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314 Cards in this Set
- Front
- Back
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Question
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Answer
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What are some s/s a patient may have if they suffer from a collagen synthesis disorder?
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Ligament laxity (hypermobility)
Fragile skin Aneurysms Bruising (vessel rigidity) Highly distensible skin Teeth issues Bone fragility *think Ehlers-Danlos |
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What determines the TYPE of collagen that is formed?
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SEQUENCE of amino acids is genetically PREDETERMINED d/t mRNA transcription/translation in rough ER
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COLLAGEN CHAINS?
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Repeating GLY-X-Y triplets
*SUPERCHAIN |
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In collagen amino acid chain composition, what amino acids are commonly found in specific positions?
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1/3 of residues are GLYCINE
PROLINE = X HYDROXYPROLINE or HYDROXYLYSINE = Y |
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What is needed to produce hydroxy- proline and lysine?
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ENZYMES
to add -OH GROUPS (HYDROXYLATION) |
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What are the 3 enzymes that hydroxylate in collagen formation?
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1. Lysyl hydroxylase acts on lysine in X or Y position
2. Prolyl-3-hydroxylase acts on proline in the X position 3. Prolyl-4-hydroxylase acts on proline in Y position |
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What must be present for HYDROXYLATION to occur? (4)
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1. IRON on enzyme
2. OXYGEN 3. VITAMIN C 4. ALPHA KETOGLUTARATE |
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INTRACELLULAR stage of COLLAGEN formation?
Don't forget the GALAXY GLUE! |
all of this takes place in the FIBROBLAST:
CARBOXYLATION occurs - GLUCOSE & GALACTOSE 3 alpha chains twist - SUPERCHAIN HELIX (GLY-X-Y) connect w/ H-bonding making PRO-COLLAGEN procollagen LEAVES FIBROBLAST enters EXTRACELLULAR space |
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EXTRACELLULAR stage of collagen formation what needs to be present?
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CLEAVE OFF TERMINAL EXTENSION of pro-collagen
via PRO-COLLAGEN PEPTIDASE |
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Name of IMMATURE forming collagen with the terminal extensions CLEAVED and how does it REACH MATURITY?
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TROPOCOLLAGEN is immature since doesn't have tensile strength; further CROSS-LINKING W/ H-BONDING is needed to form mature collagen
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How do collagen molecules assemble themselves?
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QUARTER STAGGERED ARRAY
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - *end to end w/ a gap |
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What are some pathologies associated with collagen synthesis?
SEDMOI |
Scurvy: NO HYDROXYLATION (vit C, oxy, iron, alph ketoglutarate) so stays in weak form/none!
Ehlers-Danlos: problem w/ PROCOLLAGEN PEPTIDASE so stays procollagen (can't cleave) Marfan's and osteogenesis imperfecta = hereditary, CANNOT FORM FURTHER CROSS-LINKAGES so stays at IMMATURE STAGE TROPOCOLLAGEN |
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What are 5 functions of bone?
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1. PROTECT
2. SUPPORT 3. MECHANICAL basis for MOVEMENT 4. HEMATOPOIESIS **************5. MINERAL STORAGE******************** |
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Name 2 bone MATRIX components and their functions
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TYPE I COLLAGEN: provides tensile strength; resists pulling forces
SOLIDS: provide compressive strength (Calcium, Phosphate and other crystalline structures) |
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What are 3 important characteristics of bone?
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1. Bone is a rigid tissue that ADAPTS TO MECHANICAL STRESSES (WOLFF'S LAW of bone deposition based on use it or lose it)
2. CONTINUOUS deposition and removal of bone throughout life 3. SEVEN YEARS to completely turn over skeletal bone in the body |
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In what 2 ways does mesenchymal condensation give rise to bone?
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1. INTERMEMBRANOUS OSSIFICATION - direct transition of mesenchyme to bone (clavicles and parts of skull)
2. ENDOCHONDRAL OSSIFICATION -catilage model replaced by bone (long bones, needs O2) |
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What enzyme can be measured in the blood that shows increased osteoblastic activity?
PUBERTY |
Alkaline Phosphatase BONE BUILDING
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What PATHOLOGIES could show the presence of ALKALINE PHOSPHATASE in a blood test?
