic edema:especially the manifestation of right heart failure. It’s been

evidenced that a reduction of the effective circulatory blood volume and renal blood volume, as well as the decreased glomerular filtration rate occur in this condition with secondary elevation of the aldosterone secretion, tubular Na reabsorption and sodium and water retention. The increment accumulates in the venous circulation, and the increased capillary and lymphatic hydrostatic pressure leading to reduction of fluid reabsorption promotes the formation of edema. It could be first found in the legs symmetrically. Patients commonly have the evidence of heart failure, such as dyspnea, basilar rales, venous distention and hepatomegaly, etc.

  1. Nephrogenic edema:The primary alternation in this disorder is a diminished colloid oncotic pressure due to massive losses of protein into the urine and retention of sodium and water by the kidney. Edema usually starts from the eyelids and face and tends to be most pronounced in the morning, accompanied by abnormal urinalysis, hypertension or renal insufficiency.

  2. Hepatogenic edema:Ascites and biochemical and clinical evidence of hepatic cirrhosis suggest the edema of hepatic origin. Edema may occurs from the ankle and extends upwards, but scarcely involving the head, face and upper extremities. This condition is characterized by hepatic venous outflow blockade, which in turn causes expansion of the splanchnic blood volume and increased hepatic lymph formation. These alternations are frequently complicted by hypo-albuminemia secondary to reduced hepatic synthesis and reduce the effective arterial blood volume even further leading to activation of the RAA system.

  3. Malnutrition:A diet grossly deficient in protein over a prolonged period , protein-losing enteropathy and severe burn may produce hypoproteinemia and edema. Before edema occurs from the lower extremities, there may be a history of weight loss.


  4. Idiopathic edema:This syndrome, which occurs almost exclusively in women, is characterized by periodic episodes of edema(unrelated to the menstrual cycle),frequently accompanied by abdominal distention. Etiology is unclear.

  5. Miscellaneous:These include hypothyroidism, in which the edema(myxedema) may be located typically in the pretibial region and which may also be associated with periorbital puffiness. Exogenous hyperadrenocortism, premenstrual nervous syndrome, pregnancy, and administration of estrogens and vasodilators, particularly the calcium antagonist nifedipine, may also all cause edema.

  1. Localized edema:Edema originates from local venous or lymphatic obstruction or increase of the capillary permeability, such as local inflammation, thrombosis, thrombophlebitis, filariasis, etc.




  1. Approach to the Patient

An important first question is whether the edema is localized or generalized. If it is

localized, those phenomena that may be responsible should be concentrated upon. Hydrothorax and ascites are forms of localized edema. Either may be a consequence of local venous or lymphatic obstruction, as in inflammatory or neoplastic disease.

If the edema is generalized, it should be determined, first, if there is serious hypoalbuminemia, e.g.serum albumin<2.5g/dl. If so, the history, physical examination, urinalysis, and other laboratory data will help evaluate the question of cirrhosis, severe malnutrition, protein-losing gastroenteropathy, or the nephrotic syndrome as the underlying disorder. If hypoalbuminemia is not present, it should be determined if there is evidence of congestive heart failure of a severity to promote generalized edema. Finally, it should be determined whether the patient has an adequate urine output, or if there is significant oliguria or even anuria.

Chapter 4 Mucocutaneous Hemorrhage
Mucocutaneous hemorrhage is due to the dysfunction of hemostasis blood coagulation. The clinical feature is, spontaneous bleeding in general or regional mucocutaneous, or maintainable hemorrhage after mild damage.

Etiology mechanism and Pathogenesis The basic mechanism of mucocutaneous hemorrhage as follows: 1 Capillary wall defect. 2 abnormal of platelet number or function. 3 Coagulation factors absence or activities reduce. 4 Anticoagulation factors increase within the blood. The defect of one of above factors will cause the deficiencies of hemostasis and coagulation functions, lead mucocutaneous hemorrhage.



  1. Capillary wall defect Normally, the local vascular constricts reflexly to seal the damaged vascular endothelium and reduce blood flow as soon as the capillary trauma. Then, the capillary is constricted continuously to play the role of hemostasis which acted as the platelet secretion of serotonin as the vasoconstrictor. When the capillary wall has congenital defect or camage, it can’t normally play the role of hemostasis by constriction, and then lead to mucocutaneous hemorrhage. It’s usually seen in:

  1. Hereditary hemorrhagenic capillary dilatatasis,

  2. Anaphylactoid purpura, non-thrombocytopenic purpura, purpura senilis and methanical purpura.

  3. Severe infection, chemical agents or drugs toxicosis and abnormal metabolism such as vitamin C or deficiency, uremia, arteriosclerosis.
  1. Platelet abnormality Platelet play the main role in hemostaic process. Platelets adhere and aggregate in the injured vessel, form the white thrombi to block wound. The enzyme system of platelet membranes can actuate to form thromboxane A2 which further aggregates platelets and enhances vasoconstriction to amplify local hemostasis. Platelet also release the platelet factors and thrombocytin to serve the clotting process or clot constriction, promote the hemostasis effection. The abnormalities of platelet number or function will cause the mucocutaneous hemorrhage. It’s often seen:


  1. Thrombocytopenia: ① primary thrombocytopenia: such as primary thrombocytopenic purpura, neonatorum thrombocytopenia. ② secondary thrombopenia: like drugs, infection, aplastic anemia, leukemia, hypersplenia, etc.

  2. Platelet dysfunction: by congenital thrombasthenia, giant platelet syndrom, and also acquired as drugs, hepatic disease, uremia.

  3. Thrombocytosis: there are primary thrombocythemia and secondary due to affection of infection, post splenectomize, chronic mylocytic leukemia.

  1. Coagulation abnormality Hemostasis process is much complex, in which there are many coagulation factors. It’s the chain reaction activated by pre-enzyme. It’ll cause coagulation disorder then mucocutaneous hemorrage that any one of coagulation factors defect or dysfunction. Which often been seen in clinic are: ① congenital: hemophilia, hypofibrinogenemia, deficiency of factor V, hypoprothrombinia. ② secondary, deficiency of vitamin K, severe hepatic disease.

  2. Anticogulant agents increased in blood circulation abnormal proteinemia, heparan anticogulants increased or over-dose of anticoagulant.

Clinical manifestation Red of dark red blotch is formed by mucocutaneous hemorrhage. Usually, it isn’t above skin and not fade after stressed. That’s called purpura.

In vascular defects and platelet abnormalities, hemorrhage is usually cutaneous and/or mucosal, which presences petechiae, ecchymosis. While tissue hematoma and internal organs bleeding are rare. In clotting factors deficiency, hemorrhage is often internal organs, intra-muscle or soft tissue hematoma, and also intra-anticular. There are family history or hepatic disease history in hemorrhage of coagulation disorders.



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