PGY 412Exam # 2 Study Guide: Fluid and Electrolyte, Cardiovascular, and Respiratory DisordersFluid and Electrolyte Disorders- Total body water is distributed between two major compartments separated by the cell membrane called the intracellular (ICF) and extracellular fluid compartments (ECF). The extracellular fluid is subdivided into to interstitial fluid and the plasma, which are separated by the capillary wall.- Water is able to move freely between each compartment, but two forces are responsiblefor determining the direction of movement. Hydrostatic pressure is responsible for pushing fluid into the interstitial space while osmotic (oncotic) pressure pulls fluid from the interstitial space. - Osmotic pressure differences between the ICF and ECF cause water movement across the cell membrane. The membrane is highly permeable to water, so a change in the osmolarity (same as osmolality in this class) in the ECF will result in the rapid movement of water (fluid shift). Generally, the ICF and ECF are in osmotic equilibrium. - Anti-diuretic hormone (ADH) regulates renal water excretion by changing the permeability of the distal tubule and the collecting duct. ADH secretion is stimulated by changes in the osmolarity of body fluids, and the volume and pressure of the vascular system. - When the osmolarity of body fluid increases, or the volume or pressure is reduced, an individual will perceive thirst. - Since sodium is the major determinant for plasma osmolarity, disorders of the water balance will alter the plasma concentration of Na+. This will affect the volume of ECF, notits osmolarity. - Generally, sodium input is equal to the sodium output, keeping the volume of ECF constant. Primary ECF volume sensors are located in the vasculature. Low pressure baroreceptors (cardiac atria and pulmonary vessels) respond to volume changes. High pressure baroreceptors (aorta, carotid sinus, afferent arterioles of kidneys) respond to arterial blood pressure changes. - When ECF decreases, sodium excretion is decreased via the renin-angiotensin-aldosterone system. When ECF increases, atrial natriuretic peptide (ANP) increases the excretion of sodium. Both of these substances (ANP and aldosterone) affect the reabsorption of sodium at the collecting duct. - Potassium levels are controlled by several different hormones. Insulin, epinephrine and aldosterone increase potassium uptake by stimulating Na+/K+ ATPase.- KEYo Etiology = causeso Pathogenesis = progress of diseaseo Manifestations Symptoms = subjective experience Signs = visible  Sequelae = outcomes that persist Complications = new disease caused by original disease- Edema – accumulation of fluid within the interstitial spaces- Hyperosmolarity Imbalance o Hypernatremia = high sodium concentrationo Caused by water deficit or sodium excess- Hypoosmolarity Imbalanceo Hyponatremia = low sodium concentrationo Caused by water excess or sodium depletion- Volume imbalances are ordinarily imbalances in the amount of sodium in the ECFo Volume Contractiono Volume Expansion - Hypokalemia- Hyperkalemia- Changes in EKG due to potassium imbalance Cardiovascular DisordersLecture 1: Atherosclerosis and Hypertension- It is important to know the path that bloodtakes in the cardiovascular system,including the location and names of thevalves. o LAB RAT = Left Atrium Bicuspid, RightAtrium Tricuspid- The arterial side has high pressure whilethe venous side has low pressure and highcapacitance- The atria contract first, followed by theventricles- The ventricles are more powerful than the atria, so malfunctions in the pumping of the atria are not as dangerous as those in the ventricles- Arterial Wallo Intima – endothelial cells – inhibit clotting in blood vesselso Media – muscular part of smooth muscle cells – contract and expando Adventitia – nerves and capillaries that supply the muscular layer; contains fibroblasts- Atherosclerosis – derived from the Greek word referring to the thickening of the arterial intima (sclerosis = hardening) and accumulation of lipid (athere)o Lesions Aorta – aneurysmal disease Femoral and popliteal arteries – peripheral vascular disease Carotid arteries – stroke Renal arteries – renovascular hypertension- RAS- Regulate water output Coronary arteries – ischemic heart disease or myocardial infarctiono Disease Progression Endothelial injury  Fatty streak formation Fibrous plaque Complicated lesiono Risk Factors for Coronary Atherosclerosis Non-modifiable- Age (men >44, women >54)- Family history of CAD (coronary artery disease) Modifiable- Hyperlipidemia (LDL) – high >159 mg/dl- Hypertension- Smoking- Diabetes Mellitus- Obesity- Physical inactivity- Hyperhomocystinemia – elevated homocysteine levels in blood Negative Risk factor- High HDL- Hypertensiono Most common cardiovascular disease  Prevalence increases with age 50 % of people from age 60-69 Further increased in ages >70o Elevated arterial pressure – increased workload Pathological changes in the vasculature and hypertrophy of the left ventricle (does most of the work) Principle cause of stroke Major risk factor for coronary artery disease- Myocardial infarction – heart attack- Sudden cardiac death- Major contributor to cardiac failure and renal insufficiency – leads to renal damage (kidney failure)o CriteriaClassification Systolic DiastolicNormal <120 And <80Pre-hypertension 120-139 Or 80-89Hypertension stage 1 140-159 Or 90-99Hypertension stage 2 >160 Or >100o Symptoms – nonspecific (headache or dizziness) or absent (“silent killer”)o Etiology Primary – 95% cases of essential hypertension have unknown etiology Secondary – another disease process (pheocromocytoma – abnormal increase in epinephrine and norepinephrine due to tumor in adrenal medulla) o Treatment Pharmacological interventions Non-pharmacologic Therapy- Reducing sodium intake- Dietary Approaches to Stop Hypertension (DASH diet)- Moderate alcohol consumption- Increasing physical activity- Losing weight- Smoking cessationo Vascular Changes Cardiac workload increased Retinal vascular changes Cerebrovascular occlusion or rupture – stroke Myocardial infarction Angina due to ischemia Renal failure- Hyperhomocystinemiao Homocysteine – amino acid produced by the bodyo Normal level – 5-15