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FRACTURE * NEOPLASM * INFECTION
HOW MUCH? HOW FAST? |
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What could cause disruption in a growth plate?
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Fx, infection, CA of cartilage, metabolic problem, dwarfism, endocrine problem
VIT DEFICIENCY |
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mononucleate bone-forming cells that descend from osteoprogenitor cells.
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osteoBLASTS:
(from the Greek words for "bone" and "germ" or embryonic) are mononucleate cells that are responsible for bone formation; in essence, osteoblasts are specialized fibroblasts that in addition to fibroblastic products, express bone sialoprotein and osteocalcin. - wiki |
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LEAST SPECIALIZED CELL IN THE BODY
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FIBROBLAST
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Osteoblasts produce a matrix of _______, which is composed mainly of Type ___collagen. Osteoblasts are also responsible for __________ of this matrix.
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Osteoblasts produce a matrix of OSTEOID, which is composed mainly of Type I collagen. Osteoblasts are also responsible for MINERALIZATION of this matrix.
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What were the 2 methods used to PREVENT limb length discrepancies with POLIOmyelitis?
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Removal of growth plate
Put pressure on growth plate by stapling to epiphysis to metaphysis |
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secrete OSTEOID
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osteoBLASTS
*Although the term osteoblast implies an immature cell type, osteoblasts are in fact the mature bone cells entirely responsible for generating bone tissue in animals and humans. |
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Fibroblasts are derived from embryologic __________.
They are classified by (3)? |
MESODERM
MORPHOLOGY, STAINING, & FUNCTION |
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Osteoblasts arise from ____________cells located in the deeper layer of periosteum and the bone marrow.
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OSTEOPROGENITOR
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How does membranous (woven) bone grow?
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By process of ACCRETION: adding bone to the surface and edges of the bone (i.e. closing of fontanels)
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function of collagen
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holds cells together and provides STRUCTURAL INTEGRITY
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Secretes the EXTRA CELLULAR MATRIX
*notice the question is not asking what secretes the bone matrix |
FIBROBLASTS
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Long bone (endochondral ossification) grow by process of __________,
whereas cranial vault and clavicles (intramembranous ossification) grow by layering, or ______________. |
APPOSITION = long bones
ACCRETION (layering) = skull + clavs |
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young collagen
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TROPOCOLLAGEN
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Describe APPOSITIONAL bone growth
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APPOSITIONAL bone growth outward (layers upon layers):
osteoProgenitors become... OSTEOBLASTS that secrete soft OSTEOID, the uncalcified bone MATRIX that eventually mineralizes around them. |
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located on the surface of osteoid seams and make a protein mixture known as osteoid,
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osteoBLASTS live on the osteoid seam and make osteoid
which mineralizes to become bone. The osteiod seam is a narrow region of newly formed organic matrix, not yet mineralized, located on the surface of a bone. |
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Contents of ECM secreted by fibroblasts
PFEC this noise! |
Collagen
Proteoglycans Elastin Fibronectin & other structural proteins |
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Osteoid that won't mineralize due to some insufficiency results in _________ in children and _________ in adults.
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RICKETS = kids
OSTEOMALACIA = adults |
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What are 3 requirements of healthy bone?
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1. CALCIUM EQUILIBRIUM and other metabolites in blood and bone 2. LONGITUDINAL STRESS , pressure or load on the bone
3. Viable BLOOD supply to oxygenate bone cells. |
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type of cell that synthesizes the extracellular matrix and collagen
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FIBROBLAST
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What has been shown to increase urinary calcium levels and why?
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Prolonged bed rest; d/t lack of LONGITUDINAL PRESSURE on bones; levels unaffected by heavy bicycle ergometer work.
3 HRS A DAY STANDING WILL SUFFICE |
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the defining feature of connective tissue in animals.
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ECM
extracellular matrix The ECM regulates a cell's dynamic behavior. In addition, it sequesters a wide range of cellular growth factors, and acts as a local depot for them - wiki |
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H.M.S.
