Summary

This document provides an overview of acid-base balance, covering four types of imbalances (metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis). It also explains how to interpret acid-base balance using given values, the importance of the anion gap, and the components of blood.

Full Transcript

- [Acid-base balance] - **[Four types of imbalances]** - [Metabolic acidosis]: excessive build-up of acid or an excessive loss of bicarb- look at anion gap- caused by too much acid - It will have a LOW pH because of its acidic state and...

- [Acid-base balance] - **[Four types of imbalances]** - [Metabolic acidosis]: excessive build-up of acid or an excessive loss of bicarb- look at anion gap- caused by too much acid - It will have a LOW pH because of its acidic state and LOW bicarb. - PH= LOW CO2= OK HCO3= LOW - [Metabolic alkalosis:] loss of acid from blood resulting in excess bicarb; can be caused by excessive vomiting or diuretics. - PH= HIGH CO2= OK HCO3=HIGH - [Respiratory Acidosis]: excessive buildup of carbon dioxide in the body, commonly caused by hypoventilation - PH=LOW CO2=HIGH HCO3= OK - [Respiratory Alkalosis]: Excessive loss of CO2, commonly caused by panic attacks, altitude sickness - PH=HIGH CO2=LOW HCO3= OK - **[Interpret acid-base balance when given values ]** - 1^st^ step is to look at the patient's history - 2^nd^ step is to look at the pH. Is It high or low? Is it alkalosis or acidosis - 3^rd^ step is to look at the bicarb. Is it high, low, or normal - 4^th^ look at the CO2 is it high, low, or normal - Look and see do the PH and abnormal bicarb or CO2 go in the same direction. If yes, it's metabolic equal; if they go in opposite it is respiratory. - **[The importance of anion gap tells us if metabolic acidosis is acid buildup or loss of bicarb]** - Normal anion gap is 12 mmol/l - [Normal anion gap]= too little bicarb can be from excessive diarrhea, pancreatic issues, or renal tube acidosis. - [Elevated anion gap]= excessive buildup of acid; can be from lactic acidosis, ketoacidosis, renal failure, medication, metabolic disorders. - [Components of blood] - **[Plasma vs serum: both come from liquid portions of blood once cells are removed]** - [Plasma]: liquid portion of the blood; liquid that remains when clotting is prevented with the addition of an anticoagulant - Composed of water, proteins, and other solutes - [Albumin]: maintains oncotic pressure - [Globulins]: play a role in immune defense - [Clotting factors]: fibrinogen and prothrombin - [Serum]: a liquid that remains after the blood is clotted - [Plasma protein] - **[Myeloid vs lymphoid cell lines]** - [The myeloid cell line] produces RBC, WBC, platelets - RBC- erythrocytes - WBC: neutrophils, lymphocytes, monocytes, eosinophils, and basophils- never let my engine blow-too many signals infection - [The lymphoid cell line] produces immune cells B and T - **[Role of EPO: a decrease in EPO causes a reduction in hemoglobin because EPO is a hormone produced by the kidney that promotes the formation of red blood cells. LOW oxygen in the blood, meaning not enough hemoglobin, can cause an increase in EPO.]** - [EPO compensates for low o2 by increasing production] - Kidneys detect low o2 in blood- causing an increase in EPO. This increase then increases the amount of red blood cells- this increases hemoglobin which increases oxygen carrying capacity of blood. When the kidney detects increased o2, the EPO production shuts down - **[Hemoglobin- where it is made, what's needed to make it, how it is recycled, and how it functions]** - Hemoglobin is an iron-containing protein in RBCs that carries oxygen from the lungs to other body parts. It also helps return CO2 from tissues to the lungs. - The body needs iron to make hemoglobin; therefore, a decrease in iron decreases in hemoglobin. - A person's SPO2 is the percentage of hemoglobin that is carrying oxygen out of all hemoglobin - In order [to make hemoglobin], the body needs - Vitamin C- to keep in a 2+ state - copper- bring it from tissues to bone marrow - b6, pantothenic acid- make heme ring - folate, b12 ,and b2- carry hemoglobin where heme resides - to recycle hemoglobin - RBCs return to the spleen to die, and then macrophages eat them and dispose of the toxic components. - Heme then comes off the