is posterior to the symphysis pubis. The sizre of the bladder varies with the amount of urine it contain. It can hold 300 – 500 ml of urine before internal pressure rises and signals the need to empty the bladder through micturation.
serves as a storage site for urine.
the bladder lies immediately in front of the rectum.
the bladder lies next to the vagina and the uterus.
Acidosis- excessive accumulation of acids or excessive loss of bicarbonate in body fluids.
Alkalosis- excessive accumulation of bases or loss of acid in body fluids.
4 sub types:
METABOLIC ACIDOSIS ↓ ↓ Anorexia Nausea and vomiting Abdominal pain Weakness Fatigue General malaise Decreasing level of consciousness Dysrhythmias Bradycardia Warm, flushed face Hyperventilation acid production. acid excretion bicarbonate loss chloride pH HCO 3 PaCO 2 Rate and depth of respirations increase, eliminating additional CO 2 (bicarbonate deficit)- is characterized by low ph (<7.35) and low bicarbonate (<22 mEq/L). It may be caused by excess acid or loss of bicarbonate from the body.. Manifestation Causes ABG Compensatory Mechanism Definition
METABOLIC ALKALOSIS Confusion Decreasing level of consciousness Hyperreflexia Tetany Dsyrhythias Hypotension Seizures Respiratory failure bicarbonate excess pH HCO 3 PaCO 2 Rate and depth of respirations decrease, retaining CO 2 Metabolic alkalosis (bicarbonate excess) is characterized by high ph(>7.45) and high bicarbonate (>26mEq/L).It may be caused by loss of acid or excess bicarbonate in the body. Manifestation Causes ABG Compensatory Mechanism Definition
Diagnostic Tests: ABG – pH > 7.45 and bicarbonate > 26 mEq/L; PaCO2 is >45 mmHg Serum electrolytes - ↓ potassium-serum (< 3.5 mEq/L) and decreased chloride (< 95 mEq/L). Serum bicarbonate level is high. Urine pH - low (pH 1 to 3) if metabolic acidosis is caused by hypokalemia ECG pattern – show changes similar to hypokalemia. Medical management: Prescribing K ( potassium salt ) if hypokalemia is present or NaCl solutions to correct volume depletion when extracellular fluid volume has decrease rapidly.
RESPIRATORY ACIDOSIS ACUTE Headache Warm, flushed skin Blurred vision Irritability , altered mental status Decreasing LOC Cardiac arrest. CHRONIC Weakness Dull headache Sleep disturbance with daytime sleepiness Impaired memory Personality changes Retained CO 2 and excess carbonic acid. ↓ pH HCO 3 PaCO 2 Kidneys conserved bicarbonate to restore carbonic acid: bicarbonate ratio of 1:20 characterized by a pH of < 7.35 and a PaCO2 greater that 45 mmHg. It may be acute or chronic . In chronic respiratory acidosis, the bicarbonate is higher than 26 mEq/L as the kidneys compensate by retaining bicarbonate. Manifestation Causes ABG Compensatory Mechanism Definition
DIAGNOSTIC EXAM ABG’s show pH less than7.35 and Paco2 of more than mmHg Serum electrolytes may show hypochloremia (chloride level < 98mEq/L) in chronic respiratory acidosis. Pulmonary Function Test may be done to determine if chronic lung diseases is the cause of the respiratory acidosis. MEDICATION: Bronchodilator drugs Antibiotics prescribed to treat respiratory infections IV sodium bicarbonate
RESPIRATORY ALKALOSIS Dizziness Numbness and tingling around mouth , of hands and feet Palpitations Dyspnea Chest tightness Anxiety/panic Tremors, tetany seizures, loss of consciousness Loss of CO2 and deficient carbonic acid. pH ↓ HCO 3 ↓ PaCO 2 Kidneys excrete bicarbonate and conserve Hydrogen ions to restore carbonic acid: bicarbonate ratio Respiratory alkalosis is characterized by a pH greater than 7.45 and Paco2 of less than 35 mmHg. It is always caused by hyperventilation leading to a carbon dioxide deficit. Manifestation Causes ABG Compensatory Mechanism Definition
DIAGNOSTIC EXAMS ABG’s generally show a pH greater than 7.45 and Paco2 less than 35 mmHg. In chronic hyperventilation, there is a compensatory decrease in serum bicarbonate to less than 22 mEq/ L and the pH may be near normal. MEDICATIONS: sedative or anxiety
A nonspecific disorder in which the kidneys are damaged, causing them to leak large amounts of protein from the blood into the urine.
tiny blood vessels in the kidneys that filter waste and extra water from the blood is damaged.
High blood pressure
Increased aldosterone secretion Decreased Renal function Salt and water retention Decreased renal function Edema NEPHROTIC SYNDROME Reduced intravascular oncotic pressure Loss of fluid into the interstitial space Reduced plasma volume
Nephritis – describes a group of inflammatory but non infectious diseases characterized by wide spread kidney damage.
Glomerulonephritis – is a type of nephritis that occurs most frequently in children and young adults.
- twice in men than women.
appears about 2-3 weeks after an URTI with group A beta-hemolytic streptococci, impetigo and viral infections such as mumps, hepatitis B or HIV may precede to A.G.
Antigen( group A beta hemolytic streptococcus Antigen-antibody product Deposition of the antigens-antibody complex in glomerulus Increased production of epithelial cells lining the glomerulus Leukocyte infiltration of the glomerulus Thickening of the glomerular filtration membrane Scarring and loss of glomerular filtration membrane Decreased glomerular filtrations PATHOPHYSIOLOGY
A slow progressive disease characterized by inflammation of the glomeruli.
causing irreversible damage to the nephrons.
post streptoccal Glomerulonephritis
rapidly progressive Glomerulonephritis
generalized edema known as Anasarca (fluid shift from intravascular to interstitial & intacellular location.
Slow, progressive destruction of the glomerolus Cortex layer shrinks to 1-2 mm in thickness Bands of scar tissue distort the remaining cortex Surface of the kidney becomes rough & irregular shape Scarring at the glomeruli & tubules Thickenned branches of the renal artery Severe glomerular change End stage renal disease PATHOPHYSIOLOGY GLOMERULONEPHRITIS CHRONIC