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331 Cards in this Set
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Hematocrit - definition |
The ratio of volume of blood cells to the volume of the whole blood. |
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Hematocrit - cell distribution |
RBC - 99% Leukocytes 0.1-0.2% Thrombocytes: 0.8-0.9% |
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Hematocrit - normal range |
Male: 42-52% Female: 37-47% |
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Hematocrit - evaluation of result |
Low hematocrit value - Anemia or recent bleeding High hematocrit value - Polycytemia - Dehydration - Physiological |
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Hayem´s solution |
A hypertonic salt which prevents the RBCs from sticking together. Since it´s a hypertonic solution it shrinks the ER. |
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Burker´s chamber |
A type of counting chambers. Hemocytometers. |
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RBC counting dilution |
Diluted 1:100 with hayem´s solution.
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L-law |
Left hand or lower sides of the area are counted, while the right side and the upper sides are not. |
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Burker chamber squares |
Large square - used for leukocytes - 1/5*1/5mm Small square - RBC - 1/20*1/20 mm Rectangle - RBC and thrombocytes - 1/5*1/20mm |
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RBC count - calculation and evaluation |
RBC/ul = RBC count (40-40 small sq)/volume (1/4000mm^3) * dilution(100x) Low RBC - anemia - Decreased production of RBC in bm - Increased rate of RBC loss High RBC - polyglobublia -Polycythemia vera - Acclimatization to high altitude |
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RBC - normal range |
Male: 4.5 -6 million/ul Female: 3.8-5.2 million/ul |
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What does the mean RBC diameter tell us? |
The mean diameter and distribution width gives us information regarding anemias and other hematological disorders. |
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RBC mean size - procedure |
Must be diluted with NaCl solution. If the blood sample is not diluted enough the RBC will stack in layers, and size can´t be measured. If the sample is over diluted the cells will float, and can´t be measured. |
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RBC mean size - Evaluation |
Price-Jones curve Normal curve - 7-8um mean size Left curve - Small RBC - Microcytosis - Ex. Fe deficiency Right curve - Large RBC -Macrocytosis - Vitamin B12 defiency |
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Platelet count - direct vs indirect |
Indirect is done by counting the platelet in blood smear and comparing them to RBC count. This is just an estimation.
Direct method requires thrombocyte-rich plasma and can be done by: - Lysin RBC in procain - Low speed centrifugation - Reer-Ecker´s solution
We use the Reer-ecker´s solution |
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Platelet count - Dilution |
We use Reer-ecker´s solution
- A few drops of Loffler´s methylene blue dissolved in 3.8% Na-citrate Contain anticoagulant |
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Platelet count - normal range |
Normal range of thrombocytes is 150.000-400.000/ul |
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Platelet count - evaluation |
Low - Thrombocytopenia -Production is decreased - Breakdown is increased - Usage increased High - trombocytosis - Essential - Reactive |
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WBC count |
A test to determine the number of leukocytes in the blood. It does not differentiate between the different types of WBC.
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WBC count - Dilution |
It´s diluted 1:10 with Turk´s solution. |
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Turk´s solution |
Used in WBC count It contains 1% acetic acid which hemolyses RBC, but not WBC. it also contains gentian violet which stains the nucleus of WBC. -Doesn't´t hemolys WBC because they are resistant. |
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WBC count - Burker´s chamber |
Count WBC in 20 large squares |
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WBC count - evaluation |
Normal range: 4000 -10000/ul Low - Leukopaenia - Toxic bone marrow effects - Some infections High - Leukocytosis - inflammation - Strenuous exercise - Epilepsy - EMotional stress, labour etc. |
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Differential leukocyte count |
Performed using stained blood smears. This procedure is the Pappenheim´s procedure, which used the May-Grunwald-Giemsa staining.
First stained with May-Grunwald, then the giemsa stain. |
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Pappenheim´s procedure |
Used the May-Grunwald-Giemsa staining |
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Neutrophilic leukocytosis |
Acute bacterial inflammation
Sterile inflammation |
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Eosinophilic leukocytosis |
Allergic disorders
Parasitic infections Malignancy Systemic autoimmune diseases |
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Basophilic leukocytosis |
Inflammatory reactions Myeloproliferative diseass |
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Monocytosis |
Chronic bacterial infections Systemic autoimmune diseases Inflammatory bowl diseases |
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Lymphocytosis |
Viral infections Pertussis |
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Reticulocytes |
Reticulocytes are immature RBC´s which we find in circulation. Around 1% of RBC are replaced each day by reticulocytes. Reticulocytes still have remnants of protein translation machinery. |
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Supravital dyes |
Supra vital dyes stain unfixed cells outside the body. Degradation of cells causes the preparation only to be viable for a short period of time. Brilliant cresyl blue |
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Briliant cresyl blue stain solution |
A supravital dye we use to stain reticulocyte, during counting. |
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Reticulocyte count - Range |
Normal range: 0.7-1.5% |
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Reticulocyte - Aregenerative status |
Aregenereative status is when you have a low reticulocyte count. - Aplastic anaemia |
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Reticulocyte - hyperregenerative status |
Hyperregerative status is when you have a high reticulocyte count. Haemolytic anaemia or haemorrhagic aneaemia |
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ESR |
Erythrocyte sedimentation rate is the rate at which RBC settle down in a tube in one hour. It´s measured in mm/hour. Westergren´s method is used, dilution 4:1 with Na-citrate solution. Sodium-citrate is an anticoagulant |
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ESR - factors affecting |
- Shape and size of RBC - RBC count - Viscosity of plasma - Albumin/globulin - fibrinogen ratio |
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Rouleaux |
