EXAMS 3 Flashcards
function of the kidney (vitamin D)
- homeostasis (electrolytes and water)
- excretion (urea, electrolytes and water)
production of kidney / target of kidney
PRODUCTION
erythropoietin
angiotensin
TARGET
aldosterone
ADH
vitamin d kidney
increases calcium absorption from the gastrointestinal tract
regulates calcium deposition in bone
causes of urinary tract obstruction
- developmental defects
- calculi (stones)
- pregnancy
- benign prostatic hyperplasia
- scar tissue resulting from infection and inflammation
- tumors
neurological disorders such as spinal cord
damaging effects of urinary obstruction
stasis of urine = predisposes to infection and stone formation
development of backpressure = interferes with renal blood flow and destroys kidney tissue
manifestations of urinary obstruction
DEPENDS on
- site, cause and rapidity in which condition develops
COMMIN SYMPTOMS OF URINARY OBSTRUCTION
- pain
- sign and symptoms of UTI
- manifestations of renal dysfunctions
definition of kidney stones
- crystalline structures that form from components of urine
requirements for formation of KIDNEY STONE
- urinary environment that supports continued crystallization of stone components
- concentration of stone components in the urine
- ability of stone components to complex and form stones
- the presence of substances that inhibits stone formation
types of kidney stones
- calcium stones ( oxalate or phosphate ) = HARD SINGLE BROWN
- magnesium ammonium phosphate stones( stag horn) = SMOOTH ROUND WHITE
- uric acid stones = MULTIPLE YELLOWISH, RADIOLUSCENT
- cystine stones = seen in cystinuria RADIO OPAQUE DUE TO SULPHUR
kidney stone treatment PREVENTATIVE
diet restriction
calcium salt supplementation
thiazide
cellulose phosphate
general kidney stones treatment
preventative
treatment for pain
removing stones
antibiotic for infection
removing stones kidney stone
ureteroscopic removal
percutaneous removal
extracorporeal lithotripsy
diagnosis of kidney stones
urinalysis
radiography
intravenous pyelography
ultrasonography
types of UTI
asymptomatic bacteriuria
symptomatic infections
lower UTIs - cystitis
upper UTIs - pyelonephritis
uncomplicated UTIs
E. coli
staphylococcus saprophytic
complicated UTI
gram positive cocci
S.aureus, group B streptococcus
diagnosis and treatment of UTIs
diagnosis based on symptoms and examination of the urine for prescience of micro organisms
- x ray file, ultrasonography, CT and renal scans are used to identify contributing factors
- urine dipstick
- TREATMENT OF ITI IS BASED ON THE PATHOGEN CAUSING THE INFECTION
causes of glomerulonephritis
disease that provoke a proliferation inflammation of the endothelial, mesangial, epithelia cells of the glomeruli
inflammatory process of glomerulonephritis
- damages the capillary wall
- permits red blood cells to escape into the urine
- produces hemodynamic changes that decrease the GFR
immune mechanisms of glomerulonephritis
glomerular antibodies
circulating antigen antibody complexes
characteristics of glomerulonephritis
- hematuria with red cell casts
- a diminished glomerular filtration rate (GFR)
- azotemia (presence of nitrogenous wastes in the blood)
- Oliguria
- hypertension
proximal tubular disorder
affects bicarbonate reabssorption
distal tubular defects
affect the secretion of fixed metabolic acids
peritoneal dialysis
removes nitrogenous waste products such as excess fluid and electrolyte from the blood by means or peritoneal membrane
APPROX 10-15% patients are receiving peritoneal dialysis
hemodialysis
- removes nitrogenous waste products excess fluids and electrolytes from the blood by the means of ARTIFICIAL KIDNEY
APPROX 90% of all dialysis patients receives hemodialysis
renal failure
a condition in which kidneys fails to remove metabolic end products from the blood and regulate the fluid, electrolytes, and pH balance of the extracellular fluids
underlying causes of renal failure
- renal disease
- systemic disease
- urologic defects of nonrenal origin
prevention and early diagnosis of active renal failure
