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Renal Pathology
Pathophysiology 8 - disorders of the renal system
| Question | Answer |
|---|---|
| describe the location of the hilus and its significance | the hilus is a concave cleft, and it is at this point where the ureters, blood vessels, and nerves enter the kidney |
| describe functions of the nephron | - control concentration of water and soluble materials - eliminates waste products - regulates blood volume, pH, blood pressure - controls electrolyte level |
| who does the nephron control the concentration of water and soluble materials | - filtering blood - reabsorbing needed products - excreting waste products as urine |
| name the structures of the nephron | - glomerular capsule (renal corpuscle) - renal tubule |
| what is the function of the glomerular capsule (renal corpusle) | filters the blood |
| what is the function of the renal tubule | - reabsorb needed materials |
| what is the function of the collecting ducts | carry remaining materials away as urine |
| discuss the structures in the renal cortex | - houses the glomeruli and convoluted tubules (proximal and distal) - hoses blood vessles |
| discuss the structures found in the renal medulla | inner medulla - loop of Henle and the cone-shaped masses (renal pyramids) |
| what are cortical nephrons | - 85% of all nephrons - originate superficially in the cortex - shorter loops of Henle (extend only short distance into medulla) |
| what are juxtamedullary nephrons | - 15% of all nephrons - originate deeper in the cortex - loops of Henle are thinner and extend into medulla entirely |
| name the two different systems that supplies blood to the nephron | - glomerulus - peritubular capillary network |
| what is the role of the blood supply to the glomerulus | - glomerulus is between 2 arterioles (afferent and efferent) - both arterioles are high resistance and high-pressure vessels - forces solutes out of the blood |
| what is the role of the peritubular capillary network | - low pressure vessels - better suited for reabsorption - capillaries surround the tubules in their entirety allowing rapid movement of solutes and water |
| name two specialized structures of the glomerular capillaries that contribute to the filtration of blood | - fenestrations - podocytes |
| list the 4 segments of the nephron tubule | 1) the proximal convoluted tubule (highly coiled...drains Bowman's capsule) 2) loop of Henle 3) distal convoluted tubule 4) collecting tubule (joins other nephron tubules to collect the filtrate) |
| what are the 3 processes involved in urine formation | 1) filtration 2) reabsorption 3) secretion |
| where does filtration occur | renal corpuscle |
| where does reabsorption and secretion occur | renal tubules |
| what is the normal value of the GFR | normal glomerular filtration rate (GFR) is 120-125 mL/min |
| discuss why the normal GFR value is important | maintenance of a relatively constant GFR is important for adequate reabsorption of water and other needed nutrients from the filtrate |
| list the 3 regulatory mechanisms of the GFR | 1) renal autoregulation 2) nervous system control 3) hormonal control |
| list 3 ways that the kidney acts as an endocrine organ | 1) renin-angiotensin-aldosterone (RAA) 2) erythropoietin (EPO...RBC production regulation) 3) Vitamin D activation (calcium metabolism) |
| describe the action of ADH | -acts on collecting tubule - increases water absorption - inhibits urine output - increases number of water channels in the cell membrane of the collecting duct |
| what is the main action of aldosterone | - increases the blood volume and pressure |
| describe action(s) of aldosterone | - place several types of ion channels in cells of collecting ducts - sodium-hydrogen ion channel (Na+ reabsorption and excretion of H+) - Na+ pumped out - water follows salt - increases K+ reabsorption |
| define hyponatremia using blood values | plasma concentration falls below 135 mEq/L |
| define hypernatremia using blood values | plasma Na+ levels rise above 145 mEq/L with a serum osmolality greater than 295 mOsm/kg |
| define hypokalemia using blood values | plasma levels fall below 3.5 mEq/L |
| define hyperkalemia using blood values | plasma levels rise above 5 mEq/L |
| define hypocalcemia using blood values | plasma levels fall below 8.5 mg/dL |
| define hypercalcemia using blood values | plasma levels are greater than 10.5 mg.dL |
| define hypomagnesemia using blood values | plasma levels are less than 1.8 mg/dL |
| define hypermagnesemia using blood values | plasma levels rising above 3.0 mg/dL |