Columns which RBC form when they stick together. It affects the ESR, since it lowers surface to volume. Negative charge due to acidic residues and albumin block rouleaux formation. But globulins and fibrinogen carry less negative charge, and therefore acts as glue to stick RBC´s together. |
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What causes increased ESR? |
Increases due to pregnancy, infections, inflammations and tumor diseases. |
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Westergren method and tubes |
Used in erythrocyte sedimentation rate. |
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ESR - normal range |
Male: 2-6 mm/hour Female: 3-10 mm/hour |
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ESR - evaluation |
High ESR - Pregnancy - Inflammation - Tumor - Anaemia - Hydraemia Low ESR - Hypofibrinogenaemia - Macrocytic anaemia - Polycytaemia - Exsiccosis |
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Viscosity - factors |
Linear: Formed elements-Hct, WBC, RBC shape Plasma proteins and lipids Vessels diameter Inverse: Flow rate Temperature Blood: 4-6 Plasma: 1.8-2 |
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Osmotic resistance |
Osmotic resistance is the minimum concentration of NaCl the RBC can withstand without hemolys. We use different NaCl solutions |
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Osmotic resistance - hypotonic |
Hypotonic solution causes the RBC to take up water and swell. If the osmotic concentration is to small the membrane ruptures and hemolysis occurs. |
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Osmotic resistance - isotonic |
RBC retain their bioconcave shape |
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Osmotic resistance - hypertonic |
They shrink because of water loss to the hypertonic solution. |
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Osmotic resistance - Evaluation
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Clear supernatant + sediment -> no hemolysis Reddish supernatant + sediment -> partial hemolysis Red liquid -> Complete hemolysis |
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Osmotic resistance - normal range |
Min resistance: 0.46-0.42% NaCl Max resistance: 0.34-0.30% Nacl |
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MCV |
Mean corposcular volume - Avg volume of red blood cells - MCV= Htc/RBC-count Normal range 80-95 Fl - High values indicate macrocytosis - Low values indicate microcytosis |
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MCH |
Mean corpuscular hemoglobin - Hb content in one RBC - MCH= Hb/RBC-count Normal range : 26-36pg - Hyper - Hypochrom |
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MCHC |
Mean corpuscular hemoglobin concentration - Average Hb- concentration - MCHC= Hb/Htc Normal range: 310-360g/liter |
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Drabkin´s method |
Used in determination of hemoglobin concentration. Involves osmotic hemolysis of RBC and transformation of hemoglobin molecules to cyan-hemiglobin. - Very stable and can be determined photometrically. |
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Drabkin-reagents
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Used in hemoglobin concentration determination Potassium ferricyanid Potassium cyanide Potassium dihydroen phosphate |
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Hb concentration - Photometry |
Photometry of sample and control at 540 nm. Comparison with control tube which validates answers. Csample/Cstd=Esample/Estd |
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Hb concentration - Normal range |
120-180 g/L |
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Hb concentration - evaluation |
Reduced - Anemia - Hyperhydration Increased - Polycythemia - Exsiccosis |
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Hb spectroscopy |
O2- Hb - 542 and 578 nm Desoxy - Hb - 555 nm Co - Hb - 539 and 570 nm Met- Hb - 540, 580, 630 |
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Hb gas compounds - Oxygenated Hb |
O2 bind to Hb Two stripes in yellow field N arterial blood of a healthy person |
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Hb gas compounds - Desoxygenated Hb |
CO2 bind to HB 1 stripe at yellow field N in small amounts in venous blood If absolute amount increase, bluish-purple discoloration of skin |
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Hb gas compounds - Carb-Hb |
Carboxyhemoglobin 2 stripes of yellow and green Can not release oxygen in presence of moderate reducing agents. Doesn´t change when sodium-dithonite is added |
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Hb gas compunds - Met-Hb |
Created by oxidizing hemoglobin to methemoglobin with potassium-ferrycyanide Met binds O2 stronger than Hb. Not deoxygenated by slight reducing agents. |
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Bleeding time |
Time from puncture until cessation of blood. Tells us the efficiency of the hemostasic processes in the capillaries, and the function of platelets and vascular reactions. |
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Bleeding time normal range |
2-3 minutes Longer than 5 minutes indicate thrombocytopenia or impairment of platelets function |
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Clotting time |
The time it takes for a blood samples coagulate when placed on glass. It reflects the activity of the intrinsic pathway of blood coagulation system. Stop when first fibrin fiber appears |
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Clotting time - normal range |
5-10 minutes
Increasing temperatur decreases the clotting time |
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Prothrombin time |
Test reflects the extrinsic pathway. The time needed for the first fibrin fiber to appear reflect the the activity of the extrinsic pathway. Can be used to check vitamin K status or liver function. Use thromboplastin + Ca reagent |
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Prothrombin time - normal range |
15-20 sec |
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INR |
International normalized ratio INR=(PT/NPT)^isi PT- patient prothrombin time NPT - Normal prothrombin time ISI - internation sensitivity index 1-1.25 |
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ABO blood typing |
Composed of four main blood types. A, B, AB and O. O type - only H A or B type - either A or B antigens AB type - Both A and B antigens Blood to be diluted with NaCl |
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Bombay blood type |
Lack the H antigens and AB. Not a universal donor |
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AB type |
A universal recipient |
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Landsteiner law |
A person does not have antibody to his own antigens. Each person has antibody to the antigen he lacks. |
Agglutinogens and agglutigens |
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Agglutinogens |
Antigens Glicolipids or glicoproteins on the RBC surface Difference between antigenes is determined by epitopes. |
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Agglutinins |
Antibodies
LgM -> plasma Human blood contains natural Antibodies against those agglutinogens that we dont have in our ABO system. LgG in Rh. |
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ABO determination - 1 sided test vs 2 sided |
1 sided test - known serum + unknown blood. 2 sided test - Known serum + unknown blood. - Known blood + unknown serum |