- those with pre existing renal insufficiency and diabetes
- elderly persons due to the effects of aging on renal reserve
ACUTE RENAL FAILURE
- abrupt in onset
- often reversible if recognized early and treated appropriately
CHRONIC RENAL FAILURE
- end result of irreparable damage to the kidneys
- develops slowly, usually over the course of a number of years
CAUSES OF ACUTE RENAL FAILURE (PRERENAL)
- hypovolemja
- decreased vascular filling
- heart failure and cardiogenic shock
- decreased renal perfusion due to vasoactive mediators, drugs, diagnostic agents
causes of acute renal failure (POSTRENAL)
bilateral ureteral obstruction
bladder outlet obstruction
COMMON CAUSES OF CHRONIC RENAL DISEASE
hypertension diabetes mellitus polycystic kidney disease obstructions of the urinary tract glomerulonephritis cancers autoimmune disorders diseases of the heart or lungs chronic use of pain medication
medical management treatment of renal failure
- dialysis ( hemo and peritoneal )
- transplantation
DIETARY MANAGEMENT
- protein
- carbohydrates, fat, calories
- potassium
- sodium and fluid intake
common causes of neurogenic bladder
- stroke and advanced age
- parkinson’s disease
- spinal cord injury
- injury to the sacral cord or spinal roots
- radical pelvic surgery
- diabetic neuropathies
- multiple sclerosis
spastic bladder dysfunction (neurogenic bladder)
- failure to store urine
- neurologic lesions above the sacral cord allow neurons in the micturition center to function reflexively without control from the CNS centers
flaccid bladder dysfunction
- bladder emptying is impaired
- neurologic disorders affect motor neurons in the sacral cord or peripheral nerves that control destrusor muscles contraction and bladder emptying
goals of treatment neurogenic bladder disorders
- prevent bladder overdistention, UTI, life threatening renal damage
- reduce the undesirable social and psychological effects of the disorder
treatments for neurogenic bladder disorders
- catheterization
- bladder retraining
- pharm manipulation
- surgical procedures
stress incontinence
- involuntary loss of urine during coughing laughing sneezing or lifting
urge incontinence
involuntary loss of urine associated with a strong desire to void (urgency)
overflow incontinence
involuntary loss of urine that occurs with intravesicular pressure exceeds the maximal urethral pressure because of bladder distraction in the absence of detrusor activity
MIXED INCONTINENCE = combination and urge incontinence
what is shock
tissues are not adequately perfused, causes general widespread impairment of cellular metabolism ( glucose and oxygen )
factors of shocks
defective heart function
blood volume changes
metabolic or toxic changes
manifestations of shock
- include hypotension
- tachycardia
- increased respiratory rate
circulatory failure shock (hypoperfusion of organs)
acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate resulting in cellular hypoxia
risk factors of multiple organ dysfunction syndrome (MODS)
sepsis, prolonged periods of hypotension, hepatic dysfunction, infarcted bowel, advanced aged, severe trauma, alcohol abuse
causes of multiple organ dysfunction syndrome (MODS)
most common: sepsis, septic shock
other (severe injury, trauma, burns, major surgery)
manifestations of MODS
respiratory hepatic renal GI myocordial failure
TREATMENR OF multiple organ dysfunction syndrome (MODS)
- respiratory system: mechanical ventilation
- GI system: enteral feeding or hyperalimnetation (increase calories for hypermetabolic state)
- renal system ( dialysis or continuous help filtration for fluid and electrolyte balance
cardiovascular- intro pic drugs or vasopressors
cardiogenic shock
inability of the heart to pump adequate blood to meet body’s demands
CAUSES: MI mysocaridal comtusion, sustained arrhythmias, cardiac surgery
CLINICAL MANIFESTATIONS: cardiac output
hypovolemic shock
insufficient intravascular fluid
- occurs with acute loss of 15 or 20% of circulating blood volume
MANIFESTATIONS : thirst, increased HR, cool and clammy skin, decreased arterial blood pressure, decreased urine output, changes in mentation, poor skin tugor