dying RBC and is broken into the heme ring and iron. - The heme ring is carried on albumin as bilirubin and taken to the liver, which converts it to urobilinogen. - Iron is taken by transferrin and secreted w bile by the liver, then is taken to the liver and bone marrow to make more RBC and then stored and released in the spleen to make more RBC - Which then is taken directly to the bone marrow for more heme synthesis - **Oxygen hemoglobin disassociation curve** - Left shift vs right shift - [Left shift: oxygen will stay with or go to hemoglobin when] - Alkalosis - Temperature is low - The low partial pressure of CO2 - This means that hemoglobin has a higher affinity for oxygen under these circumstances it wants oxygen to go to it and stay with it - [Right shift: oxygen will leave hemoglobin and go to tissues in cases of ] - Acidosis - High temperature - This means hemoglobin has a lower affinity for oxygen under these circumstances. It wants oxygen to leave it and go to the tissues - **Anemia** - [Three classifications] - **[Normocytic normochromic: normal cells, normal color]** - Results from low RBC or high RBC consumption - Causes of [low production]: bone marrow defects, bone marrow mass crowding, leukemia-preventing production, chronic disease - Causes of [high consumption]: hemorrhage, hemolysis, malignancy - **[Microcytic hypochromic: small cells with low color]** - Results from not enough heme and, therefore, defects in hemoglobin synthesis (heme makes RBC bright red, hence lack of heme low color) - Causes can be chronic blood loss, iron deficiency, and hemoglobin defects - **[Macrocytic normochromic: big cells' standard color]** - Heme is fine; hence, the standard color - Causes are typically folate or b12 deficiency - [What would you expect to see on the CBC report if someone has a specific type of anemia? ] - A decrease in hemoglobin and a decrease in hematocrit - Size and shape of rbc - A hgb lower than 13.5 for men or 12.0 for women - A hematocrit between 35 and 47 percent for women and 40 -52 percent for men - **[Sickle cell anemia: an autosomal recessive disease that causes hemoglobin molecules to be detective resulting in weak RBCs that die earlier than healthy RBC]** - s/s include bilateral pain, extremity edema, acute chest syndrome, glomerular disease, infection - proteins undergo polymerization, causing sickling of RBCs - low oxygen causes red blood cells to change their shape, causing RBCS that are sickle-shaped, sticky, and tough, which causes clumping, which blocks blood flow to tissues - causes the development of hemoglobin S- a variant that is less effective at carrying o2 and will cause the shape of an RBC to change into a crescent shape under times of cellular stress. The crescent shape causes them to get stuck in small blood vessels, which blocks blood flow and causes damage to the vessels. This causes a sickle cell crisis- a chain reaction of further hypoxemia, more rbc sickening, more damage, and more ischemia. - **[Two types of hemophilia: A and B]** - Deficiency in factor 8 classic hemophilia: hemophilia A - Factor 8-produced in endothelium - Deficient in factor Christmas disease: hemophilia B - vWF: circulated in blood carrying factor 8 promotes platelet adhesion to endothelial surfaces as well as platelet aggregation - **Clotting** - **[Role of platelets]** - Regulate blood flow to damaged areas of blood vessels - Form platelets plug to stop further bleeding - Activate further aspects of the clotting cascade - Initiate repair processes, including eventual clot breakdown - - Stages of the clotting cascade - Where clotting factors are made - **[Clot degradation and counteractions to clotting]** - [Counteraction to clotting] - Endothelial surfaces - Prostaglandins: inhibit platelet aggregation - Nitric oxide: inhibits platelet adhesion and aggregation - Proteins C and S: made in liver, inactivate clotting factors - Tissue factor inhibitor - Anti thrombin III: turns off thrombin - **[Role of Vitamin K]** - Makes coagulation factors functional: factors II, VII X, and Vitamin K - Comes from plant and intestinal bacteria - Proteins C and s are also vitamin k K-dependent - **[lab tests]** - D-dimers - PT-measures time it takes for blood to clot

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