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In vitro vs in vivo - blood typing |
In vitro the blood precipitation = agglutination In vivo hemolysis |
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Rh blood group |
Contain D, E, C, c, f, e Ag, D-Ag. D is the strongest antigen. Europe: 85% Rh+ and 15 Rh- |
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Which antigen penetrates the placenta? |
D-Ag |
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Rh- determination |
Anti-D serum and NaCl for control |
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Tidal volume |
Air moved into or out of lungs during one cycle of quiet breath 500 ml |
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Eupnoea vs dyspnoea vs apnoea |
Eupnoea is normal good, unlabored ventilation. Dyspnoea is uncomfortable awareness of breathing, shortness of breath. Apnoea is temporary suspension of breathing. |
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Inspiratory reserve volume |
The additional air that can forcibly be inhaled after inspiration of tidal volume. 2500 ml. |
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Expiratory reserve volume |
The additional volume of air which can forcible be exhaled after normal expiration. 1000 ml. |
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Residual volume |
Volume which cannot be exhaled voluntarily. About 1500 ml. |
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Inspiratory capacity |
Volume of air that can be inhaled during a full inhalation from resting expiratory postion. It´s equal to tidal volume plus inspiratory reserve volume. 3000 ml |
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Vital capacity |
Maximum amount of air a person can exhale from lungs after maximum inhalation. Avg of 4000 ml in males and 3100 in females. |
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Functional residual capacity |
Volume of air present in lungs after normal expiration. Cannot me measured with spirometer, since it includes the residual volume. 2500 ml |
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Total lung capacity |
Volume in the lungs at maximal inflation. The normal value is 5500 ml |
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MBC |
Maximal breathing capacity
The maximum amount of gas a person can inhale and exhale per minute by breathing as quickly and deeply as possible. 70-200 l/min |
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FEV |
Forced expiratory volume The volume exhaled during the first seconds of a forced expiratory maneuver. |
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Obstructive respiratory disorders |
Bronchial asthma, chronic bronchitis or emphysema. This causes FEV1 to decrease and tiffany index is decreased, in relation to VC. Increased RV Increased TLC |
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Restrictive respiratory disorder |
Chest deformity or reduction of pulmonary surface causing decreased lung volume. VC and TLC is smaller tha normal. FEV1 is decreased due to reduction in VC. But tiffanea-index is normal |
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Hyperventilation |
Occurs when rate and quantity of alveolar ventilation of CO2 exceeds the body´s production of CO2
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Valsalva maneuver |
Performed by doing forceful attempted exhalation against closed glottis. This creates a positive intrapleural pressure, which blocks the blood from entering the right side of the heart from the central veins. This causes the body to compensate with sympathetic activity. -Increased heart rate, vasoconstriction and increased total peripheral resistance. |
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Muller maneuver |
Forced inspiration made with closed glottis. This creates negative intreplauleral pressure, flooding the lungs and heart with blood. The stroke volume will decrease du to increased wall tension. This leads to weak radial pulse. Frank-Starling law |
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Intrapulmonary pressure during normal inhalation and exhalation |
Intrapulmonary is lower during normal inhalation and higher during normal exhalation |
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Intrapleural pressure during normal inhalation and exhalation |
Pressure remains negative til the end of exhalation. During inhalation the expansion of the thorax causes the intrapleural pressure to decrease. |
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Donder´s model |
Displays the relationship between the intrapleural and intrapulmonary pressure, and the volume changes. |
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Pulmonary compliance |
The capability of lungs and chest to distend under pressure. It´s measured by pulmonary volume change per unit of pressure change. DV/Dp |
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total pulmonary compliance |
In the case of total pulmonary compliance is the elasticity of the elastic and collagen fibers found in the parenchyme of the lung + surface tension. Saline decreases the surface tension to almost zero. |
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Pulmonary compliance - normal value
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1 liter/kPa |
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Metabolic rate - indirect |
Metabolic rate can be measured indirectly. If we measure the amount of O2 used in oxidation, which is the same as the O2 demand. The consumed O2 is than proportional with heat release. |
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Metabolic rate - influencing factors
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Temperature, position, medical substances, mental and physical state, and diet. We can measure the basal metabolic rate if we standardize these influencing factors. |
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Resistance of the respiratory system |
Elastic resistance: 80-90% - Elastic resistance of the lungs - Elastic resistance of the chest wall Resistance of airways: 10-20% - Sympathetic causes less resistance (dilation) - Parasympathetic causes resistance (constriction) |
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Belák-Illényi apperatus |
Used to measure the oxygen consumption of a rat. When the rat consumes O2 it produces CO2 and water vape, this decrease in O2 is adjusted by fluid administration, which directly equals the O2 volume consumed. |
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In situ |
On site |
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Electrical stimulation of heart - systole |
No effect since the heart muscle is in a absolute refractory period. |
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Electrical stimulation of heart - diastole |
This causes premature ventricular contraction, or PVC. This is followed by a compensational pause. Both of these can be seen on the ECG. The pacemaker is not effected by this, so the heart rhythm returns to normal. |
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PVC or ES |
Premature ventricular contraction or extrasystole - caused by electrical simulation during diastolic phase. |
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Electrical stimulation of heart in systole with serial stimuli |
No effect since the cardiac muscle is in absolute refractory period during the whole systole.
