Exam2 - Movement/Support + Perfusion Flashcards
Dorsal to ventral, what is the order of the spinal cord coverings?
Dura mater
Arachnoid mater
Pia mater
How does spinal anaesthesia differ from epidural anaesthesia? How are they similar?
They are both analgesics (pain relief) and anaesthetics (numbing).
Epidural location is the fatty epidural space between dura and dorsal vertebrae. A catheter is threaded and it’s hooked up to a continuous drip.
Epidurals medicate afferent nerves. They do not enter the spinal fluid.
The spinal anaesthetic location is in the subarachnoid space. It is an injection (no drip) and wears off in two hours. It enters the space with spinal fluid.
Which nerves are afferent and which are efferent? (Dorsal vs ventral)
Dorsal nerves are afferent (sensory relay to brain)
Ventral nerves are efferent (motor relay to body)
What does RANK-L do? Who releases it? What initiates its release?
Rank ligand. Activates bone resorption by attaching to RANKL receptors on osteoclasts.
Released by osteoblasts.
When blood calcium levels decrease, parathyroid gland releases PTH, which tells the osteoblasts to release RANKL.
What is OPG and what does it do? Who releases it? What initiates its release?
Osteoprotegrin.
It supports bone formation by attaching to RANKL so it can’t attach to osteoclasts. Prevents osteoclasts from resorbing and allows osteoblasts to build bone.
Released by osteoblasts.
Its release is initiated by testosterone, estrogen, and weight-bearing exercise.
What effects do low blood calcium levels have on osteoblasts and/or osteoclasts?
Parathyroid gland releases PTH in response to low Ca++ levels.
PTH stimulates RANKL release by osteoclasts.
Osteoclasts resorption releases Ca++ into bloodstream.
(PTH release slows when Ca++ levels rise).
What effect do high blood calcium levels have on osteoblasts and/or osteoclasts?
With high blood Ca++ levels, the thyroid releases Calcitonin, which tells osteoclasts to stop resorption activity.
(PTH release will also slow).
What is RANK?
RANK is the receptor for RANKL (found on osteoclasts)
What are the risk factors for osteoporosis?
**Post-menopause (low estrogen=low OPG release) Insufficient dietary Ca++ before age 30 Poor Ca++ absorption Vitamin D deficiency Excess caffeine/nicotine/alcohol Inadequate weight-bearing exercise Endocrine disorders (like excess PTH)
Where is osteoporosis most likely to occur?
In porous parts of bone, like the femoral neck of the trochanter, the wrist, and the thoracic and lumbar spine.
What are the three types of fractures we talked about and any risks associated with them?
Closed fracture
Open fracture (broken skin = increased risk for infection)
Pathologic fracture
(Note: if any of the above are breaks fo the femur, there is a high risk for blood loss leading to hypovolemic shock).
What is compartment syndrome and why does it happen?
Inflammatory response can lead to fluid increase/swelling, that puts pressure on arteries, veins, nerves, muscle in the compartment.
It can happen if a hard cast is put on a broken limb too soon, or inside the abdomen (unrelated to casting).
What signs and symptoms are associated with compartment syndrome?
Swelling, skin color change (pallor), signs of occluded blood supply on other end of cast:
- decreased SpO2
- decreased cap refill
- decreased pulse strength
- decreased sensation (due to hypoxic cell injury)
Monitor circulation, motion and sensation.
What are the types of spinal cord injuries we talked about that can lead to spinal shock? Are they primary or secondary neurologic injuries?
Concussion: (violent shaking of brain tissue or spinal cord tissue up against bone. From force of acceleration, deceleration, or rotation).
Contusion: (bruising of neural tissue)
These are all primary neurologic injuries.
Laceration: (tearing of neural tissue)
What is transection and why isn’t it associated with spinal shock?
Transection is a complete severing of the spinal cord. There will be total and irreversible loss of function below the level of the cord injury.
(Spinal shock is temporary)
What is a secondary neurologic injury?
When spinal blood flow is obstructed due to an inflammatory response. The obstruction leads to ischemia and necrosis of neural tissue.
What is spinal shock and why does it happen? Is it a primary or a secondary neurologic injury?