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HEREDITY
METABOLIC SYSTEMIC *if not localized |
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Like other cells of connective tissue, fibroblasts are derived from primitive __________ Thus they express the intermediate filament protein vimentin, a feature used as a marker to distinguish their __________origin.
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MESOderm = the middle derm
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What is a fracture?
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DISCONTINUITY
A break in the cortex can be applied to any anatomy with a cortex |
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Makes up 25% of all mammalian protein
ie, for every quarter of a century you age, 25% of your face sags |
COLLAGEN
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What is the most common lesion in bone and the most common cause?
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Fracture d/t trauma
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CARTILAGE cells make TYPE ____ collagen.
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TYPE 2 = CAR(TWO)ILAGE only
*all the rest have type 1, which is vascular |
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Why need ascorbic acid for intracellular procollagen synthesis?
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keeps Fe+ happy on enzyme
SCURVY INTERRUPTS THE HYDROXYLATION STEP *deficiency leads to SCURVY (can't add -OH so if you have scurvy, you can't make type I collagen) |
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What can predispose someone to fracture?
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Anything that alters the structural integrity of the bone
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Why need ALPHA KETOGLUTERATE for intercellular procollagen synth?
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SUBSTRATE!
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Is a fracture as a pathology the same as a pathological fracture?
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No, all fractures are pathologies but
a pathological fracture IS a fracture through DISEASED bone. |
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what is observed in a patient
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signs
*symptoms are the pt. complaint |
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What is the difference b/w an open and closed fracture?
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A closed fracture doesn't break the skin while an open one does.
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What is an avulsion fracture?
* to AVULSE something |
Tearing away of bone fragment; pull from ligament, tendon or muscle
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2 STAGES of collagen synthesis
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INTRACELLULAR: from AMINO ACID TO PRO-COLLAGEN
EXTRACELLULAR: from PRO-COLLAGEN to MATURE COLLAGEN |
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What is an occult fracture, what should be done and what are common bones affected?
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A radiographically invisible fracture; re-radiograph in 7-10 days; scaphoid (FOOSH) and ribs
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What determines the TYPE I or II collagen?
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GENETICALLY PREDETERMINED SEQUENCE OF A.A.'S
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What is a bone bruise?
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Hemorrhage
Edema Trabecular microfracture (shearing of vasculature inside bone), NOT SEEN ON X-RAY but can be seen on MRI |
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Proline and Hydroxyproline are ____ ACIDS = rigid cyclic structure limits rotation ability of chain
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IMI-NO likey the movement. PRO LINES ARE STRAIGHT AND RIGID LINES!
STRUCTURAL INTEGRITY due to limited motion *proline & hydroxyproline are rigid IMINO acids of COLLAGEN |
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What is fracture orientation based on?
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MECHANISM of injury
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Describe transverse fractures.
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They are uncommon and can be from a high velocity injury (falling from heights). They are often pathologic,
Paget's "banana" fracture. |
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s m a l l e s t amino acid (relative to collagen)
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g l y c i n e
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Describe oblique fractures.
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They usually occur on shaft of tubular (long) bone and are 45 degrees to long axis and are VERY COMMON in normal, healthy bone.
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The collagen chain HELICAL in nature and needs ________ to have HELICAL STRUCTURE.
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g l y c i n e
the MOST COMMON! 1/3 of all residues! Proline makes it straight (imino) and SUGAR (glycine) makes it curly! |
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Describe spiral/torsion fractures.
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They can be d/t torsion and axial compression, they are angulated with pointed ends.
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SUPERCHAIN collagen sequence
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Glycine (first!) - Proline (X) - Hydroxyproline (Y) OR Hydroxylysine (Y)
= collagen |
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What is a green stick fracture?
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INCOMPLETE FX
CHILDREN due to organic:inorganic ratio breaks on CONVEX (OUTER) side |
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If you don't have vitamin C, you can't add the ____ group to proline and lysine during the __________ stage of making of procollagen.
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-OH
during INTRACELLULAR stage of procollagen making. |
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What is a torus fracture?
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Buckling fracture, resembles bump on radiograph.
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If we are NOT needing molecular oxygen, what type of collagen are we making? Why?
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type II - cartilage is anoxic
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What is a comminuted fracture?