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Thermal stimulation - sinus node |
Effect of warming: frequency of contractions increases. Effects of cooling: frequency of contraction decreases. No change in magnitude of contractions. |
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Thermal stimulation - Ventricular muscle |
Effect of heating: Magnitude increases Effects of cooling: Magnitude decreases NO change in frequencies. |
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Stannius-ligature I |
This causes binding off sinus venosus.
Pacemaker frequency of sinus venosus remains the same, but the contractions stops. After 15-20 minutes the heart restarts with a lower heart rate. Not only sinus has pacemaker activity, the atrium takes over. |
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Bowditch's all or nothing law |
If that stimulus exceeds the threshold potential, the nerve or muscle fiber will give a complete response; otherwise, there is no response. |
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Ligature of stannius II |
Binding of the atrio-ventricular border Blocking the AV. Ventricular stop beating, but atria continue in same rhythm. After a while ventricle starts contacting in a separate frequency, lower than the atrial one. Specific regions of ventricles has a pacemaker function, but slower than original. |
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Atrio-ventricular dissociation |
Happens during ligature of stannius II. It causes the atrium and the ventricle to beat totally independent. |
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Ligature of stannius III |
Apex is cut of from the heart and placed in ringer´s solution. No spontaneous contractions since the ventricular working fibers have no pacemaker activity. Mechanical or electrical stimuli causes contraction. So conduction and contraction remains. |
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Summation of frog heart |
Summation is when we have a series of subtreshold stimuli are added together, and at a critical momentthey evoke the maximal contraction of the heart. |
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ECG |
Electrocardiogram
Registration of voltage changes Impulses towards the electrode gives positive curve. Impulses away from the electrode gives negative curve. |
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Einthoven´s triangle |
Lead dependent changes of amplitudes of the ECG waves are explained by einthoven´s triangel. I - Right arm- left arm II- Right arm - left foot III - Left arm - left foot |
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Einthoven´s rule |
I+III=II |
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P- wave |
Positive wave Atrial depolarization D: 0.1 sec A: 0.1-0.2 mV P-wave is positive in I, II, aVF, V4-V6 sometimes negative in: III, V1, V2 Always negative in aVR |
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Atrial repolarization in ECG |
Cannot be seen, as it will merge with QRS. |
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PQ interval |
Beginning of the P wave and ends at the beginning of the QRS complex. Time that signal from SA node to reach the ventricles. D: 0.12-0.20 sec |
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Atrioventricular transmission |
The time it takes for the signal to travel from SA node to reach the ventricles. PQ interval |
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H wave |
Found in the PQ segment, but not visible in a regular ECG. |
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QRS complex |
Ventricular depolarization 1st negative wave is the Q wave. First positive after Q wave is R wave A: Q: 1/4 of R, R: 1-21 mm, S:1/3 of R D: 0.1 s Positive: I, II, III, aVF Negative: aVR |
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QRS - 5 parameters
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1. Duration of QRS complex 2. Amplitude of QRS 3. Presence, duration and amplitude of Q 4. Electrical axis 5. Transition zone in chest leads |
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QRS - 1. duration of QRS complex |
Duration of QRS should be between 0.04 and 0.1 s. Measurement should be done in standard limb leads. |
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QRS - 2. amplitude of QRS complex |
The amplitude has to be minimum of 0.5 mV in frontal leads. Maximum in limb leads of 20 mm |
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QRS - 3. Presence, duration and amplitude of Q wave |
W wave is important in diagnosis myocardial infarction. D: 0.03s A: 1-2mm |
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QRS - 4. Electrical axis |
Between -30 and 100* |
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Determination of E and J point |
E point is at the end of the PQ segment J point is at the end of the QRS complex. |
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ST segment |
Starts at the end of S wave and lasts until the beginning of T wave. Isoelectric at rest |
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T wave |
T wave is produced by ventricular repolarization. A: 5-15 mm D: 0.15-0.25 sec Positive in I, II, aVF and V4-V6 Negative in aVR Variable in III, aVL, V1-V3 |
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aVR |
aVR always gives negative P and T wave. |
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QT interval |
Electrical systole starts at the beginning of Q and ends at T D:0.4 sec Highly heart rate dependent. |
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U wave
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Rare waveform that can in some causes lead to wrong diagnosis if its not considered. |
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ECG - heart rate determination |
1. When heart beats are rhythmic we measure between two successive R waves. 2. Estimation - 1 thick division between heart rates is 300, 2 is 150 and 3 is 100 per minute. 3. Based on 3 seconds mark on the edge of the ECG paper. |
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PCG |
Phonocardiography The amplitudes of the waves are determined by the frequency. 1st heart sound is the closure of AV valves 2nd heart sound is the closure of semilunar valves. 3rd is the vibration of the ventricular walls, |
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Blood pressure measuring |
Blood pressure can measured directly (animals only) and indirectly. Indirectly with a sphygmomanometer + stethoscope |
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Pulsoxymeter |
Measures finger pulse and oxygen saturation of hemoglobin. Arterial oxygen saturation should be 95-100% |
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Blood pressure with sphygomomanometer |
Inflate sphygomomanometer to above 180 mmHg, collapsing major arteries in the arm. Then slowly release air. Sound is produced by turbulent blood flow 1st sound is systolic blood pressure -The blood flowing in the artery is greater than the pressure in the cuff. As the pressure drop and all sound disappear we have diastolic pressure. |
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Korotkov sounds |
Turbulent blood flow producing sound during blood pressure measurement with sphygomomanometer. |
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Physical fitness index |
Harvard step-test 1. step up and down 30 times per minute. 2. rest for 1 min 3. check pulse after 1, 2 and 3 minutes PFI=Exercise duration*100 / sum of counted pulse*2 Age-dependent index |
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weak vs strong vagus stimulation
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The heart rate decreases due to weak vagus stimulation. While strong stimulation current stops the heart. Because the vagus nerve is inhibitory of the heart. |
