Physiology Test 2 Book Flashcards
Polyuria?
Increased urination
Polydipsia?
high level of fluid intake, increased thirst
How do loop diuretics work such as furanosamide would partially act by decreasing the osmolarity of the renal interstital fluid?
Loop diuretics work in the thick ascending limb of the loop of henle which is crucial to the establishing the counter current multiplier hyperosmolarity. It makes the renal interstitial fluid hyperosmotic.
Unwanted side effect of carbonic anhydrase inhibitors?
Acidosis due to the decrease in bicarbonate re-absorption and loss in the urine
Osmotic diuretics such as mannitol work where and what is the mechanism?
They inhibit water and solute reabsorption by increasing the osmolarity of tubular fluid in the proximal tubules
Thiazide diuretics work where and what is the mechanism?
They inhibit NaCl co transport in luminal membrane and work in the early distal tubules
Carbonic anhydrase inhibitors work where and how?
Inhibit H secretion and bicarb reabsorption which reduces Na reabsorption in proximal tubules
Aldosterone antagonists work where and how?
Inhibit aldosterone on tubular receptor and decrease Na reabsorption and decrease K secretion in the Collecting tubules
Where do sodium channel blockers work and how?
Block entry of Na into na channels of luminal membrane and decrease Na reabsorption and decrease K secretion. Collecting tubules
General function of diuretics?
Increase the rate of urine volume output, most commonly used to treat edema and hypertension
What can cause pre-renal AKI?
It is due to decreased blood flow through the kidneys this can be caused by heart failure due to a decreased CO and low BP or severe hemorrhaging.
How does an intrarenal AKI occur?
From abnormalities within the kidney affecting blood vessels, glomeruli, or tubules
How does a post renal AKI occur?
results from obstruction of the urinary collecting system. Most common cause is kidney stones
What is oliguria?
decreased urine output, usually accompanied with a prerenal AKI due to decreased BP and GFR.
What is anuria?
complete cessation of urination due to renal blood flow extremely reduced
Acute Glomerulonephritis?
Type of intrarenal AKI caused by abnormal immue reaction damaging glomeruli. STREPTOCOCCAL infection
Tubular necrosis?
Cause of intrarenal acute renal failure. Destruction of epithelial cells in tubules due to severe ischemia or blood loss or poisons/medications destroying the epithelial cells
Tubular cells slough off and block nephrons so urine output doesn’t occur. If BM isn’t damaged then new tubular epi cells can grow along surface of membrane and repair within 10-20 days.
Acute tubular necrosis?
caused by severe renal ischemia due to circulatory shock. Tubular cells slough off and block nephrons so urine output doesn’t occur
Post renal AKI?
Multiple abnormalities in lower urinary tract that block or partially block urine flow. Caused by: bilateral obstruction of ureters bladder obstruction, urethra obstruction
physiological affects of AKI?
Retention of water and other waste products leading to edema and high BP
Benign nephrosclerosis?
Most common form of kidney disease is a vascular lesion in arteries in kidney leaking plasma through membrane of vessels.
Glomerulosclerosis?
Damaged kidney tissues becomes replaced by fibrous tissue
What is the most important stimuli for increasing H secretion by tubules in acidosis?
Increase in pCO2 of ECF in respiratory acidosis AND an increase in H concentration of ECF
What occurs in alkalosis?
H secretion is reduced too low to achieve complete HCO3 reabsorption increasing the amount of HCO3 excretion.
Under pathological conditions what hormone can cause an increase in H+ secretion?
Aldosterone as seen in patients with Conn’s syndrome. They increase secretion of H into tubular fluid and increases the amount of HCO3 added back to blood usually causing alkalosis.
Compensatory response of respiratory acidosis?
Addition of new bicarb to the ECF by the kidneys which increases HCO3 plasma levels
Metabolic acidosis compensatory response?
In met. acid. there is a decrease in pH and rise in H ecf concentration. The primary abnormality is a decrease in Bicarb. Response includes increasing ventillation rate which decreases pCO2 and also renal compensation of adding bicarb to ECF
Respiratory alkalosis compensatory response?
response to a primary reduction in Pco2 is to reduce plasma HCO3 concentration caused by increased renal excretion of HCO3
Metabolic alkalosis compensatory response?
caused by rise in ECF bicarb concentration it is compensatoed for decreasing ventillation which raises pCO2 and increase renal bicarb excretion.
Achalasia?
lower esophageal sphincter fails to relax during swallowing
Achlorhydria?
stomach fails to secrete HCl pH of gastric secretions fails to fall below 6.5
Sprue?
Malabsorption by small intestinal mucosa
Hirschprung’s disease?
megacolon. Constipation so severe bowel movements only occur every few days or once a week. Caused by deficiency or lackof ganglion cells in myenteric plexus in sigmoid colon
Where do fats go instead of portal blood?
Absorbed into intestinal lymphatics and then conducted to systemic blood by the thoracic duct. Bypassing the liver.
What causes increased blood flow during GI activity?
vasodilator substances such as peptide hm’s cholecystokinin, vasoactive intestinal peptide, gastrin, and secretin.
GI glands also relase Kallidin and Bradykinin also vasodilators.
Decreased o2 concentration in the gut wall increases blood flow.