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2 or more fragments have seperated, bone has been crushed or pulverized, can be called a "butterfly fragment"
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Ferrous ion NEEDED on enzyme (intracellular) to prevent
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bruising, bleeding
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What is a noncomminuted fracture?
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Bone has one break and 2 fragments.
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Molecular oxygen needed (intracellular) because
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you can't add -OH gps w/o it (unless making type II then don't need it for cartilage)
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COMPRESSION fracture?
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AXIAL compression usually of the VERTEBRAE
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What is the mechanism of injury in a clay shoveler's or coal miner's fracture?
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Avulsion; occurs in the spine.
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What is a fatigue fracture and where does it occur?
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Stress fracture or march fracture; in healthy bone. d/t abnormal stress on normal bone, repetitive stress, gradual formation of microfracture.
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What is an insufficiency fracture?
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Stress fracture through DISEASED bone; a form of pathologic fracture.
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In EXTRACELLULAR stage, you cleave off terminal extension from procollagen. What is problem w/ Ehlers-Danlos sufferers?
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Can't cleave and therefore CANNOT ORGANIZE COLLAGEN BECAUSE EXTENSIONS STILL ATTACHED!
Problem w/ skin distensibility due to faulty PROCOLLAGEN PEPTIDASE that can't cleave. |
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3 PHASES FRACTURE REPAIR?
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1. INFLAMMATORY
2. REPARATIVE 3. REMODELING |
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In EXTRACELLULAR stage of collagen formation, what goes wrong w/ MARFAN'S victims?
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Further CROSS LINKING via INTERCHAIN & INTRACHAIN HYDROGEN BONDS is necessary to form mature collagen. Marfan's cannot do this so THEIR COLLAGEN NEVER GROWS UP! Remains as TROPOCOLLAGEN.
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What are the first 4 things that occur in the INFLAMMATORY I phase of fracture repair (1-2 DAYS post fracture)?
R.H.T.N. |
1. RUPTURE of blood vessels in both soft tissue and bone
2.HEMATOMA (CAULKING) fills gaps, surrounds and seals off injury 3. Immediate TEARING of periosteum 4. NECROSIS of bone and soft tissue. |
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BRIEFLY describe bone formation
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avascular CARTILAGE model (via endochondral ossification)
introduced to OXYGEN via FIBROBLASTS then MINERALS via BLOOD |
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What occurs in the INFLAMMATORY II phase of fracture repair 2-5 DAYS post fracture?
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1. FIBRIN MESH develops
2. FIBROBLASTS migrate into area & deposit AVASCULAR CARTILAGE b/w bone ends 3. NECROSIS and MACROPHAGE SUNSHINE CLEANING activity continues. |
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Bone is the only tissue tat
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replaces itself with itself.
Be like bone. Do tat. |
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What occurs in the INFLAMMATORY III phase of fracture repair 5-10 DAYS post fracture?
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1. Soft tissue callus (PROCALLUS)
2. MACS STILL CLEANING UP |
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cessation of growth occurs ___ years EARLIER in FEMALES than in males
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3
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REPARATIVE phase of fracture repair?
How to REPAIR 4 HAZY relations with Russia? Wide-Class Nukes are Never Called to Blast! |
How to REPAIR 4 HAZY relations with Russia? WIDE-CLASs NUkes are NEver CALLed to BLAST!
HAZY CLOUD ON X-RAY WIDENED fracture zone due to osteoCLASTIC and monoNUCLEAR cell activity. NEOvascularization. CALLUS formation begins. OSTEOBLASTIC activity significant after neovascularization begins. |
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Increased osteoblastic cativity (puberty) increases production of the enzyme ___________, which can be measured in the blood
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ALKALINE PHOSPHATASE = made by OSTEOBLASTS
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REMODELING THE HOUSE phase of fracture repair?
A CALLUS SEAL and a STRONG WOLFF went BLASTING & CLASTING about during the REMODEL |
CALLUS SEALS bone,
Bone adjusts its strength and shape (WOLFF'S LAW) Osteoclasts and -blasts are involved with INCREASED ACTIVITY RELATIVE TO NORMAL BONE |
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When does a fracture happen?