| 3 mechanisms of control for blood pH | - chemical buffer system - brainstem respiratory center - renal system |
| common causes of acute postinfections glomerulonephritis | - streptococcus and staphylococcus bacterial infections - viral infections (hepatitis) - parasitic infections |
| risk factors for the formation of renal calculi | - levels of stone components in the blood and urine - anatomical changes or urinary tract structurs - metabolic and endocrine function - dietary and intestinal absorbtion - past history of UTIs - supersaturated urine |
| list the 4 types of kidney stones | - calcium stones - magnesium ammonium phosphate stones - uric acid stones - cystine stones |
| describe calcium stones | - results from increased concentrations of calcium in blood and urine - secondary to increased bone resorption (immobility), bone disease, hyperparathyroidism |
| describe magnesium ammonium phosphate stones | - alkaline urine (usually results from UTIs) - urease (enzyme from bacteria...breaks urea in to ammonia and CO2) - stones size increase as levels of bacteria rise ~ 15% of all kidney stones |
| describe uric acid stones | - coincides with gout - when pH is more acidic - not visible on X-ray films ~ 7% of stones |
| describe cystine stones | - rare (1-3%) - most common among children - results of cystinuria (decreased tubular absorption of cystine, result of genetic defect in renal transport) |
| describe renal colic pain | - brought on by stretching of collecting ducts/ureters - stones 1-5mm diameter move through ureter and block flow - acute, sharp pain in waves - pain in upper, lateral quadrant of abdomen ("flank pain") - can be accompanied by clammy skin and n/v |
| describe non-colicky pain | - stones that distended the renal pelvis or renal calyces - deep, dull ache in flank area - varies in intensity from severe to mild |
| what are the 3 categories of acute renal failure | - prerenal - postrenal - intrarenal |
| what are the 2 types of ATN | - ischemic - nephrotoxic |
| what are the 3 phases of ATN | - initiating - maintenance - recovery |
| what blood values are closely monitored in renal failure | BUN creatinine levels |
| describe the three parts of hemodialysis | 1) blood delivery system 2) a dialyzer 3) dialysis fluid delivery |
| how does hemodialysis work | - blood circulates through dialyzer - dialysate (dialysis fluid) moves on outside of tubules - molecules move in both directions - blood flows back into the body via a shunt |
| how is vascular access achieved for hemodialysis | - shunt (implantation of tubing into an artery and a vein)or more commonly through an arteriovenous fistula (anastomosis of an artery to a vein) |
| why are dialysis patients put on blood thinners | - to prevent blood clotting during treatment |
| name a blood thinner that you would give to a patient on blood thinners | heparin |
| list some common symptoms that accompany dialysis treatment | - nausea - vomiting - muscle cramps - headache - chest pain - vertico |
| the frequency of hemodialysis treatments | 3 times weekly ---lasting 3-4 hours |
| describe peritoneal dialysis | - same principles of hemodialysis - catheter placed in peritoneal cavity and exits on side of abdomen - sterile solution run through catheter - fluid remains in cavity (allowing metabolic waste to diffuse into solution) - fluid is drained |
| what is one of the major concerns about peritoneal dialysis | risk of infection at catheter site |
| what are the determinants of transplantation success | - overall health of the recipient - degree of compatibility btwn the donor and the recipient - management of recipient immunosuppression |
| in the proximal tubule, what is reabsorbed | - sodium - chlorine - bicarbonate - potassium - glucose - amino acids |
| in the proximal tubule, what is secreted | - organic acids and bases |
| in the thin descending loop of Henle, what is reabsorbed | water |
| in the thick ascending loop of Henle, was is reabsorbed | - sodium - chlorine - potassium - calcium - bicarbonate - magnesium |
| in the thick ascending loop of Henle, what is secreted | protons (H+) |
| in the early distal convoluted tubule, what is reabsorbed | - sodium - chloride - calcium - magnesium |
| in the late distal convoluted tubule/collecting duct, what is reabsorbed by the principle cells | - sodium - chloride |
| in the late distal convoluted tubule/collecting duct, what is reabsorbed by the intercalated cells | - bicarbonate - potassium |
| in the late distal convoluted tubule/collecting duct, what is secreted by the principle cells | - potassium |
| ADH acts on which cells cells | principal cells of the late distal tubule and collecting duct |
