Physiology Flashcards
(36 cards)
You encounter a patient with a rare viral disorder that erodes the cartilage from the long bones especially of the distal femur and proximal tibia. The bodies repairing of this structure would most likely convert which type of cartilage into which new material? A) fibrocartillage into elastic cartilage B) Hyline cartilage into fibrocartillage C) Hyline cartilage into elastic cartilage D) Periosteum into hyline cartilage The early stages of this condition leading to inflammation and pain and increased friction would be called what?
B) The cartilage of long bone is hyline cartilage and when repaired becomes fibrocartilage, which has more type 1 collagen making it stronger but also doesn’t bear weight well at the joint due to its rigidity. Initially this would be considered osteomalacia and later athritis.
A patient presents with stiffness of the back and a PE reveals a fairly healthy 5’2” 14 y/o girl. After viewing an x-ray of the back you discover some suspicious finding in her inter-vertebral disks, which appear more dense than usual; though she has no signs of tumor. How would you generally classify her condition? A) Achondroplasia B) Arthritis C) Chondrodystrophy D) osteosarcoma
C. Chondrodystrophies are a group of disorders in which cartilage is ossified into bone. The problem is with the fibrous cartilage of the inter-vertebral disk. This is a cartilage issue and the only one that fits. Her height is not an issue due to her age, and arthritis isn’t a good fit.
What is a precursor to a fibroblast? Hematopoetic stem cell Fibrocyte Chondrocyte Messenchymal cell Osteoclast precursor?
Messenchymal cell Monocyte
What general process causes the circular formations of lamelae?
Bone remodeling
What is endochondral ossification?
In conjunction with intramembranous ossificiation it is one of two essential processes during fetal development by which bone tissue is created; cartilage is present in this process. The formation and growth of long bones as well as the healing of bone is what defines this process.
WHAT DO YOU THINK IS HIGH YIELD FOR THIS LECTURE?
PRECURSOR CELLS TISSUE ID
What is marfan’s syndrome?
Defect in fibrillin 1 which is the primary component in microfibrils which attach to elastin. It is essential for the proper formation of ECM, including the formation of elastic fibers. Can lead to aortic aneurysm Increased TGF-B activity: neg affects vascular smooth muscle development Inflammation
Connectve tissue proper is of two types. What are they and which tissue compose them?
Dense and loose connective tissue Dense- regular (tendons, ligaments) irregular- skin, dermis, periosteum/chondrium Elastic- EEEE + aorta, vocal cords, epiglottis, eustacian tubes Loose- areolar, adipose, and reticular
What is syndesmosis, synchondrosis, and diarthrosis?
Syndesmosis- Bone united by the same ligament (interosseus membrane of the tibia and fibula) Synchondrosi- same cartillage- cartilage joints, like costal cartilage Diathrosis is the same thing as a synovial joint.
When a joint is injured and hyline cartilage is replaced with fibrous cartilage how does the collagen content differ in the newly repaired joint?
Fibrocartilage has more collagen Type I, so its stronger, but less flexible.
How is osteoblast formation different from osteoclast?
Mesenchymal stem cell–> osteoprogenitor cell–> osteoblast–> osteoclast Hematopoietic stem cell–> myeloid stem cell-> monocyte–> osteoclast precursor–> osteoclast
Pain sensation has what four qualities?
Location
Modality-type or quality
Intensity-sharp or dull
Duration/Frequency
What is a receptive field? What type of neurons innervate it, and how many neurons can innervate it?
Is a area sensitive to stimuli such as touch temperature pressure pain etc.
First order neurons innervate it and can be either inhibitory or excitatory; one or many.
Which type of first order neuron utilizes an interneuron as an intermediate to the second order neuron?
A) Excitatory first order neuron
B) motor neuron
C) Inhibitory first order neuron
D) Inhibitory motor neuron
C) inhibitory first order neuron
The excitatory first order neuron acts directly on the second order neuron and motor neurons don’t make sense in this sensory contex.
How does a sensory neuron compare to a motor neuron, or a projection interneuron?
The sensory neurons soma is between the free nerve ending on one end and the terminal buttons on the other. This is contrasted with both the motor neuron and the projection interneuron and others whose soma are surrounded by dendrites receiving signals from other neurons.
You’re on your way back to town after a long camping trip with your friends when you decide to stop and eat and a mexican restarant known for its habenaro peppers. How does your body interpret the capsaicin in your mouth as spicy? What type of nociceptor is involved and what fiber type does it utilize to process this information?
Your body has Transient receptor potential (TRP) channels that respond to different modalities: hot, cold, chem, mechanical. When activated the channel opens and ions flow into the nociceptor causing depolarization of the membrane potential.
Spicey food would utilize a polymodal nociceptor with a nonmyelinated C fiber. This receptor handles high-intensity mech, chem, or thermal signals.
As you continue to eat spicy peppers and the nociceptors activated stay above threshold how will this be interpreted by your body? Are there other ways to replicate this effect?
