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midterm

Terms in this set (71)

ACE inhibitor drugs
Produce vasodilation and decrease blood pressure (benazepril, and catopril)
diuretics
medications administered to increase urine secretion in order to rid the body of excess water and salt
Calcium Channel Blockers
agents that inhibit the entry of calcium ions into heart muscle cells, causing a slowing of the heart rate, a lessening of the demand for oxygen and nutrients, and a relaxing of the smooth muscle cells of the blood vessels to cause dilation; used to prevent or treat angina pectoris, some arrhythmias, and hypertension
Angiotension II Receptor Blockers
medications block the action of angiotensin II
beta blockers
decrease heart rate and dilate arteries by blocking beta receptors
glomerulonephritis
Triggering event, ag-ab complex formation and deposition in glomerulus, activation of complement system and WBC infiltration, GFR injury and leakage this causes and also coagulation cascade activation and fibrin deposit, decreased capillary perfusion, and decreased GFR, proteinuria/hematuria, edema, increased serum creatinine, azotemia oliguria
prerenal
Caused by renal hypoperfusion due to hypotension, decreased CO, or decreased blood volume. Most common cause of AKI
intrarenal
caused by ATN, Acute glomerulonephritis and
Post renal
Caused by blockage/obstruction to ureter or urethra (BPH, Calculi, inflammation tumor) - OLIGURIA
Na H2O retention leads to
increased vascular volume, HTn, edema then HF
K retention leads to
hyperkalemia, dysrhthmias
phosphate retention leads to
hypocalcemia then skeletal changes
acid base imbalances from kidney disease leads to
metabolic acidosis, and respiratory compensation
kidney disease leads to decrease in nitrogenous waste elimination
then uremia, azotemia, pruritis, coagulopathies, neuro, CV / Skeletal changes
Kidney disease leads to
decrease in erythropoeitin production which leads to anemia
Vitamin D activation in kidney failure leads to
hypocalcemia then skeletal changes
proteinuria leads to decreased albumin
muscle protein losses, edema and muscle wasting
Normocytic
normal erythrocyte volume
Macrocytic
increased erythrocyte volume
microcytic
decreased erythrocyte volume
normochromic
normal hemoglobin content
high MCHC
Increased hemoglobin content
Low MCHC
decreased hemoglobin content
Macrocytic normochromic anemia
large cell size that are normochromic or have normal hemoglobin
Macrocytic anemia
due to folate or vitamin B12(cobalamin) deficiency
pernicious anemia
either congenital or acquired deficiency of intrinsic factor or a genetic disorder of DNA synthesis.
Microcytic-hypochromic
anemia presents with small abnormally shaped erythrocytes (microcytic) that aren't able to carry a normal hemoglobin concentration (hypochromic). There are a number of types of this anemia, which can be as simple as iron-deficiency anemia to Thalassemia.
Cause of Thalassemia
inherited autosomal recessive genetic defect of globin synthesis.
Normocytic-normochromic anemia presents with erythrocytes that are of normal size and shape (normocytic) and can carry a normal concentration of hemoglobin (normochromic).
So how can you have anemia with normal erythrocytes that carry a normal amount of hemoglobin? By having a decreased number of erythrocytes to carry enough hemoglobin to meet the oxygen needs of the cells in the body! Anemia in this category includes aplastic anemia that results from a decreased number of stem cells, posthemorrhagic anemia from blood loss, hemolytic anemia from the premature destruction of erythrocytes, sickle cell anemia from abnormal shape of hemoglobin, and chronic disease anemia from an unusually high demand for new erythrocytes.
Why is iron deficiency anemia common in children between 6 months and 2 years of age?
not enough dairy or iron in the diet
anemia decrease in oxygen carrying of the RBC
palpatations , dizzy, pale, orthostatic dizzy, dypsnea on exertion
Severe anemia
angina stroke, hf, tissue infarction, shock
anemia affects volume
can cause tachycardia, murmur, decreased u/o edema
too many blood cells polycthemia
You could suffer from polycythemia because you are dehydrated and have too many red blood cells in each volume of whole blood (relative polycythemia). In relative polycythemia, the blood becomes very concentrated. This condition can be easily treated with rehydration of the individual. Absolute polycythemia exists when the body has produced too many red blood cells. The major risk associated with polycythemia occurs because of the increased viscosity of blood that has too many cells per volume. Concentrated blood has a high viscosity and requires more effort to circulate and places an extra workload on the myocardium. There is also an increased risk of viscous blood pooling in the periphery and clogging blood vessels with microemboli.
S1
the first heart sound, heard when the atrioventricular (mitral and tricuspid) valves close at the start of systole
S2
End of systole The second heart sound, "dub" or S2, is caused by the closure of the aortic and pulmonic valves, marking the end of systole.
