① Primary hemostasis defect: caused by PLT and vessel wall defects → Use PLT counting and BT ② Second-stage hemostasis defect: caused by coagulation factor deficiency or the presence of pathological anticoagulant substances → choose APTT and PT ③ Hyperfibrinolytic bleeding: caused by degradation of fibrinogen and certain coagulation factors by plasmin → FDPs and D2 polymers

screening test ① Bleeding time BT: TBT measurement; 6.9±2.1min>9 abnormality; BT↑→ PLT quantity and function decreased (thrombocytopenic purpura ITP), coagulation factor deficiency (VWD, DIC), vascular abnormalities, drug effects ② Band arm test/CFT/CRT: Observe the number of bleeding points within a certain range (5cm) when the arm is pressurized for 8 minutes and the venous return is blocked; m＜5, cw＜10; bleeding points↑→vascular structure and function, PLT quantity and quality, VWD, HBP , diabetes, sepsis, VitC deficiency, uremia, cirrhosis △Henoch-Schonlein purpura: Positive band-arm test, does not affect bleeding time, and has nothing to do with PLT

Screening test: ①PLT count ②Blood clot contraction: decrease is seen in PLT reduction and asthenia, no fibrinogen; increase is seen in VIII deficiency

Diagnostic tests: ①PLT adhesion and aggregation test → decreased (PLT weakness, VWD, myeloproliferative diseases); increased (hypercoagulability-myocardial infarction, cerebral infarction, venous thrombosis, diabetes) △The strongest aggregation effect is TXA2; platelet aggregation refers to the adhesion between PLTs △Thrombothethenia-GPⅡbⅢa deficiency→decreased platelet aggregation function ② Platelet-associated immunoglobulin (PAIg measurement): Increased levels are seen in various purpuras (purpura IgG increases significantly after blood transfusion), lymphoma, leukemia, SLE, MM, and chronic active hepatitis ③Platelets release type I particles (ADP, 5-HT, Ca2); type II particles (IVV fibrinogen, platelet growth factor, β-platelet globulin); induce platelet aggregation (divalent ions, vWF, platelet membrane glycoprotein)

screening test ① Activated partial thromboplastin time measurement APTT: concept; 31-43s, abnormal exceeding 10s normal; clinical significance - endogenous coagulation factors (12,11,9-B, 8-A) common pathway (1,2,5, 10): Prolong/shorten/heparin treatment monitoring/diagnosis Lupus anticoagulant factor (LA) → binds to phospholipids, so APTT, PT, and TT will be prolonged ②Plasma prothrombin time measurement PT concept, PTR, INR; 11-13s, abnormal for 3 seconds more than the control; clinical significance - exogenous coagulation factors (3,7) common approach: prolongation/shortening/oral anticoagulant monitoring ( INR for warfarin)

① Thrombin time TT: The time from adding standardized thrombin to the tested plasma to the beginning of fibrin filaments; 16-18s is abnormal for more than 3 seconds; prolongation is seen in fibrinogen ↓, FDPs heparin-like substances ↑; shortening has no clinical significance; A Aniline blue correction ② Detection of AT-Ⅲ (serine protease inhibitor): Increased levels are seen in the acute bleeding phase of hemophilia, leukemia, and aplastic anemia; decreased levels are seen in liver disease, prothrombotic state, and thrombotic diseases

① Plasma protamine sulfate paracoagulation 3P test → Fibrin monomer is precipitated by protamine sulfate to form a paracoagulant → DIC screening (early and mid-stage, secondary fibrinolysis) ②D-dimer→Secondary fibrinolysis specific product ③FDP measurement→primary and secondary hyperfibrinolysis Primary → tPA (tissue type), uPA (urokinase type); secondary → ⅪaⅫa, α1α2, thrombin

①GFR (120-160ml/min) ②CL=UV/P (4 types) ③Three Musketeers: Scr (male 53-106, female 44-97), BUN (3.2-7.1) - not early stage, degree of elevation and lesions Consistent with sex, BUN dialysis adequacy index and evaluation; UA (male 150-416, female 89-357) - early stage, the degree of increase is inconsistent with the nature of the disease ④Ccr (80-120ml/min): method; clinical significance (early reflection sensitive indicators, fourth period, evaluation) △In order to exclude the influence of extra-renal factors→Scr and BUN are measured together

UA is a purine metabolite that can come from the body or from food decomposition, and is mainly synthesized by the liver; most of it is filtered by the glomerulus, and 90% is reabsorbed by the renal tubules → blood UA is affected by these two ①UA↑: Impaired glomerular filtration - more sensitive; abnormal increase in synthesis (gout, hematological malignancy); fasting due to lead poisoning; long-term use of diuretics ②UA↓: Impaired renal tubular reabsorption; reduced synthesis (severe impairment of liver function); cadmium poisoning with large amounts of hormones