| in the late distal convoluted tubule/collecting duct, what is secretion by the principle cells | protons (H+) |
| ultimately, what is the stimulant for renin release | hypotension or hypovolemia, renal hypoperfusion |
| diagnostic tests for renal calculi | (based on sypmtomology) - UA - x-ray - CT - intravenous pyelography (IVP) - abdominal ultrasound |
| how does a UA test for a renal calculi | - urine pH - presence of stone forming crystals - infection - hematourea |
| CT used for renal calculi | most common diagnostic tool |
| treatment for acute renal colic | - pain management - antibiotic therapy |
| kidney stones that are _________ mm in diameter or less will pass on their own | 5 |
| what to do after a kidney stone has passed | focus on prevention of future stones |
| what lifestyle changes should be done to prevent kidney stones | - increased fluid intake - decrease in food that contributes to kidney stones |
| what is a ureteroscopic removal (under fluoroscopic guidance) | - small probe inserted to urethra/bladder/ureter - ureter dilated allowing physician to grasp fragment/stone |
| what is a percutaneous nephrolithotomy | - small gauge needle directly into flank - area is dilated - nephroscope placed in renal pelvis ***allows for removal of stones up to 1 cm*** ***larger stones must be broken down first*** |
| what is the extracorporeal shockwave lithotripsy | - use of acoustic shock wave to break stones to smaller fragments - stent will be placed in ureter to ensure proper drainage |
| describe stage 1 of Kidney Disease | Kidney damage with normal GFR |
| what is the GFR of Stage 1 kidney disease | 90 mL/min 1.73 m^2 or above |
| describe stage 2 kidney disease | kidney disease with mild decrease in GFR |
| what is the GFR of Stage 2 kidney disease | 60-89 mL/min |
| describe stage 3a and 3 b kidney disease | moderate decrease in GFR |
| what is the GFR of stage 3a kidney disease | 45-59 mL/min |
| what is the GFR of stage 3b kidney disease | 30-44 mL/min |
| describe stage 4 kidney disease | severe reduction in GFR |
| what is the GFR in stage 4 kidney disease | 15-29 mL/min |
| describe stage 5 kidney disease | kidney failure |
| what is GFR for kidney failure | less than 15 mL/min |
| what is hyponatremia | when plasma concentrations falls below 135 mEq/mL |
| name the two ways hyponatremia can present | - hypertonic - hypotonic |
| what is hypertonic hyponatremia | when water shifts from intracellular fluid to the extracellular fluid |
| when is hypertonic hyponatremia most likely to occur | in situations with hyperglycemia ---- increased sodium levels in plasma in response to increased glucose levels ---- ECF becomes diluted as water follows salt into plasma |
| what is hypotonic hyponatremia | - most common type - caused by water retention |
| three classifications of hypotonic hyponatremia | - hypovolemic - hypervolemic - euvolemic |
| what is hypovolemic hypotonic hyponatremia | when water and sodium are lost ---- mostly due to excessive sweating (exercise) ---- adrenal disease (decreased aldosterone levels) |
| what is hypervolemic hypotonic hyponatremia | when hyponatremia is accompanied by edema ---- heart failure ---- liver disease ---- renal disease |
| what is euvolemic hypotonic hyponatremia | when there is a retention of water with a dilution of sodium while ECF volume remains at normal levels ---- when ADH is higher than normal ---- common during post-op periods |
| early signs of hyponatremia | - fatigue - muscle cramps - weakness |
| more severe signs of hyponatremia | - nausea - vomiting - abdominal cramping - diarrhea |
| how can the nervous system be affected by hyponatremia | affected by the increased intracellular fluid. symptoms can include: - lethargy - headaches - disorientation/confusion - gross motor weakness - seizures (extreme) - coma (extreme) |
| how is a diagnosis of hyponatremia made | - blood work - urinalysis |
| how is hyponatremia treated | focus on underlying cause - (water intoxication) limit fluids and change meds - administer saline solution |
| what is hypernatremia | - when blood plasma levels rise above mEq/L with a serum osmolality greater than 295 mOsm/kg - deficit of water in relation to body's sodium level |
| what is the earliest sign for hypernatremia | thirst |
| list some other signs of hypernatremia | - decreased urine output - rise in body temp - flushed skin - dry mucous membranes - decreased salivation - difficulty swallowing |
| if the nervous system becomes affected by hypernatremia, what symptoms occur | - agitation - headaches - restlessness - seizures (extreme) - coma (extreme) |