right heart failure secondary to a pulmonary cause is called
cor pulmonale
use a beta agonist on the bronchioles
sympathetics dilate
use of anticholinergics on the bronchiole
parasympathetics constrict
Heart Failure
cardiac dysfunction caused by inability of the heart to provide adequate cardiac output, resulting in inadequate tissue perfusion
Heart Failure symptoms
- dyspnea, fatigue, edema, pulmonary HTN, decreased urine output, orthopnea, cough with frothy sputum
Neurohumoral, inflammatory & metabolic processes
- Catecholamine's
sympathetic nervous system activation initially compensates for a decrease in cardiac output by increasing heart rate and peripheral vascular resistance
- RAAS (renin-angiotensin-aldosterone-system)
activation of RAAS causes not only increase in preload and afterload but also causes direct toxicity to the myocardium
Aldosterone
causes salt and water retention by the kidney and contributes to dysrhythmias
- Arginine Vasopressin (antidiuretic hormone)
causes peripheral vasoconstriction and renal fluid retention
Hematopoiesis
- the site of blood cell formation
- Begins in yolk sac at beginning of 3rd week gestation
- Shifts to fetal liver & spleen by week 8
- Shifts to bone marrow by 5th month
- To red marrow of all bones to make blood cells from birth - 5yrs
- Red marrow primarily located in ilium, vertebrae, cranium & jaw, sternum & ribs, humerus & femur after 20yrs
Hematopoietic Stem Cells (HSCs) proliferate (rapidly increase) and differentiate under the control of numerous growth factors and cytokines to form the 3 types of cells found in peripheral blood:
- RBCs
- WBCs
- Platelets
Risk Factors and Causes for Developing Any Type of Anemia:
Causes - impaired RBC production, excessive blood loss, increased RBC destruction
Risk Factors:
- Diet lacking certain vitamins (low iron, vitamin B12, folate)
- Intestinal disorders (Chron's, celiac disease)
- Menstruation
- Pregnancy
- Family History
Erythrocyte Function and Lifespan:
Erythrocyte - mature RBC that lacks a nucleus, ribosomes, and mitochondria
Lifespan in circulation is approximately 100-120 days
Primarily responsible for tissue oxygenation
Erythropoietin:
a growth factor that is made by the kidney and liver in response to tissue hypoxia
- Stimulated by androgens (testosterone)
Erythropoiesis
formation of red blood cells
Iron-Deficiency Anemia
Problem - Insufficient Iron (Fe) availability, small cells and low Hgb levels
Causes - inadequate dietary intake, chronic and or occult bleeding (hemorrhage, colitis, cirrhosis, GI ulcer), decrease ability to utilize Iron for heme synthesis)
Pathophysiology - insufficient Fe levels or inability for mitochondria to utilize Fe effectively leading to decrease Hgb synthesis leading to smaller, paler cells
Sickle Cell Anemia:
Problem - inherited disorder of erythrocytes (hemoglobinopathies)
Causes - inherited autosomal recessive genetic disorder
Pathophysiology - single amino acid change on beta-chain.
- Oxidative stress (hypoxia), anxiety, fever, cold, dehydration - decrease oxygen binding to Hgb and increases sickling tendencies
Thalassemia:
Problem - inherited disorder of erythrocytes (hemoglobinopathies)
Causes - inherited autosomal recessive genetic disorder
Pathophysiology - single or multiple amino acid changes on alpha- and/or beta-chains
Pernicious Anemia Causes:
Problem - unusually large cells, but normal Hgb levels. Not enough "building blocks" (vitamins, folic acid or B12) to make DNA, so erythroblasts continue to enlarge instead of undergoing cell division (megaloblastic)
Causes - autoimmune reaction, gastritis, gastrectomy (loss of GI cells producing intrinsic factor (IF)
Pathophysiology - malabsorption of B12 due to lowered IF production/secretion
hemolytic anemia
Problem - low cell number (cell size and Hgb level are normal)
Causes - Infection, transfusion reaction, hemolytic disease of newborn (Rh incompatibility), autoimmune reaction, drug induced
Pathophysiology - premature destruction of RBC due to enzymes/toxins produced by infectious agent, mediated by own immune system, or the effects of certain chemicals/drugs
Functions of Hemoglobin
Oxygen-carrying protein in the RBC.
Hemoglobin-packed blood cells take up oxygen in the lungs and exchange it for carbon dioxide in the tissues
cystitis
Almost 90% of cystitis is caused by E. coli (80% to 85%) or Staphylococcus saprophyticus (10%). The organisms are usually introduced by retrograde movement along the urinary tract, and women are much more susceptible to cystitis than men, secondary to the short length of the urethra in women. The immune system will respond, in both sexes, to invading organisms that come in contact with the bladder wall.
cystitis The body's normal protective factors also include the following.
Maintaining acidic urine (high hydrogen ion concentration), which inhibits bacterial growth
Maintaining a low concentration of salts (osmolality), which increases the bacteriostatic property of urine
A lack of glucose in the urine, because glucose supports bacterial growth
Maintaining a high urea concentration, because urea is bacteriostatic
An abundance of glycoproteins in the urine, which are slimy substances that interfere with bacterial adherence
Producing a dilute urine that washes out bacteria
pylonephritis
Pyelonephritis refers to an infectious process within the upper ureter or kidney, but often is associated with the pelvis, calyces, and medulla of the kidney. The condition may affect one or both kidneys and may be either acute or chronic in nature. Table 38-4 in your text lists the common predisposing factors along with the pathologic mechanisms of pyelonephritis. Rather than memorize this table, try to understand the processes involved.
a measure of distensibility
compliance
the structure that participates in gas exchange
acinus
where the bronchi and pulmonary vessels enter the lungs
hila
where the trachea divides into the two main bronchi
carina
stimulation of the carina causes
coughing
the mononuclear phagocytic cells in the lung are called the
macrophages
presence of pus in the pleural cavity
empyema
Hyperventilation causes decreased
paco2
presence of fluid in the pleural space is called
effusion
Dypsnea
difficulty breathing
orthopnea
difficulty breathing when lying down
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