① Phenol red excretion rate as a rough indicator ② Determination of some small molecular proteins: β2MG (5mg/L) and α1MG → can be freely filtered by the glomerulus, reabsorbed and decomposed by the renal tubules → elevated blood levels indicate glomerular filtration Obstacles, elevated levels in urine indicate renal tubular reabsorption impairment, which can reflect glomerular function impairment earlier; RBP; NAG

① Day and night urine density (Mohs): method, reference value (nocturia <750ml, day and night (3-4): 1, at least once > 1.018, difference > 0.009), clinical significance ② 3h urine density ④ Osmotic pressure: Reference value (P275-305, U600-1000, urine/plasma (3-4): 1, U/P=1 or 300 isotonic urine); late stage of chronic nephritis → complete loss of renal tubular concentration and dilution function → isotonic urine; Diabetes insipidus → loss of concentrating function → hypotonic urine

①Ammonium chloride load (acid load) → distal renal tubule Ⅰ ② Bicarbonate ion reabsorption and excretion (alkali load) → proximal Ⅱ ③Ⅰ: distal H secretion disorder; Ⅱ: proximal HCO3- reabsorption disorder; Ⅲ : near and far; IV: acid substitute combined with high potassium

STP(60-80)=A(40-55) G(20-30); A/G(1.5-2.5:1)→A/G<1 ratio is inverted; STP and A have nothing to do with gender but age, A It is related to plasma colloid osmotic pressure, G is related to immunity △The decrease in STP is parallel to the decrease in A, and the increase in STP is accompanied by an increase in G → due to liver compensation and long half-life → it takes a certain course of disease to change → detects chronic liver damage and reflects the storage function of liver parenchymal cells ①STP and A decrease: STP＜60, A＜20; source ↓ consumption loss ↑ dilution ②STP and A increase: dehydration shock, insufficient drinking water, insufficient adrenocortical hormones → hemoconcentration, but the absolute amount does not increase ③STP and G increase (γ): STP＞80, G＞35; chronic inflammation, chronic hepatic autoimmune M-globulinemia ④G reduction: reduction in synthesis ←Infants, adrenocortical hormones, immunosuppressants, congenital

Serum protein electrophoresis

Blood ammonia measurement

①UCB(1.7-10.2);CB(0-6.8);STB(3.4-17.1) ②Clinical significance: Determine the presence and extent of jaundice (4); Determine the cause of jaundice (4); Determine the type of jaundice (based on CB/STB; based on STB, CB, UCB)

①Isoenzyme ② Principle: Some enzymes exist in liver C → liver C is damaged and released into the blood → the concentration in serum increases → the activity of enzymes in serum reflects the pathological state of the liver and is a sensitive indicator for diagnosing liver diseases ③Classification: Enzymes reflecting necrosis of lesions (ALT-GPT, AST-GOT); liver and gallbladder stasis (ALP, GGT); liver fibrosis (MAO, PH); liver cell synthesis function (AchE) ④ Determination of serum enzymes: ALT, AST → viral hepatitis (acute ALT, slow AST); ALP (type 4) → diagnosis of hepatobiliary system diseases, cholestasis enzymatic indicators; GGT → elevated alcoholism, normal bone disease; MAO ⑤ Reasonable selection and application of inspection items: ALT and AST (distribution, clinical significance); ALP (distribution, clinical significance); GGT (distribution, clinical significance); MAO (clinical significance)

①Acute viral hepatitis: →The increase in ALT is more obvious; chronic viral hepatitis →The increase in AST is more obvious. If ALT/AST<1, it indicates that chronic hepatitis has entered the active stage. ② Bile enzyme separation - in acute severe hepatitis → AST is more obviously elevated ③Alcoholic liver damage→γGT increases most obviously ④ Cirrhosis→MAO, ALT>AST

FBG increased but did not reach hyperglycemia - impaired fasting glucose (IFG), >7-hyperglycemia (mild, moderate or severe), >9-positive urine glucose

<3.9-low blood sugar; <2.8-hypoglycemia

75g glucose; 5

Ⅰ: Fasting insulin ↓, low and flat release curve after oral administration of G Ⅱ: Normal fasting insulin, delayed release of insulin after oral administration of G

Proinsulin is released when it is converted into insulin under the action of proteolytic enzymes → Understand insulin secretion metabolism, pancreatic beta cell reserve

① Retrospective monitoring (reflecting average blood sugar in the past 2-3 months) ② Special diagnostic value when blood sugar and urine sugar fluctuate greatly ③ Evaluate the degree of diabetes control

HbA1c: 4-6%. Once generated, it is no longer dissociated. The metabolic cycle is basically the same as the RBC life span.