| how is hypernatremia diagnosed | - physical exam with indications of dehydration - blood work |
| how is hypernatremia treated | treating underlying causes - replenishing fluids or intravenously |
| what is hypokalemia | when plasma potassium levels fall below 3.5 mEq/L |
| what are the three main causes of hypokalemia | - inadequate intake (most common) - excessive GI, renal, skin losses - redistribution between ICF and ECF compartments |
| 80-90% of potassium loss occurs via | urine (with remainder of being excreted through stool and sweat) |
| hypokalemia is common in the treatment of | diabetic ketoacidosis |
| GI symptoms of hypokalemia | - atony of intestinal smooth muscle - nausea - vomiting - constipation - abdominal distention |
| the most serious effects of hypokalemia occur on which system | cardiovascular |
| side effects of cardiovascular presentation of hypokalemia | - postural hypotension - bradycardia - ectopic ventricular arrhythmias |
| how is hypokalemia treated | - increase dietary potassium - (if rapid replacement is needed) IV replacement |
| what is hyperkalemia | when plasma levels rise above 5 mEq/L |
| why is hyperkalemia a rare condition | the body is extremely effected in the prevention of potassium accumulation in the ECF |
| three main causes of hyperkalemia | - decreased renal excretion - excessively rapid administration - movement of potassium from the ICF to the ECF compartment |
| the *most common* cause of hyperkalemia is | decreased renal function (renal failure) |
| burn and crush injuries will release potassium from the cell into the ECF, what type of hyperkalemia is this | potassium moved into the ECF from the cells, leading to an increased potassium levels |
| how doe signs and symptoms of hyperkalemia manifest themselves | through a decrease in neuromuscular activity |
| clinical presentation of hyperkalemia | - muscle weakness - dyspnea - heart issues (leading to ventricular fibrillation/cardiac arrest...extreme) |
| how is hyperkalemia diagnosed | - patient history (diet, potassium sparing drugs, episodes of muscular weakness, history of kidney disease) - physical exam (muscular weakness and volume depletion) - blood work - EKG |
| how is hyperkalemia treated | - administration of calcium - administration of sodium bicarbonate (or insulin) - intravenous infusions of insulin and glucose |
| what is hypocalcemia | plasma calcium levels falling below 8.5mg/dL |
| hypocalcemia is common place among those who are | critically ill |
| four categories of hypocalcemia | - impaired ability to draw calcium from bone stores - abnormal loss of calcium from kidneys - increased protein binding leading to greater abound of calcium in non-ionized form - soft tissue sequestration |
| list a few things that can lead to the suppression of PTH on bone reabsorption | - hypoparathyroidism - elevated levels of vitamin D - magnesium deficiencies |
| hypocalcemia will result when GFR falls below | 59 mL/min |
| acute presentation of hypocalcemia presentation | - increased neuromuscular excitability - paresthesias (tingling) - tetany (muscle spasms) |
| presentation of severe hypocalcemia | - seizures - hypotension - dangerous dysrhythmias (heart block or v. fib) |
| effects of chronic hypocalcemia | - issues with skeletal system - bone pain/deformities - fractures are common |
| how is acute hypocalcemia treated | always emergent - calcium infusion |
| how is chronic hypocalcemia treated | oral supplimentation |
| what is hypercalcemia | when plasma calcium levels are greater than 10.5 mg/dL |
| what are the two most common causes of hypercalcemia | - increased bone reabsorbtion of calcium due to noplasmic activity - hyperparathyroidism |
| clinical presentation of hypercalcemia | - stupor - weakness - muscle flaccidity - possible acute psychoses (behavioral alterations) - increased cardiac contractility and ventricular arrhythmias - constipation - nausea - vomiting |
| hypercalcemia treatment | - rehydration (lots of fluid replacement) - increase excretion of calcium in urine (use of diuretics and NaCl for excretion of calcium) |
| what is hypomagnesemia | when plasma concentration of magnesium is less than 1.8 mg/dL |
| hypomagnesemia results from | - malnutrition and starvation - diarrhea = decreased absorption in intestines |
| clinical presentation of hypomagnesemia | - usually in conjunction with hypocalcemia and hypokalemia (will have similar signs and symptoms) - personality changes - tremors - tachycardia - hypertension - ventricular dysrhythmias |
| treatment for hypomagnesemia | - replacement therapy (route depends on severity) - severe cases = parenteral administration |