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Effects of ions on the isolated frog heart - Calcium |
Calcium - stops in systole because we increase the extracellular concentration, which prevents the muscle cell form pumping out calcium, and the cell can´t repolarize. |
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Effects of ions on the isolated frog heart- Potassium |
Potassium - heart stops in diastole We increase the potassium concentration, and the late potassium pumps can´t pump out. Because of this the cell will not be depolarized. |
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Effects of ions on the isolated frog heart- Physiological saline |
Will stop heart in diastole The cells runs out of calcium and potassium if there isn´t a supply from extracellular fluids. |
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Effects of adrenalin on frog heart |
Epinephrine is a sympathetic stimulant. Increases therefor contractions and heart rate. Positive inotropic (amplitude of contractions) Positive chronotropic (HR) |
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Effect of acetylcholine |
Acetylcholine is a parasympathetic stimulant, suppressing the heart. It gives a negative inotropic (contractions) and negative chronotropy (HR) Can cause heart to stop in diastole Antropine inhibits the effects of acetylcholine. |
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Primary waves |
Changes of the cardiac cycle cause primary waves. |
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Secondary wave |
According to herin-breuer reflex Which is triggered to prevent overfilling of lungs
Inspiration: HR up, BP up Expiration: HR down, BP down |
Herin-Breuer reflex |
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Tertiary waves |
Called meyer waves Cause increased BP when chemoreceptors are stimulated.
Hypoxia can lead to Meyer waves |
Meyer waves |
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Effect of adrenaline - small dose |
In small dose moderately decreases blood pressure. B2 receptors are closer, and therefore mostly affected. These cause vasodilation, which causes drop in blood pressure. |
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Effect of adrenaline - Large dose |
Large dose of epinephrine causes increase of blood pressure and heart rate. In the viscera, further out the A1 receptors are found in larger numbers than beta. The alpha 1 causes vasoconstriction and the B1 causes increased heart rate. a1 -> BP( vasoconstriction) B1 -> increased heart rate |
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Loven reflex - weak electrical stimulation |
Sensory nerve stimulation Causes increase in vasomotor activity and rise in BP. local vasodilations override, causing a depressor response |
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Loven reflex |
Sensory nerve stimulation Local vasodilation General vasoconstriction Pressor response, causing increases BP, RR and TV. |
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Effect of acetylcholine |
decrease in blood pressure and heart rate |
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Baroreceptor mechanism |
A mechanism that keeps the arterial blood pressure almost constant. Baroreceptors are stretch receptors in the walls of vessels. Carotid sinus and aortic arch monitor the arterial blood pressure. |
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Pressure falls in carotid sinus |
This causes a lower baroreceptor activity. This causes an overall vasoconstriction and heart rate and respiration rise |
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Asphyxia or hypoxia |
Strong stressor, leads to adrenalin release. This result in increased blood pressure and dyspnea. |
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Depressor reflex |
Stretch of arterial wall causes decrease in blood pressure and heart rate. Baroreceptors |
Arterial wall |
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Transection of vagus nerve - peripheral and central |
Peripheral will induce decrease blood pressure, heart and respiratory rate. Central - weak stimulation cause irregular respiration, strong stops respiration. Since the vagus nerve carries afferent fibers from lung baroreceptors. During stimulation these tell the brain that the lungs are filled. |
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Endothelin |
Produced by endothelium. constricts blood vessels |
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Nitric oxide |
Vasodilator produced by endothelium |
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ERDF |
Vasodialtor produced by endothelium |
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Prostacyclin |
Vasodilator produced by endothelium
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Increased lactate concentration, hydrogen ion concentration, potassium ions concentration and reduced oxygen tension causes vaso.. |
Vasodilation |
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What causes a right shift in the oxygen-hemoglobin saturation curve? |
Acidosis and an increase in 2,3-diphosphglycerat |
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How is urine moved from kidney to bladder? |
Peristaltic contractions |
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What is the difference between the glomerular filtrate and the plasma |
The filtrate has less proteins, as they are not filtrated out. |
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What does the juxtaglomerular apperatus regulate? |
It regulates the glomerular filtration. |
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What increases the glomerular filtration rate |
Increased sympathetic stimulation, dilation of afferent arterioles, constriction of efferent arterioles. |
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ANH |
A powerful vasodilator |
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How is glucose and amino reabsorbed in kidneys? |
Secondary active transport |
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How can substances move from blood into tubular fluid |
Via tubular secretion and glomerular filtration |
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What produces 1,25-dihydroxycholecalciferol |
Kidney |
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Which blood flow is higher in the kidney
Cortical or medullary |
Cortical |
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When can airways resistance be measured? |
Only when air is flowing into or out of the lungs |
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How is CO2 mostly carried in the blood |
As bicarbonate ions in the plasma |
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What would lack of ADH cause |
It would cause maximally diluted urine, as ADH functions are as a vasopressin. keeping water in the body |
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What´s the function of thick ascending limb cells in the kidney |
Actively transporting Na+, K+ and Cl- |
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Arterial pH below 7.35
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Metabolic acidosis |
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Damage to glossopharyngeal nerve effects |
Pharyngeal phase of swelling and the carotid sinus reflex. |
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Receptive relaxation in stomach |
During this period there is no efferent input via the vagus nerve |
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Gastrin secretion is inhibited by? |
Inhibited by H+ levels
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Gastrin secretion is stimulated by?