distributive or vasodilatory shock
loss of BLOOD VESSEL TONE, enlarged vascular compartment, displacement of vascular volume away from the heart and central circulation
3 shock that share the basic circulatory pattern of distributive shock = neurogenic, anaphylactic, septic shock
neurogenic shock ( distributive )
- caused by decreased sympathies control of blood vessel tone, sympathetic outflow to the blood vessels
RARE AND USUALLY TRANSITORY
anaphylactic shock
severe reactions
warm/burning sensation of the skin, itching l, choking, wheezing, chest tightness, dyspnea
TREATMENT: remove the trigger, administer oxygen, antihistamine, corticosteroids, epinephrine ( EpiPen)
Sepsis
suspected or proven infection, plus a systemic inflammatory response ( FEVER TACHYCARDIA, TACHYPNEA, elevated WBC altered mental state hyperglycemia IN THE ABSENSE IF DIABETES
treatment of sepsis
- airway management to treat hypoxenua
- early administration of fluids within the first 3 hours
- broad spectrum antibiotic PRIORITY TREATMENT
- central venous access is recommended for IV fluids, medications, frequent blood draws
septic shock
most common type of vasodilatory shock associated with sever infection and the systemic response to infection
MANIFESTATIONS of septic shock
- HYPOtension and warm, flushed skin
- fever and increased leukocytes are present
- an elevated serum lactate or metabolic acidosis
obstructive shock
circulatory shock that results from mechanical obstruction of the flow of blood through the central circulation
causes of obstructive shock
- dissecting aortic aneurysms, cardia tamponade, pneumothorax, atrial myxoma, and evisceration of abdominal contents into the thoracic cavity
TREATMENT: pulmonary embolectomy, pericardiocentesis or the insertion of a chest tube for correction of a tension pneumothorax or hemothorax
COMPLICATIONS OF SHOCK
- pulmonary injury
- acute renal failure
- gastrointestinal ulceration
- disseminated intravascular coagulation (DIC)
- multiple organ dysfunction syndrome (MODS)
parkinson’s disease
a degenerative disorder of basal ganglia function and results in variable combinations of tremor, rigid, bradykinesia
CHARACTERISTICS: destruct nigrostriatal pathway, reduction in striata concentration of DOPAMINE
myasthenia gravis (NEUROMUSCULAR JUMCTIOMS)
disorder of transmission at the neuromuscular junction THAT AFFECT THE COMMUNICATION BETWEEN MOTONEURON AND INNERVATED MUSCLE CELL
CAUSE: cashed by antibody mediated LOSS OF ACH in the neuromuscular junction
multiple sclerosis ( EXACERBATIONS AND REMISSIONS OVER MANY YEARS IN SEVERAL DIFFERENT SITES CNS)
demyelinating disease of the CNS
- most common non traumatic cause of neurologic disability among young and middle aged adults
INITIAL: normal or near normal between neurologic functions between exacerbations
As the disease progresses, there’s less improvement between exacerbations and increasing neurologic dysfunction
AMYOTROPHIC LATERAL SCLEROSIS (ALS)
devastating neurologic disorder that SELECTIVELY AFFECTS MOTOR FUNCTION
disease typically follows a progressive course with a mean survival period of 2-5 years from the onset of symptoms
dawn phenomenon
- early morning glucose elevation WITHOUT nocturnal hypoglycemia
- related to nocturnal growth hormone elevation
TREATMENT: alter timing and dose of insulin
somogyi effect ( TYPE 1 DM )
most common in type 1 DM and in children
- hypoglycemia with rebound hyperglycemia
- counter regulatory hormones in GLUCONEOGENESIS
inflammatory bowel disease ( ulcerative colitis, chrons disease)
chrons disease: can affect anywhere ( patches )
- recurrent granulomatous type of inflammation that can affect anywhere from mouth to anus )
ulcerative colitis: nonspecific and continuos of the colon
chronic stable ANGINA
- associated with a fixed coronary obstruction DISPARITY BETWEEN CORONARY BLOOD FLOW AND METABOLIC DEMANDS OF THE MYOCARDIUM
CAUSES
- atherosclerotic plaque disruption
- platelet aggregation
cushing syndrome
excess cortisol level