| what is hypermagnesemia | when plasma magnesium levels can raise above 3.0 mg/dL |
| why is hypermagnesemia rare | the kidneys have a great ability to excrete magnesium |
| hypermagnesemia is rare, when it does occur why does it occur | renal insufficiency or disease or the overconsumption of foods/supplements containing magnesium |
| clinical presentation of hypermagnesemia | - diminished neuromuscular function - hyporelexia - muscular weakness - confusion - drop in BP (severe cases) - respiratory paralysis - heart block - cardiac arrest |
| treatment of hypermagnesemia | intravenous administration of calcium (inhibits effects of magnesium) |
| what is acidosis | when blood pH is < 7.35 |
| what is alkalosis | when blood pH > 7.45 |
| what is normal blood pH levels | 7.35-7.45 |
| what is normal PCO2 | 35-45 mmHg |
| what is normal HCO3 | 22-26 mEq/L |
| what is respiratory acidosis | blood pH < 7.35 due to higher than normal CO2 pressure (PCO2 > 45) |
| what causes respiratory acidosis | shallow breathing or limited gas exchange |
| which diseases are associated with respiratory acidosis | - cystic fibrosis - emphysema - pneumonia |
| what is the clinical presentation of respiratory acidosis | - hypoxemia - change in pH in CSF - headaches - blurred vision - irritability - muscle spasms - psychological changes - paralysis (severe) - respiratory depression (severe) - coma (severe) |
| respiratory acidosis treatment | - improving ventilation (mechanical ventilation is required) |
| what is respiratory alkalosis | blood pH >7.45 due to lower than normal CO2 pressure (PCO2 < 35 mm) |
| what is the cause of respiratory alkalosis is almost always caused by | hyperventilation (over-breathing) |
| respiratory acidosis/alkalosis may cause the renal system to attempt to correct these disorders through | renal compensation |
| clinical presentation of respiratory of alkalosis | - reduction in serum calcium levels - increased neuromuscular excitability (hyperexcitability) - decreased cerebral blood flow - light-headedness - dizziness - numbness - tingling - sweating - palpitations - dyspnea - short period apnea |
| treatment for respiratory alkalosis | - supplemental oxygen - (under psychological stress) treat underlying anxiety |
| what is metabolic acidosis | when blood pH is < 7.35 due to a lower than normal HCO3- concentration (PCO2 will be in normal limits) |
| what normally causes metabolic acidosis | buildup of acidic metabolic waste in blood stream (i.e. acetic acid from ETOH overdose, lactic acid, diabetic ketosis, or extreme diarrhea) |
| clinical presentation of metabolic acidosis | difficult to diagnosis (usually brought on by other disease and sx mimic underlying cause) - increase RR - dyspnea at rest - weakness/fatigue - malaise - dull headache - decrease in CO (severe) - fatal arrythmias (severe) |
| what are compensatory mechanisms of metabolic acidosis | - changes in normal breathing patterns - rapid respiratory rate |
| what is the treatment for metabolic acidosis | - revolves around the underlying cause of condition - administration of supplemental sodium bicarb. |
| what is metabolic alkalosis | - blood pH > 7.5 and higher than normal HCO3- (PCO2 will be within normal limits) |
| common causes of metabolic alkalosis | - vomiting - excess intake of antacids - constipation |
| how does the respiratory system help correct metabolic acidosis or alkalosis | respiratory compensation |
| clinical presentation so metabolic alkalosis | similar s/s with volume depletion - less frequent neurological symptoms but can include ------ mental confusion ------ hyperactive reflexes ------ tetany |
| treatment for metabolic alkalosis | focus on correcting underlying condition - replace fluid with n/s solution - administration of potassium and chloride |
| Respiratory acidosis - pH - PCO2 - HCO3- | pH < 7.35 PCO2 > 45 mm HCO3- > 26 mEq/L (if compensated) |
| respiratory acidosis - body compensation | increase kidney retention of HCO3- |
| respiratory alkalosis - pH - PCO2 - HCO3- | - pH > 7.45 - PCO2 <35 mm - HCO3- <22 mEq/L (if compensated) |
| respiratory alkalosis - body compensation | decreased kidney retention of HCO3- |
| metabolic acidosis - pH - PCO2 - HCO3- | - pH >7.35 - PCO2 < 35 mm (if compensated) - HCO3- < 22 mEq/L |
| metabolic acidosis - body compensation | hyperventilation to increase CO2 elimination |
| metabolic alkalosis - pH - PCO2 - HCO3- | - pH > 7.45 - PCO2 > 45 mm (if compensated) - HCO3- > 26 mEq/L |
| metabolic alkalosis - body compensation | hypoventilation to decrease CO2 elimination |
Created by:
kandriot
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