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Activated by stretch, peptides and neural signals |
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Gastrin - function |
Acid secretion and motility Mucosal growth in gut and stomach |
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What trigger the enterogastric inhibitory reflex? |
Acidic or hypertonic solutions in duodenum |
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Where are bile salts synthesized? |
In the hepatocytes, only. |
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In which phase of stomach secretion does the greatest amount of secretion take place? |
Gastric phase |
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Difference between serum and plasma |
Plasma has fibrinogen |
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When is erythroblastosis fetalis most likely to become a problem in Rh-negative mothers as? |
Second Rh-positive fetus develops |
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Term for slow heart rate |
bradycardia |
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Term for fast heart rate |
Tachycardia |
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What prevents overfilling of lungs during normal respiration? |
Hering-Bruer reflex |
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function of LDL |
Transport of lipids from the liver to tissues Reverse of HDL´s function |
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HDL function |
Transport of the lipids from the tissues to livers. Reverse of LDL´s function |
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Growls from stomach is part of which phase |
The cephalic phase |
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Which type of ingested food would stay for the longest period in the stomach? |
Meal with high concentrations of lipids. |
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Which part of the GI system does the following: Storage of undigested material absorption of water Absorption of electrolytes |
Large intestine |
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When does the breakdown of proteins vs carbohydrates begin? |
Protein: Stomach Carbohydrates: salivary glands |
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Intestinal epithelial cell secretion Brush border |
Maltase, aminopeptidase, lactase, sucrase |
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Function of chylomicrons |
Enables fat and cholesterole to move in the blood stream |
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Gastrocolic reflex |
Is a reflex controlling motility in the GI tract, in the colon. Gastrin, CCK, serotonin |
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Histamin secretion in stomach causes |
This can caused hyper secretion of HCL acids by parietal cells.
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Stimulation of b1 |
Increase in heart rate, impulse conduction, contraction. Positive chronotropic, dromotropic and inotropic effect |
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Stimulation of a1 |
Vasoconstriction of blood vessls |
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Stimulation of b2 |
Smooth muscle relaxation |
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Blocked forced inspiration |
Muller manoeuvre |
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Blocked forced expiration |
Valsalva manoeurvre |
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Blocking forced expiration 1.Decreased or increases peripheral resistance 2.Decreased or elevated jugular venous pressure 3. Drop or increased blood pressure 4. Tachycardia or bradycardia 5. Increased blood volume in systemic or pulmonary circulation? |
1. Increased peripheral resistance 2. Eleveated jugular venous pressure 3. Drop in arterial blood pressure 4. Tachycardia 5. Increased blood volume in systemic |
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Blocking forced inspiration 1.Increased or decreased pO2 in blood 2.Decreased or elevated jugular venous pressure3. Drop or increased blood pressure 4. Tachycardia or bradycardia 5. Increased blood volume in systemic or pulmonary circulation? |
1. Decreased pO2 in blood 2. Elevated jugular venous pressure ??? 3. Drop in arterial blood pressure 4. tachycardia 5. Increased blood volume in pulmonary circulation |
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What leukocytes is increased in numbers during allergic diseases? |
Eosinophil |
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What can inhibit blood clotting? |
Antithrombin, heparin Deficiency in vit k |
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How to demonstrate summation of electric stimuli? |
Apply below threshold stimulus, and increase frequency of it. |
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A slide with cover slip is needed in? |
Determination of retikulocyte count |
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Hyperventilation results in what? |
Decreased frequency of respiration |
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Carotid sinus reflex |
Stretch of arterial wall. Causes decrease in BP and HR. Receptors are baroreceptors |
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Chemoreflex |
Caused by hypoxia. Causes increased HR, TPR and BP. Chemoreceptors |
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Bezold-Jarish reflex
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Stretch of ventricular wall. Decrease in HP and BP Pressure receptors |
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Brainbridge reflex |
Increase central venous pressure and therefore stretch in atrial wall. Increase in HR and BP Baroreceptors |
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Cushing reflex |
Increased intracranial pressure Decrease in HR and increase in BP. intercranial baroreceptors |
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Lovenreflex |
Painful stimulus Causes increase in BP, HR and TPR |
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Goltz reflex |
Mechanical stimulus of the abdomen causing decrease in heart rate |
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Oculo-cardial reflex |
Compression of eyeball causes decrease in heart rate. |
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Atrialrenal reflex
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Stretch in the atrial wall. Baroreceptors in the right atrium |
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Systemic vs pulmonary circulation - cardiac ouput |
Cardiac output can be measured on each side, and they are equivalent. |
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Small dose of epinephrine causes |
Vasodilation, or a decrease in the total peripheral resistance |
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Transpulmonary pressure equals |
Alveolar pressure minus intrapleural pressure |
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At the end of expiration it elastic recoil of the lung or chest wall the greatest? |
At the end of respiration at rest the inward directed elastic recoil of the lung balances the outward elastic recoil of the chest wall.