A temporary loss of function due to swelling around the nerves in the spinal cord. (Despite the word “shock,” has nothing to do with vascular supply).
Mast cells detect concussion/contusion/laceration and begin the inflammatory process.
Spinal shock is a secondary neurologic injury - it is due to swelling.
What are dermatomes and what are some ways we use them?
Dermatomes mapped out sections of the body that correlate with spinal nerves.
We use them to test for sensation at different levels:
- C3/C4 on side of neck
- T6 at nipple line: critical level for neurogenic shock/failure of vital processes. Monitor for patients with an indwelling epidural cath. If loss of sensation rises to T8/T7, get a BVM an a provider.
Shingles: location of skin blisters tells you where in the nerve fibers varicella is acting up. Provider can give cortisone shots along the nerve route to treat.
What is the most common cause of lower back pain?
Acute lumbar disc herniation due to poor body mechanics.
Herniation in towards the spinal cord puts pressure on the capillary beds there.
Local ischemia d/t occluded blood flow. Mast cells detect and send out chemotactic factors to initiate inflammatory response.
(Slide says most low back pain is idiopathic).
What is degenerative joint disease?
Also called osteoarthritis. It occurs in load-bearing synovial joints. Excess wear and tear leads to degradation of cartilage. Bone rubs on bone, leading to inflammation. Sometimes associated with crepitus (crunching sound from bone fragments in joint)
Biggest risk factor is a BMI greater than 30.
Age also increases risk d/t decreased cartilage
Also, joint stress/trauma
genetic & environmental factors
What is Rheumatoid Arthritis?
Autoimmune condition where your adaptive immune system attacks the synovial membrane, thinking its antigens are foreign invaders.
Chronic inflammatory process in joints leads to fibrotic scarring. Synovial membranes experience hyperplasia, developing nodules called “pannus” that are most visible on surface joints. Limit movement.
Describe the immune process behind rheumatoid arthritis
Rheumatoid factor attaches to the synovial membrane cells, initiating the inflammatory response.
Neutrophils and Macrophages start to phagocytize damaged tissue.
Macrophages present the antigen to CD4 cells
CD4 cells connect with naive B cells and initiate their differentiation into plasma & memory B cells.
Lots of antibodies produced against synovial cells.
(A positive test for rheumatoid arthritis will reveal elevated levels of rheumatoid factor).
What is the primary symptom of Gout? What causes it?
Red swelling, pain, and eventually a hard nodule called a “tophi” in the big toe.
Caused by uric acid crystals that form in the synovial fluid and slightly lower temps of the toe.
-Uric acid can accumulate because of hyperuricemia (elevated blood uric acid levels). Decreased kidney function, high purine diets, conditions with rapid cell turnover and repair (like burns) can increase risk.
What gives cartilage its cushioning characteristics and why doesn’t it heal? What happens instead?
Cartilage attracts water, which helps to cushion loads.
- chondrocytes don’t proliferate
- don’t receive nutrients through a blood supply, but rather through diffusion.
Cartilage is prone to calcification:
- calcified cartilage can’t properly diffuse nutrients
- this leads to swelling and death of chondrocytes
- eventually, bone will replace cartilage.
What can you do to promote bone repair/growth?
Change your diet:
- extra Ca++
- extra protein
- vitamin D
- antioxidants to combat any inflammatory ROSs from damage.
Avoid: nicotine, excess caffeine, alcohol
Add weight-bearing exercise to increase OPG release.
What is a soft callus?
Forms when bone has been damaged and is in the process of regrowing (osteoblasts). Includes new blood vessels and collagen (thanks to macrophages).
Weight-bearing in the first 2-3 weeks of bone repair can cause deformities.
(The soft callus will become harder, but the bone won’t fully heal for about 4 months)
What leads to scoliosis and why do people have surgery to correct it?
It’s due to genetic factors and occurs during rapid growth in adolescence.
Surgery consists of the severing of all muscles, placing in traction, total spinal fusion, titanium rods and screws.
Corrective surgery is because the curvature in the spine can put pressure on the lung tissue leading to shortness of breath, and pressure on the heart, leading to low cardiac output.
What happens to sensory input once it arrives at the brain?