Diagnostic criteria (3) → Repeat test on another day

①Ig (present in the gamma globulin region): G (maximum secondary immune response through the placenta), A (SIgA local resistance to mucosal infection, newborns obtain from breast milk), M (maximum primary immune response-cold agglutination test-the strongest agglutination effect) - Intrauterine infection - is a natural blood type antibody), E (parasite allergy, the lowest content), D ②Serum M protein: Multiple myeloma-IgG is the most common; Macroglobulinemia-a large amount of IgM ③CH50-determination of the classic pathway; C3 (0.8-1.5 at most)-traditional and bypass acute phase response proteins; C4 (0.2-0.6)-consumptive reduction is more meaningful→↑inflammatory tumors↓nephritis autoimmune disease

①T: ERFT (64.4±6.7%)-detection quantity; LCT-detection of biological function; differentiation antigen determination: CD3-total T, CD4-Th, CD8-Ts, CD4/CD8↓-HIV ②CD19,20,22-B ③NK: ADCC (antibody-dependent cell-mediated cytotoxicity) ④CK: IL-2 (produced by T cells), TNF, IFN

tumor marker (protein, sugar, enzyme, hormone) → screening of high-risk groups, auxiliary diagnosis, observation of efficacy, detection of tumor recurrence, and judgment of prognosis ①AFP→Liver cancer (>300), gonad embryonic tumors (testicular cancer, ovarian cancer, teratoma) ②CEA→Broad spectrum non-specific, the gastrointestinal tract and certain tissues of early fetuses have the ability to synthesize CEA (rectal and colon cancer of the digestive tract) ③PSA (80% bound 20% free)→Prostate cancer ④SCC → Squamous cell carcinoma cervical cancer ⑤CA199-pancreatic cancer, hepatobiliary gastrointestinal disease, CA125-ovarian cancer but not mucinous ovarian cancer, CA153-breast cancer, bronchial lung cancer ⑥Tissue polypeptide antigen (TPA): The increase has nothing to do with the site of tumor occurrence and tissue type. Pneumonia↑ ⑦Thyroid follicular cells → calcitonin

①RF(IgM type)←denatured IgG stimulates the body to produce ② Antinuclear antibody detection: ANA; ENA (dsDNA, Sm-SLE, ribosomes, Scl-70, Jo-1, SSBSSA-Sjögren’s syndrome, nRNP-mixed connective tissue disease)

①Bacteria: ASO-rheumatoid nephritis ↑; Feida reaction-typhoid and paratyphoid fever → typhoid fever (H＜1:160, O＜1:80); paratyphoid fever (A, B, C＜1:80) → HO both increased (typhoid fever) ; H increased (immunization or recall response); O increased (early infection or cross-reaction) ②TORCH: Toxoplasma gondii, rubella, giant cell, herpes simplex ③Sexually transmitted diseases: Syphilis-RPR→TPHA, TPHA; HIV-ELISA to detect HIV antibodies→Western blotting or PT-PCR to detect RNA

①Bacteria: Indicate basic information, try to collect before using antibiotics, perform aseptic operations, and submit immediately for inspection. Do not use disinfectants for autoclaving specimen containers. ②Blood and bone marrow: Collect blood from the cubital vein during periods of rising body temperature or high temperature. Adults 10-20ml each time. Infants and young children 1-5ml, 10:1. Collect blood before next medication. Collect 3 blood at different parts at different times. Double bottles and double tests → Differentiate skin infections contaminating bacteria ③Urine: midsection, urinary catheter, bladder puncture ④ Feces: Pick out the pus, blood and mucus part, and collect the rectal swab → Infants and young children ⑤Respiratory tract: The first sputum in the morning, send for examination in time <1h ⑥ Cerebrospinal fluid: Sterile, Neisseria, Streptococcus pneumoniae, Haemophilus influenza → Insulated and sent for inspection ⑦Wounds, burn wounds, abscesses:

①Direct smear microscopy ②Isolation and culture identification-gold standard ③Serological test (antibody): The difference between the two sera is 4 times, IgM has early diagnostic significance ④Pathogen-specific antigen ⑤Pathogen nucleic acid

① Resistance mechanism: hydrolase/passivation enzyme; efflux of pump; change of target site; biofilm formation; integrator system of resistance genes ②Drug sensitivity test: K-B disk agar diffusion-SIR; dilution method-MIC; E test ③Detection experiments on key drug-resistant strains ④Detection of drug resistance genes of pathogenic bacteria

①Epidemiological characteristics: ②Inspection items and clinical applications:

①HAV ②HBV-two and a half ③HCV ④HDV

① Concept ② The most common - Gram-negative bacteria, lower respiratory tract infection