The result of multiple action potentials firing at a higher rate will be an increased intensity.
This can also be achieved by increasing the number of nociceptors involved, which results in a more intense signal being sent to the brain.
You step into a walk in freezer at costco and the door accidentally closes behind you traping you inside. The temp is 23 deg. Assuming the range for your cold receptors is 7-43 deg and your cold-pain receptors initiate below 15 deg. How would you explain the firing rate for each at around 10 deg?
A) cold receptors are decreasing their firing rate and the cold pain receptors are increasing their firing rate
B) Cold-pain receptors are decresing their firing rate and the cold receptors are increasing their firing rate
C) Their are only a few cold receptors and cold pain receptors firing
D) Their are many cold receptors firing but only a few cold-pain receptors firing
A) is correct. According to the questions stem 10 degs is in the lower range for cold receptors, meaning they will be decreasing their firing rate. Conversely 10 degs is in the upper range for cold-pain receptors, meaning they will be starting to increase their firing rate.
B) opposite of A
C) It’s not the number of receptors firiing here that matters. It’s true that intensity of a signal can be increased with an increased rate of firing or with more receptors firing. If this was the case with the cold receptors though it wouldn’t translate to cold-pain. This is because Nociceptors respond to extreem temperatures (cold and heat) to signal pain, this is not the result of many “regular” cold or warm receptors having a additive effect.
After being saved from a costco freezer entrapment you start to warm up to about 25 deg. What type of receptors facilitate this sensation and what is their fiber type?
A) Thermal nociceptors with A-delta fibers
B) Polymodal nociceptors with C-fibers
C) Regular warm receptors fiber type unknown
D) Mechanical nociceptors with A-delta fibers
C is correct
Unless the temp is extreem (>45 or <-5) you wont be utilizing thermal nociceptors (pain), just your regular warm receptors. Unless the stem explains that your set pt is decreased making you more sensitive to pain, you will not be using thermal nociceptors around room temperature 25 deg
What is the pathway for pain sensation from nociceptor to the cortex and back to the NMJ?
Nociceptor
Peripheral nerve
(brachial plexus)
Spinal cord: relay neuron, dorsal horn.
Spinothalamic tract/Thalamus
Somatosensory cortex
THEN BACK
Motor cortex
Pyramidal tract
Spinal cord: motor neuron, anterior horn
(brachial plexus)
Peripheral nerve
Neuromuscular junction
You decide to flip your tortillas by hand on the frying pan and accidentally burn your finger a bit. The nociceptors in your hand have various types of TRP channels, those with a majority of one type are named after that type. Which nociceptor type will signal the pain in your finger first, and which will come after? What is the name of this nociceptor type?
A) Thermal, Polymodal, Polymodal
B) Thermal, Polymodal, Thermal
C) Polymodal, Thermal, Polymodal
D) Polymodal, Thermal, Thermal
A is correct
Thermal nociceptors will send the pain signal first b/c they’re myelinated and polymodal will send signal after as it’s nonmyelinated. Both respond to thermal stimuli, but the receptor will be named after the polymodal nociceptor as it responds to high-intensity thermal stimuli (like heat from a frying pan).
Describe the characteristics of thermal, mechanical, polymodal, and silent nociceptors
Thermal: (>45 deg C or <-5 deg C), small diameter, thinly myelinated A-delta (Aδ) fibers, 5-30 m/s
Mechanical: intense pressure to skin, A-delta (Aδ) fibers.
Polymodal: high-intensity mechanical, chemical, or thermal (both hot and cold stimuli), small diameter, nonmyelinated C fiber, slow (< 1.0 m/s).
Silent
Found in the viscera.
Not normally activated by noxious stimuli.
Inflammation and chemical agents can reduce their firing threshold.
Highly localized visceral damage (e.g. cutting the intestine in two) often does not cause pain but diffuse nociceptor activation (e.g. ischemia, spasm, chemical stimuli) can be severe.
What are the classic chemical mediator that can activate or sensitize nociceptors? How can this effect be cyclic? How does this process usually begin? What would you call this decreased pain tolerance to noxious stimuli?
Prostaglandins and bradykinin can sensitize nociceptors.
Bradykinin activates Aδ and C fiber nociceptors directly
Increases the release and synthesis of prostaglandins from nearby cells.
This usually begins with injury-substance P release from neuron, vasodillation and histamine relase from mast cells= neurogenic inflammation. This leads to release of the above metabolites.
This decreased pain tolerance is termed Hyperalgesia-primary (increased sensitivity to damaged area), secondary (surrounding area).
How do you get referred pain?
Nociceptors from different places on the body can converge on the same relay nerurons (AT THE DORSAL HORN) which can confuse the brain about the location of the pain. This can happen during MI when receptors on the skin of the left arm converge with receptors on the heart and is interpreted as arm pain which is more common in our everyday experience.