Pathophysiology Schematic Diagram and narrative

Predisposing Factors: Family history of DM Race Age Polycystic ovary syndrome

Precipitating Factors: Obesity Sedentary lifestyle Congestive Heart Failure

Insulin Resistance

Exhaustion of Beta cells

Decrease insulin production/ secretion of insulin

Failed absorption of the glucose in the cell Protein Degradation Cell starvation Stimulation of hunger mechanism via hypothalamus Hunger A Increase Breakdown of fat

Weight loss

A POLYPHAGIA

Hypertension

Glomeruli becomes sclerotic Nephrons vasodilate

Hyperglycemia Increase blood viscosity

Hypertens ive Nephroscl e-rosis

Renal blood flow & glomerular Filtration rate

Nerve Demyelinization

Kidney filtration mechanism impaired

Capillary basement membrane thickening Diffuse glomerular sclerosis Nephropathy

Neuropathy

Macromolecule can now pass Glycosuria Decrease acidity of urine Increase urethral flora

Impaired pain sensation (Paresthesia)

Renal failure End stage renal disease

UTI

Non- healing ulcers

Delayed wound healing

Circulating blood volume Hypovolemia

POLYURIA & ALBUMINURIA

Gangrene Amputation

Hypotension, tachycardia, tachypnea

Inability to filter blood

Inability to excrete fluids and electrolytes Sodium and Water Retention Fluid Volume Blood Pressure

Inability to synthesize Vitamin D Ca absorption

Inability to produce erythropoietin Stimulation of red bone marrow RBC production

Retention of nitrogenous waste product

Calcification of bones and teeth

Uremia Anemia Affects Nervous System Accumulation of urea crystals in the skin Leakage of Fluid in pulmonary interstitial space Rapid filling of alveolar spaces Leakage of fluid and electrolytes interstitial space Edema

Altered LOC, Headache, Irritability

Pruritus

Pulmonary congestion Rales, Crackles, dyspnea, pallor and profuse sweating E D

D IF NOT TREATED Oxygen deprivation induced organ failure BAD PROGNOSIS Fluids & Electrolyte imbalance Increase number of solute relative to water

IF TREATED: Preload reducers Supplemental O2 Diuretics Anti-hypertensive drugs Bronchodilators GOOD PROGNOSIS

Potassium ion retention

Sodium ions lost

Cardiac arrhythmias

Tissue hydration

Death

POLYDIPSIA

Capillary basement membrane thickening

Thickening of blood vessel walls Occlusion of plaque

Musculoskeletal effects Impaired glucose absorption in the muscle tissue Diminished peripheral pulse Joint contractures

Abnormal retinal vascular permeability

Blood flow blocked Increase blood pressure G

Myocardial ischemia Myocardial infarction Heart failure

Scarring F

Fatigue

F Retinopathy jnljbjjnhobhkjhobjb Blurring of vision

G Poor tissue perfusion Cool extremities Weakness and fatigue Exercise intolerance Confusion Diziness

H Increase Fatty acids & glycerol

Decrease oxygen supply

Increase fat content in the blood Hyperlipidemia Formation of fatty deposits on the walls of the blood vessels

Blindness

Hypoxia

ketone bodies in the general circulation hydroxybutyric acid acetoacetic acid acetone

Atherosclerosis

Convulsions

Metabolic acidosis

Acetone breath

Nausea and vomiting

Abdominal pain

Decrease cellular potassium

Body attempts to prevent further decrease in pH

Depressed central nervous system

Poor appetite

Cardiac arrhythmias

Kussmauls respirations headache Coma

PATHOPHYSIOLOGY NARRATIVE Diabetes mellitus type 2 is a chronic disease marked by high levels of glucose in the blood. it is the most common form of diabetes. It is non-insulin dependent as well. The predisposing factors are those that put the client at risk and factors that cannot be modified. One of which is having a family history of diabetes mellitus. It can be passed on from one generation to the other. It also primarily affects people who are 4o years old and above most of which are obese. Race is also a predisposing factor especially Hispanic, Native American, African American, Asian American, Pacific Islander descent. Lastly, those who have polycystic ovarian syndrome are at risk because they have an increased insulin resistance. The precipitating factors are those that could put a person at risk to develop the illness. Only these factors can be modified. One of which is sedentary lifestyleExcessive calories, inadequate exercise and obesity can put a client at high risk of having diabetes mellitus 2. Smoking is also a precipitating factor. But the most powerful risk for DM type 2 is obesity. It is said that in obese clients insulin has decreased ability to influence glucose uptake and metabolism in the liver, skeletal muscles and adipose tissue. DM type 2 is characterized by three pathophysiologic abnormalities. These are peripheral insulin resistance, decrease insulin production and hepatic glucose production. An insulin resistance is when cells do not respond correctly to the insulin. At the early stages of the disorder, glucose tolerance remains normal, despite insulin resistance because the pancreatic beta cells compensate by increasing insulin output. As insulin resistance and the compensation progresses, it will cause the exhaustion of cells thus there would be a decrease in the production of the beta cells. The persistence of the hepatic glucose production and the inability of the cells to compensate because of the exhaustion of cells will cause the decrease absorption of the glucose in the cell. Thus cell starvation will occur. Cell starvation can lead to three things. First of which is degradation of proteins. Since there is decrease of glucose by the cells the cells turn to other sources. Protein