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When the TENSILE & COMPRESSIVE strength of bone is overcome
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What is Clinical union regarding fracture?
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Point when cast is removed, implies fracture is STABLE
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a pathologic fracture is __________ until it fails due to pathology
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ASYMPTOMATIC
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What is malunion regarding fracture?
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Fracture heals with residual DEFORMITY.
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phosphate is fundamentally important in
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all GLCOLYTIC cmpds
ATP, ADP, AMP CREATINE PHOSPHATE COFACTORS= NAD, NADPH LIPIDS (phosphatidyl choline) Covalent MODIFIER of enzymes ****Major ANION in BONE = NEGATIVE**** |
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What is non-union with regards to fracture?
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Fails to heal AFTER 6 months
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What is delayed union regarding fracture?
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Fails to heal UP TO 6 months
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What is pseudoarthrosis regarding fracture?
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Non-union fracture heals with pseudojoint
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Where does alkaline phosphatase come from?
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Secreted by osteoblasts when depositing bone.
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When would you expect to see alkaline phosphatase iINCREASED in the blood?
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GROWING children
FRACTURE NEOPLASIA |
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What does an increased erythrocyte sedimentation rate (ESR) indicate?
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INFLAMMATION
will be increased in inflammatory stage of fracture repair; not limited to conditions of bone. |
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What % change can be detected in bone scans versus plain film?
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bone scans can detect 2-4% change while films don't detect until 40-60% change has occurred; bone scans very sensitive but not specific
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What 6 body functions depend on calcium?
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1. Enzymatic reactions 2. Hormone secretion; mediates hormone events 3. Neurotransmission 4. Muscle contraction 5. Blood clotting 6. Major cation in bone and teeth
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How important is it to keep calcium w/in normal limits and what is the normal range in plasma?
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VITAL to keep Ca in normal limits;
8.6-10.6 mg/dl: 50% available, 40% bound to something (albumin) 10% CaCO3 |
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How is calcium related to intake and how does the body maintain normal levels?
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% intake absorbed is inversely related to intake; normal levels maintained by preventing overload w/ dietary surplus, w/ dietary deprivation, adaptive increase in absorption.
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What 6 body functions depend on phosphate?
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1. All glycolytic compounds
2. ATP, ADP, AMP, creatine phosphate 3. Cofactors: NAD, NADPH 4. Lipids like phosphotidyl choline 5. Covalent modifier of enzymes 6. Major anion in bone |
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What is the normal range of phosphate in plasma and how is the balance maintained?
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2.5-4.5 mg/dl;
amount absorbed in diet constant, adaptive reg. at gut is minimal, URINARY excretion is major mech. in phosphate balance. 90% conserved, 10% secreted in urine |
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What are the major regulators of plasma calcium, what hormone and how is it related to Ca levels?
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Parathyroid glands; PTH (neg. feedback); secretion PTH inversely related to plasma Ca levels
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How do levels of calcium affect the body?
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Ionized Ca regulates PTH (PARATHORMONE)secretion w/in minutes
HIGH CA+ levels over time shut down PTH synth. and stores; LOW Ca+ levels over time cause PARATHYROID GLAND HYPERtrophy |
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How does PTH moderate phosphate and calcium levels in the body?
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Role of phosphate on PTH is indirect through mech.s that lower Ca levels; If inject phosphate, Ca level drops and PTH increases; PTH moderates hyperphosphatemia created w/ injection by increasing renal excretion.
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Where does PTH act to raise Ca levels and decrease PO4?
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Bone Gut Kidney
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what organ dumps calcium if too much?
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KIDNEY
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When PTH acts on organs what happens to Ca and PO4 levels?
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Increases Ca influx in blood, increasing []; Plasma phosphate levels also rise but action of PTH on kidney causing efflux of phosphate in urine
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If calcium level drops, what happens<
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PARATHYROID releases PTH = tells kidney to hang on to calcium and dump phosphate
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Describe PTH action on bone, what cells are activated/deactivated?