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Surfactant - size of alveoli |
The surfactant has a greater effect on smaller alveoli than in larger, meaning it can reduce it's surface tension further |
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What increases the release of aldosterone and activates thirst? (vasoconstrictor) |
Angiotensin II |
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Which system returns ions and proteins to the circulatory system? |
Lymphatic system |
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Which law describes the intrinsic relationship between end-diastolic volume and stroke volume |
Frank-starling law |
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Decreased pH level can cause vaso..?
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Local vasodilation |
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Increased metabolism, CO2 production and K+ level can cause vaso..? |
Local vasodilation |
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What happens during the processing of glomerular ultrafiltrate? |
The transport maximum will be reached, and glucose which is present in excess to this will appear in the urine |
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What stimulates gallbladder contraction, pancreatic enzyme secretion and HCl seceretion by parietal cells |
Cholecystokinin |
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Renin |
An important enzyme in blood pressure regulation. It´s secreted by the liver, and it acts on angiotensin.
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Hypoventilation can cause |
Respiratory acidosis Can cause the pH of the blood to decrease |
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What does hypercapnia stimulate |
It stimulates the central chemoreceptors |
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Hyperventilation |
Decreases cerebral blood flow, increases blood pH, causes hypocapnia, and increases cardiac output. |
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Number of white blood cells
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6000–8000/μl
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WBC – percentage of each type
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62% neutrophils
2.3% eosinophils 0.4% basophils 5.3% monocytes 30% Lymphocytes |
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WBC – size'
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Eosinophils – 12
Neutrophils – 12 Basophils – 8–10 Monocytes – twice as big as an RBC |
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Physiological range of platelets
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150000 – 300000 / microliter
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Hemaglobin concentration in blood
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120–180 g/l
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Hemaglobin molecular weight
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64.5 kDa
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Iron amount and distribution
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4–5 g of iron
Hemoglobin 65–70% Storages 20–25% Myoglobin 3.5–10% Enzymes 5% Serum 1% |
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Ferritin– normal range
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17–304 μg / l
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Prothrombin concentration in normal plasma
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15 mg/dl
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Fibrinogen in plasma
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100 to 700 mg/dl
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Bleeding time
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2–3 min
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Clotting time
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5 – 10 min
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Prothrombin time
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13–22 seconds
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Normal systolic pressure
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120 mmHg
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Normal diastolic pressure
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80 mmHg
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Velocity of pulse wave – aorta
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4–6 m/sec
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Blood pressure and pulse – Baby
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80/ 50 and 110
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Blood pressure and pulse – Child
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90/60 and 100
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Blood pressure and pulse – Adolescent
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105/70 and 100
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Hematocrit normal range – male and female
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Male: 42% – 52%
Female: 37% –47% |
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RBC – male and female
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Male: 4.5 –6 million/μl
Female: 3.8–5.2 million/μl |
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Capillary dimensions – systemic and pulmonary
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systemic diameter: 6μm, length 750μm
Pulmonary diameter: 8 μm, length 350μm |
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Capillary structures – pores
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Intra–cellular: 20–25nm
Inter–cellular: 4– 4.5 nmr |
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TPR
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Total peripheral resistance
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TPR – arteries, arterioles, capillaries and veins
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Artery: 10% of TPR
Arterioles: 50–55% of TPR Capillaries: 30–35% of TPR Veins: 5% of TPR |
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Reynold´s number
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Re= (v * 2r * r)/ h
re>200 to 400 turbulent flow will occur in some parts. Re> 2000 turbulence will always occur |
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Normal right atrial pressure
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0 mm Hg
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Pressure in right ventricle
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Systolic: 25 mm Hg
Diastolic: 0 –1 mm Hg |
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Mean pulmonary arterial pressure
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15 mm Hg
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Mean pulmonary capillary pressure
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7 mm Hg
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Mean pressure in left atrium and major pulmonary veins
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about 2 mm Hg
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Blood volume in lungs
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450 ml
70ml of this in the pulmonary capillaries |
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Normal coronary blood flow
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225 ml/min
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Cerebral blood flow
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60 and 160 mm Hg
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Blood flow and oxygen consumption of organs
– Except lung |
Splanchnic area: 25–30% of CO, 25–35% O2
Kidney: 20–245 of CO, 6–7% of O2 Brain: 14–15% of CO, 18% of O2 Skeletal muscle: 15–20% of CO, 19–20% of O2 Skin, bone: 4–10% of CO, 2–5% of O2 Coronary blood flow: 5% of CO, 10–12% of O2 |
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Highest specific blood flow
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Glomus aorticum and caroticum is highest
2000–3000 ml/100g / min |
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Highest specific O2 consumption
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Heart
8ml/min/100g |
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Blood volume in splanchnic area