- Motor cortex (in cerebrum) interprets & determines response
- Sends message to thalamus
- Thalamus (sensory relay center) interprets both incoming and outgoing messages
What do we need to know about the basal ganglia?
Cluster of cells in and around the thalamus that release dopamine.
(Dopamine inhibits excess movement and smooths out good movements).
These are the cells that atrophy in Parkinson’s, decreasing dopamine and resulting in a resting tremor and other movement control issues.
What do we need to know about the cerebellum?
Home of the Reticular Activating System (RAS) - a cluster of nerve cells that helps regulate movement.
Problems in which areas of the brain can lead to coordination and movement issues? What sort of problem might cause that?
Motor cortex (cerebellum)
Thalamus
Basal ganglia
Cerebellum
Hemorrhagic stroke is one of the problems that can damage these areas.
What are some motor dysfunctions related to tone?
Hypertonia: too much muscle tone - leads to stiff, difficult to move muscles.
(Can result from blocked efferent messages - muscles tighten due to disuse)
Hypotonia: Low muscle tone, many times with reduced strength.
How does muscle tone differ from strength?
Tone is observable in activities like sitting, turning, general ADLs.
Strength relates to the ability to push, pull, lift, etc.
What type of motor dysfunction is related to strength?
Paresis: muscle weakness but normal tone
Plegia: paralysis
What type of motor dysfunction is related to movement?
Hyperkinesia: increased muscular activity, resulting in excessive abnormal movements (like tremors in Parkinson’s)
Hypokinesia: Abnormally decreased muscle movement (slow gait in Parkinson’s, or difficulty in initiating movement).
What is the most common cause of hypotonia in infants?
Lack of oxygen to the brain in the birth process leads to hypoxic cell injury to the brain. Creates motor cortex problems (no motor output).
What is disuse syndrome and how does it relate to limited mobility?
Inability to move around leads to a deterioration of body function/systems.
What does nitric oxide do? What medication do we give for MIs that mimics its effects.
Nitric Oxide (NO) causes arteries to dilate, improving blood flow.
We give Nitroglycerin during MIs because it has the same effect.
What do free radicals have to do with NO (nitric oxide) production? How do we combat their effects?
The enzyme that produces NO gets highjacked by free radicals and changes it so it produces MORE free radicals.
Due to free radical damage, arteries will stiffen and become dysfunctional - they won’t relax when they should.
Large quantities of fruits and vegetables in our diet will use up the free radicals so they can’t hijack this enzyme.
How do Aortic & Carotid Baroreceptors participate in heart rate regulation.
What is the response?
Stretch receptors that detect a pressure change in the arteries (based on the amount of stretch).
Send signals via connected nerves to the medulla oblongata.
Cardiac Control Center in oblongata has a “set point” for blood pressure. It interprets message and sends signals along efferent nerve to bring it back to set point.
If BP is too high, efferent vagus nerve (PNS fibers) to SA node, releases ACH and inhibits/slows heart rate. (Notes also say systemic dilation of arterioles and veins).
If BP is too low, efferent cardiac nerve (SNS fibers) - releases Norepinephrine and increases heart rate.
A patient has broken his wrist. Which cells will the mast cells summon during degranulation?
Phagocytes: neutrophils and monocytes/macrophages.
Your patient with the broken wrist has mast cells that will synthesize platelet-activating-factor. How is this going to help repair his bone?
It signals the liver to release clotting factors - both fibrinogen and platelets are activated for response.
Which WBC promotes angiogenesis?
Macrophages
What are 3 ways that macrophages help to repair broken bone?
- Clean up debris at site (phagocytosis). Stay a while because it can replicate.
- Grow a new blood supply so area can heal.
- Release cytokines - promote collagen and callus growth.
A fibrin mesh is being laid down at a broken bone injury site. How did the clotting cascade get started?
Mast cells synthesized platelet activating factor.
This signaled the liver to release clotting factors and fibrinogen.
What should you tell your broken-bone patient about diet and activity?
- DO eat calcium, vitamin D and protein.
- Avoid OPG inhibitors like caffeine, alcohol and nicotine.
- Avoid weight bearing exercise during soft-callus formation.