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Initially stimulates osteolysis by surface osteocytes putting free Ca into plasma; stimulates prod'n of osteoclasts and activates resorption of bone; all bone constituents liberated; PTH down regulates osteoblasts and inhibits collagen synth. (vit. D)
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long term hyperphosphatemia to skeleton
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bones INCREASED phosphorus
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What happens when PTH takes action on the kidney?
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Increase Ca reabsorption from distal tubule; MOST dramatic effect is inhibiting reabsorption of phosphate; stimulates synth. of vit D metabolite
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why vit D w/ Calcium?
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increases calcium absorption from GUT
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What happens when PTH takes action on the gut?
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Indirect: stimulates 1-25-OH2-D3 which directly increases active transport of Ca across lumen
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Vit D must be
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converted
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Summarize the function of PTH.
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Causes prompt increase of Ca and decrease of PO4 in plasma; Kidney dumps PO4 and conserves Ca initially; As plasma Ca levels rise, PTH levels accommodate, kidney filters more Ca, and urinary Ca levels rise to maintain homeostasis
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Stim. BONE RESORPTION and STIMULATE PLASMA CALCIUM LEVELS IN BODY
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1,25-(OH2) DH3 /CALCITRIOL
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What is the most common cause of hyperparathyroidism and what are the s/s of hypercalcemia?
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single parathyroid adenoma; dulled mentation, lethargy, muscle weakness and hyporeflexia, anorexia and constipation (high Ca makes harder to open Ca channels for nt release; m. contraction not affected)
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VIT D metabolite necessary for bone break down
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CALCITRIOL
PTH comes out when Ca++ levels are down |
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How does hyperparathyroidism affect the kidneys and what are sequela?
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Excessive urinary Ca filtration = renal stones; persistent hypercalcemia = reduced renal function and irreversible renal failure; Peptic ulcers sequela
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Vit D metabolite nec for bone BUILD?
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is NOT calcitriol, but we don't know if its the other one either
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How does hyperparathyroidism affect bone?
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Massive irregular resorption Weakening of bone Pain Fx (pathological) Deformities
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long term hyperparathyroidism on bone
yochum and rowe pic **************** |
loss of cortical definition
******************************************frayed, irregular, lace-like subperiosteal resorption osteolysis decreased bone density and accentuated traebecular pattern Presence of a brown rumor distinct geographic radiolucencies; slightluy expansile mimicking destructive neoplasm |
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How does hyperparathyroidism look radiologically?
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Subperiosteal erosions/resorption Bone looks splotchy Deposition Ca in soft tissues
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PTH is downregulating _________ and upregulating __________-
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********down blast, up clast********
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How does one distinguish hyperparathyroidism from other causes of hypercalcemia?
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Elevated PTH levels Elevated plasma Ca levels Decreased plasma PO4 levels
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brown tumor
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NOT a neoplasia - associated w/ hyperparathyroidism
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Explain primary hyperparathyroidism.
Using the 4 gland explanation |
common endocrine disorder - gland does not respond to rising Ca levels;
80-85% of time d/t SINGLE parathyroid ADENOMA on ONE of the glands = NORMAL GLANDS SHUT DOWN; Pt.s found through blood analysis; symptoms mild if any |
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what happens to all the liberated Ca++ in hyperparathyroidism
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deposition of calcium into SOFT TISSUES
evidence of tissue calcification in long standing disease on x-ray |
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Explain secondary hyperparathyroidism.
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Problem NOT in gland,
asked to OVER function; PTH released but Ca levels NOT rising; glands become hyperplastic; Ca levels low-normal or low (below 8.6), PO4 levels low if kidney intact; Most frequent cause is chronic renal failure or malabsorption of Ca |
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resorption pattern of spine
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losing density in middle -RUGER jersey spine (rugby) due to stripe 1, 2, 3 through vetrebrae
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What is the most common cause of HYPOparathyroidism and what occurs?
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AUTOIMMUNE IDIOPATHIC ATROPHY
receptors cannot bind to hormone = they can't see it rarely end organ resistance to PTH; Ca absorbed from gut diminished; Little vit D metabolite around; Decreased bone resorption |
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hypercalcemia blood profile
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dif by bloodwork (ie, could be hyperparathyroidism = if elevated hyperparathyroidism usually caused by an adenoma, so pumps out lots of PTH hormone. Response is UP plasma calcium levels then DECREASED plasma phosphate levels. Why?