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1/5 of total blood volume
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Skin circulation blood flow – resting condition
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100 ml/min
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Local vasodilators – Metabolits
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Local acidosis H+
K+ ion Lactate Adenosine Hypoxia (vasoconstrictor in lungs.) Hypercapnia |
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Local vasodilators – Others
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NO
PG 12 – prostacyclin Histamine Bradykinine Substance P Neurokinin A Vasoactive Intestinal polipeptide Calcitonin gene–related peptide Adenosine |
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Vasoconstricotr
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Epinephrine (via alpha 1, but dilator via beta 2. )
Norepinephrine (via alpha 1, but dilator via beta 2) Endothelin Vasopressin Angiotensin II Thromboxane A II ATP PGF |
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Intrapleural pressure during inspiration and expiration
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Inspiration:P(intrapleura)= –8 cm H20
Expiration:P(intrapleura)=–5 cm H20 |
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Alveolar ventilation
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4200 ml/min
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Saliva produced each day
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1–1,5 liter/day
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Gastic juice produced
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2.5 –3.5 liters/day
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GCP, PTP, COP, EFP
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Glomerular capillary pressure
Proximal tubular pressure Colloid osmotic pressure Effective filtration pressure |
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GCP – Afferent and efferent
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Afferent GCP: 60 Hg mmEfferent GCP: 60 Hg mm
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PTP – Afferent and efferent
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Afferent PTP: 18 Hg mmEfferent PTP: 18 Hg mm
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COP – afferent and efferent
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COP afferent: 28 Hg mm
COP efferent: 36 Hg mm |
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EFP – Afferent and efferent
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EFP afferent: 14 Hg mm
EFP efferent: 6 Hg mm |
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Renal blood flow – cardiac output
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20–24% of CO
1200–1300 ml/min |
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RPF
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Renal plasma flow: 600–800 ml/min
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GFR
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Glomerular filtration rate: 100–125 ml/min
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Ff
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Filtration factor: 0.2
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Relative blood viscosity
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4–5
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Hemoglobin concentration in blood
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120–180 g/L
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What is the effect of thrombosthenin on platelets? |
Cause the platelets to contract, we find it in the cytoplasm together with actin and myosin molecules. |
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What is the most important function of ER and golgi in platelets? |
Store large amounts of calcium ions. |
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Growth factor in platelets |
It causes vascular endothelial, vascular smooth muscle and fibroblasts to grow. Help repair damaged vascular walls. |
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Extrinsic vs intrinsic pathway |
Extrinsic pathway occurs when there is tissue trauma, while the intrisinc pathway starts with blood. They both lead to the formation of a prothrombin activator. |
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Factors in extrinsic pathway |
Factor V, VII, X Ca2+ is important in every step |
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Factors in intrinsic pathway |
Factor V, VIII, IX, X, XI, XII |
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What is vitamin K required for? |
Vitamin K is required for prothrombin production. So if prothrombin time is prolonged, it can be caused by insufficient production by the liver. |
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Function of plasmin |
Plasmin can cleave a fibrin polymer, creating fibrin degrading product. It´s important in anticlotting |
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What is the three-component model of the heart muscle? |
Made up of - Contractile element - Parallel elastic component (Frank-starling mechanism) - Series elastic component |
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What causes respiratory alkalosis, and how does it shift Hb dissociation |
Caused by hyperventilation, and shifts the HB dissociation curve to the left. |
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Metabolic alkalosis |
Caused by heavy vomiting |
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What causes respiratory acidosis and metabolic? |
Hypoventilation causes respiratory acidosis. Metabolic acidosis can be caused by build up of acidic substances, or the failure of kidneys. |
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Why does methemoglobin have a lower affinity for oxygen than deoxyhemoglobin? |
Because the iron has been oxidized to the ferric state. |
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Which immunoglobulin protects the mucous membrane? |
Ig A |
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What is produced in platelets? |
Thromboxan - A2 and serotonin |
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Rh positive vs Rh negative - blood diffusion |
A Rh positive can receive blood from Rh negative, but a patient with Rh negative cannot receive blood from a Rh positive.
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where do we find secretin? |
Duodenum |
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What activates secretin?
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It´s activated by H+ concentration increase in the stomach. |
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Effects of secretin |
Inhibit acid secretion and mucosal growth HCO3 secretion in pancreas. Bile flow and HCO3 secretion in bile ducts |
Works to balance out gastrin |
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where do we find motilin? |
Motilin is found in the small intestine |
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What activates motilin |
motilin is activated neuronal |
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Effect of motilin |
Motility during interdigestive phase. Promotes emptying of the stomach |
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Where is Glukose-dependent insulinoptropic peptide found? |
Found in the small intestine |
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What is the effect of GIP? |
It inhibits acid secretion, digestive motility in stomach and the emptying of the stomach. Promotes insulin secretion of the stomach |
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What activates GiP?
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Activated by glucose, peptides and fattyacids |
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Where is CCK found and what activates it? |
In the small intestine and it´s activated by fatty acids and amino acids. |
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Effect of CCK |
Inhibit emptying of stomach Stimulate enzyme secretion and growth in pancreas. Stimulate gallbladder emptying |
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Which GI hormones are found in the small intestine? |
Secretin, motilin, GIP, CCK. Gastrin is found in both the stomach and the duodenum. |
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