and amino acids are not stored in the body, like fat and glucose are in adipocytes and as glycogen, respectively. The largest reservoir of protein is then used by the cells resulting in increase mobilization and degradation of protein. And because of such muscle wasting is the result. Muscle wasting sffects disease outcome because it leads to weakness, disability, impaired quality of life and increased hospitalization of days. Second, increased breakdown of fat due to decrease absorption of glucose in the cell. This will be utilized by the cell for source of energy leading to increase fat content in the blood which is called hyperlipidemia. Individuals with DM have several forms of dyslipidemia. Due to the additional risks if hyperglycemia and hyperlipidemia, lipid abnormalities is present. the most common pattern of dyslipidemia is

hypertriglyceredimia and reduced HDL cholesterol. DM does not increase levels of LDL, but the small dense LDL particles found in type 2 DM are more atherogenic (substances of processes that cause atherosclerosis) because they are easily glycated and susceptible to oxidation. This will now contribute to the formation of the fatty acid deposits in the blood wall vessels resulting to atherosclerosis. Atherosclerosis, if not treated, will lead to coronary heart disease, stroke and other disorders occurring due to blood clots. Due to decrease insulin production, the glucose in the blood is not absorbed within the cell. In order for the cell to get energy to use, it uses carbohydrates, fats and proteins. But soon those will not be enough which will lead to depletion of the said cellular stores leading to the third result of cell starvation. A message will be sent to the hypothalamus to stimulate the hunger mechanism leading to Polyphagia. Because of polyphagia, the clinet will eat more, increasing the glucose in the blood. this is now known as hyperglycemia, a condition in which excessive amount of glucose circulates in the blood plasma. Hyperglycemia will now lead to the different conditions that will lead t the complications that a diabetic client will experience. Because nerve fibers do not have their own blood supply, they depend on the diffusion of nutrients and oxygen across the membrane. But, because absorption of glucose has failed, axons and dendrites are not nourished. Thus,making their transmissions slow.

This is now known as neuropathy. Neuropathys manifestations are tingling sensation, numbness, mild to total sensory loss, and paresthesia (sensation of numbness or tingling in the skin. Poor circulation is an important factor in why most wounds do not heal. Because there is impaired circulation and altered carbohydrate metabolism in diabetic clients, this will affect the peripheral circulation. Tissues such as epidermis and dermis become compromised, and thus are prone to injuries and persistent infections. Diabetes ulcers frequently develop because of this. If left untreated, client will have gangrene. Hyperglycemia acts as an osmotic diuretic; the amount of glucose filtered by the glomeruli of the kidney exceed (kidney filtration mechanism impaired) that which can be reabsorbed by the renal tubules. Glycosuria results. Because of this, the environment of the urine will become alkaline. Thus, putting the client at risk of developing infections. Because of the alkalinity of the environment, the normal flora will increase. This could predispose to the development of urinary tract infection and vaginitis in the client. Another complication of diabetes mellitus type 2 is nephropathy. Diabetic nephropathy is used to describe the combination of lesions that often occur concurrently in a diabetic kidney. Commonly, kidney lesions in diabetic people affect the glomeruli. Various glomerular changes may occur in people who develop diabetic nephropathy. This includes capillary basement membrane thickening, diffuse glomerulosclerosis and nodular glomerulosclerosis. Changes in the capillary basement membrane take the form of thickening of the basement membrane along the length of the glomeruli. Nodular glomerulosclerosis which is also known as intercapillary glomerulosclerosis or Kimmelstiel-Wilson disease, is a form of glomerulosclerosis that involves the development of nodular lesions in the glomerular capillaries of the kidneys. This will cause impaired blood flow with progressive loss of the kidneys functions resulting in renal failure. On a later stage, this will lead to end-stage renal disease (ESRD). Diabetic nephropathy is the leading cause of ESRD.

Having ESRD leads to inability to filter blood because the renal system has been stressed out and injured and as a consequence there is a retention of nitrogenous waste products which is called Uremia, which can affect the nervous system (manifesting altered LOC, Headache, and Irritability). It can accumulate urea crystals in the skin making it so itchy (pruritus). With ESRD it also leads to inability to excrete fluid and electrolytes which can lead to Na & water retention thus increasing the fluid volume making fluid shift to interstitial space causing edema, Inability to synthesize Vit. D thus decreasing the absorption of Ca decreases the calcification of bones and teeth, and problems with production of blood because of the inability of production of erythropoietin which stimulates the red bone marrow to produce RBCs. Diffuse glomerulosclerosis (glomerular sclerosis) consists of thickening of the basement membrane and the mesangial matrix. The deposits appear diffusely on the basement membranes of capillary loops of the glomeruli. There will also be increase permeability. Thus, allowing larger deposits of proteins (albumin). Hyperglycemia also acts as an osmotic diuretic which results in large amounts of water lost through urine. This will result in polyuria and albuminuria. Because of polyuria, or frequent urination, the circulating blood volume decreases. Because of this, there will be poor circulation since there is inadequate blood volume. Thus, also leading to poor wound healing which would lead to gangrene if not managed well. Also, because of polyuria, there will be imbalance in the fluids and electrolytes of the body. Because of the excretion of water in the form of urine, the amount of solute inside the body becomes relatively higher than that of the solvent. There will be imbalance in the electrolytes potassium and sodium. Because of the imbalance in potassium, there will be arrhythmias and other clinical signs that are weakness, silent distention of the abdomen, dyspnea and EKG changes. If not treated or managed, this will lead to death. Aside from potassium, there is also an imbalance in the electrolyte sodium. Sodium is lost. Since sodium is responsible for absorbing water, then the loss of it will lead to

