BIO SCI N120A Lecture Notes - Lecture 1: Glucose Tolerance Test, Efferent Arteriole, Afferent Arterioles

6 views3 pages
24 Jul 2019
School
Professor
Professor Nicholas
Course Code 06204
N120A
4 units
Lecture
Diabetes:
Hypoglycemia alpha cells glucagon forms glucose to release
Hyperglycemia beta cells insulin glucose to glycogen
Stress inhibits insulin release, increases glucagon, increases lipolysis, decreases AA and
fat storage, increases glucose/gluconeogenesis
Type I: beta cells destroyed
Type II: insulin resistant, cells don’t want to take glucose out
Insulin binds to receptor signal transduction cascade new GLUT 4 receptors brought
to surface through exocytosis glucose enters cell
Insulin = glucose uptake in muscle; no lipolysis or glucose production
Dilated afferent arteriole, constricted efferent arteriole (increased pressure), loss of
proteins so cell inflammation
o ACE inhibitor dilates the efferent arteriole to decrease pressure going out of
nephron
Symptoms: fatigue (no sugar in cells), hungry, (no glucose in cells), peeing more (excess
sugar excreted in urine, drags along fluids from tissues), excessive thirst, (kidneys can’t
bring blood sugar all in more urine), dry mouth (peeing more), blurred vision (pulls
fluid from eye tissues), weight loss (less calories), nausea (burning fat ketones),
infections, tingling in hands/feet, dry mouth, itchy skin, slow healing cuts
Tests:
o Fasting blood sugar: tests for blood sugar at that moment
o Hemoglobin A1C: tests for blood sugar over the past 2-3 months
o Oral glucose tolerance test: glucose is given, how quickly is it clearly from blood?
Treatments:
o Insulin injections
o Metformin: decreases amount of glucose produced by liver
o Erythropoietin: increase red blood cells = relieves fatigue
o Weight reduction (increases sensitivity to insulin)
o Drugs for type II: increase insulin production (chlorpropamide), decrease sugar
absorption (acarbose)
Renal failure:
Amino acids undergo deamination to form ammonia and keto acid less toxic urea
Hydrostatic pressure vs. osmotic (tries to hold fluid in) and capsular pressure (fluid
already in capsule)
Bp increases
Macular densa cells senses sodium level in distal tubule
o If low sodium, bp and hydrostatic pressure is too low and blood moving slow so
more time to absorb salt earlier
o Controls pressure in nephron by saving filtration
Renin-angiotensin-aldosterone system
o Renin: angiotensinogen angiotensin I
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