Week 4 Day 3 & 4 (excluding Nervous tissue and bone) Flashcards
Name the primary and secondary curvatures of the spine.
Primary: Thoracic and sacral
Secondary: Cervical and lumar
Describe a herniated disc
When the nucleus pulposus has breached the annulus fibrosus and impinges upon a spinal nerve.
Name the 6 functions of the spine
- Protection
- Support
- Motion and posture
- Attachments
- Flexibility
- Pivot point for head
Name the five main parts of the spine
Cervical (7), Thoracic (12), Lumbar (5) Sacral (5), Coccyx (4)
Atlantoocciptal joint allows you to ____ your head ____
Nod your head yes
Atlantoaxial joint allows you to _____ your head ___
Shake your head no
The __________ arteries supplies blood to the cervical, thoracic, lumbar and sacral regions of the spine
Segmental arteries
The largest vertebral venous plexus is the _____________ which drains into the __________ veins in the neck and trunk.
The largest vertebral venous plexus is the internal vertebral venous plexus which drains into the segmental veins in the neck and trunk.
_____ _____ provide the only significant mechanism for cholesterol excretion.
Bile salts! Bc cholesterol is turned into bile acid in the liver then to bile salt and through biliary secretion delivered to the small intestine for excretion.
____ allows for the synthesis of steroid hormones with cholesterol as a precurser
CYP450 in the liver!
_______ biosynthesis intermediates are required to make vitamin D
Cholesterol
Name the rate limiting step in cholesterol synthesis
HMG-CoA reductase
To inhibit the production of cholesterol, which enzyme do statins inhibit?
HMG-CoA reductase
What is the relationship between cholesterol and LDL, VLDL, and HDL?
LDL, VLDL, and HDL are lipoprotein transporters of cholesterol in the blood.
VLDL from the liver turns to LDL. HDL as it leave tissue.
What does lowering cholesterol via statins do to the LDLR?
Lowering cholesterol causes an increase in LDLR which causes more cholesterol to be taken in and degraded.
Name four defects in cholesterol that could lead to familial hypercholesterolemia.
- Defect in the LDLR synthesis
- Mutation causing misfolding then degradation (never makes it out of the ER)
- Mutation that prevents ligand LDL binding to receptor
- Mutation that prevents LDLR endocytosis or recycling
Describe prevalence and give the equation
Amount of the disease in a population at a given time
Prevalance = # w/disease / # people in population
Describe incidence
Development of a new disease over time