tissue dehydration. This will now lead to the third P of diabetes mellitus which is polydypsia. Lastly, because of hyperglycemia, there is more amount of solute (glucose) in the blood. This will result in increase viscosity of the blood. Stress from increased blood viscosity is a hemodynamic mechanism that increases permeability and decrease elasticity of capillaries. The retina, which is the most essential structure of the eyes, has the highest rate of oxygen consumption of any tissue in the body. But due to the destruction of its capillaries, it will be then deprived of oxygen leading to tissue anoxia (lack of oxygen). Also, over time, hyperglycemia can cause fluid to build up behind the retina. Because of these, the blood vessels that supply blood to the retina are damaged. This leads blurring of vision which latter results into blindness. Also, due to blood viscosity, the blood vessels thicken decreasing the elasticity of blood vessles. Plaque will form and occlude (coronary artery disease: atherosclerosis) the said blood vessels impeding blood supply. Because the blood that is supposed to nourish the blood vessels are impeded, the delivery of oxygen in to these are also impaired resulting into necrosis and scarring of the endothelium of these blood vessels. Because the blood is blocked, the blood pressure increases (hypertension) which if not managed, will lead to stroke. Also, when the blood flow is blocked, the heart will try to compensate by increasing its workload. As the hearts workload increases, contractility results in an increase in end diastolic blood volume in the ventricle, stretching the myofibers and increasing the size of the ventricle or also known as ventricular dilation. The increased size of the ventricle further increases the stress on the ventricular wall, adding to the workload of the heart the preload increases. One way the heart compensates for the increase workload is to increase the thickness of the heart muscle (ventricular hypertrophy) the myocardial muscle is stretched. Because of the excessive stretching of the myocardial muscle, the cardiac muscle contraction will become ineffective.

The heart muscle will be weakened. It cannot effectively pump blood, thus, blood flow to the lung is restricted. Because of such, the blood that is supposed to flow into the system will backflow into the right ventricle and to the right atrium. When the right ventricle fails, congestion of the viscera and the peripheral tissue predominates. This occurs because the right side of the heart cannot eject blood and cannot accommodate all the blood that normally returns to it from the venous circulation. This will lead to increase pressure in the great veins and distendible organs. There will be dependent peripheral edema as a result of increase pressure in the capillary vessel. The increase in venous pressure will also lead to jugular vein distention. There will also be the enlargening of the liver (hepatomegaly) and of the spleen (splenomegaly). Hepatomegaly result from the venous engorgement of the liver. The increase pressure may interfere with the livers ability to perform. As hepatic dysfunction progr esses, pressure within the portal and peritoneal vessels increase to force fluid into the abdominal cavity, a condtion known as ascites. The hypertrophy is not accompanied by an adequate increase in capillary blood supply, resulting in increased demand for oxygen by the cardiac muscles. Because of the lack of nourishment needed, the contraction of the cardiac muscles decrease. With that, the cardiac output decreases. The decrease in ejected ventricular volume causes the sympathetic nervous system to increase the heart rate. Because of such, the systemic perfusion becomes inadequate. To increase the circulating blood, the neurohormonal pathways are activated. The neurohormone like the atrial natriuretic peptide/factor (ANP), endothelin, and prostacyclin are continually stimulated. The release of neurohormones lead to an increase in preload and afterload, which increases stress on the ventricular wall, causing an increased in the workload of the heart. With this, the cardiac output decreases as well. Because of such, the perfusion becomes inadequate and the wall tension increases. INCREASE PULMONARY PRESSURE Increase pulmonary pressure causes decreased oxygenation, the amount of blood ejected from the left ventricle decreases (forward failure). The relaxation of the left ventricle becomes impaired thus it cannot pump the blood out of the ventricle to the

body. The increased left ventricular end-diastolic blood volume increases the left atrium into the left ventricle during diastole. This exceeds the hydrostatic pressure and osmotic pressure in the capillaries of the lungs. Pulmonary venous blood volume and pressure rise, forcing fluid (fluids shifting) from the pulmonary capillaries into the interstitium, bronchioles, bronchi and alveoli. This results in pulmonary congestion wherein the lung expansion decreases which will manifest dyspnea. Also, because of fluid shifting, fluid is trapped in the pulmonary trees, thus, hearing crackles upon auscultation.