Kidney is being told to DUMP THE PHOSPHATE so u will drive a hypOphosphatemia. Adenoma overriding so Ca++ stay up but phosphate levels stay low. |
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What are the clinical s/s of hypoparathyroidism?
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Those of hypocalcemia: hyperactive reflexes, spontaneous m. contractions, convulsions and laryngeal spasm w/ airway obstruction
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WHY WOULD THE BLOOD PROFILE OF HYPERPARATHYROIDISM BE UP CALCIUM A ND DOWN PHOSPHATE?
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Why? Kidney is being told to DUMP THE PHOSPHATE so u will drive a hypOphophatemia. Adenoma overriding so Ca++ stay up but phosphate levels stay low.
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Describe plasma levels with Hypoparathyroidism:
Ca++ level? Phosphate level? If gland destruction, results in? If end organ failure to detect, results in? |
Too much ATP(hosphate), not enough Calcium for neurotransmission.
LOW Ca++ HIGH Phosphate Gland destruction: nobody is asking, "Where's the Calcium?" - no PTH because the gland is dead. End organ failure: HIGH PTH because nobody shows up to pick it up from the airport. No one cares, end organ unresponsive. Plasma PTH levels low in gland destruction because nothing is making it (MOST COMMON); Plasma PTH levels ELEVATED when target tissue UNresponsive because nothing picks it up |
|
|
2nd hyperparathyroidism patient profile
|
primary adenoma is NOT on the glad as in primary. Glands are okay BUT calcium levels are not coming up. They contineue to respond to "where's the calcium?" so they kick out hormone.
Glands will hypertrophy because working overtime - high plasma PTH but low plasma Ca. If kidney okay, low Phosphate. Of bone/gut/kidney, = KIDNEY PROBLEM!!! |
|
|
How do you treat a pt with hypoparathyroidism?
|
supplement w/ 1-25-(OH)2-D3 supplement w/ calcium
|
|
|
If LOSING PLASMA CALCIUM LEVELS, BLAME THE _______ FIRST.
|
KIDNEY
chronic renal failure Ca still coimg out of bone, still being pulled out of gut but STILL GOING DOWN THE DRAIN due to kidney. |
|
|
What is calcitonin?
|
Hormone produced by parafollicular cells of the thyroid gland; PTH raises plasma Ca levels and calcitonin acts to lower plasma Ca
|
|
|
who is to blame in secondary hyper parathyroidism
|
kidney
|
|
|
What are the actions of calcitonin? (3)
|
1. Binds to membrane receptors, and cAMP levels increase 2. cAMP as second messenger initiates calcitonin action 3. Ca is sequestered into mitochondria which acts to lower cytosolic [Ca], lowering plasma [] by allowing more Ca into the cell
|
|
|
HYPOcalcemia symps and signs
|
hyperactive reflexes due to UPREG of receptors to any Ca ion floating by = spasm!
spontaneous muscle contractions convulsions laryngeal spasm = airway obstruction |
|
|
CALCITONIN effects? (4)
|
1 plasma Calcium DECREASES rapidly (magnitude of fall related to baseline rate of bone turnover)
2. INHIBITION of osteolysis and bone resorption by bone cells 3. ANTAGONIST to PTH w/ respect to Ca 4. Same results as PTH on PHOSPHATE w/ diff. mechanism |
|
|
Why is PHSOPHATE ELEVATED in hypOPARATHYROIDISM?
|
ABSENCE OF SIGNAL TO KIDNEY to dump phosphate
(more than 4.5 mg/dec of blood) |
|
|
vit D deficiency - what causes a decrease in rate of bone mineralization?
|
STRONGLY NEGATIVE PHOSPHATE balance
+ DECREASE IN CA+ LEVELS = decreased bone building |
|
|
What does vitamin D effect in gut, bone and where is the final active metabolite converted?
|
Increases Ca absorption from gut; important effect of bone deposition and resorption; Must be converted through series of reactions in liver and kidney
|
|
|
In vit D deficiency, a fall in plasma calcium level will be buffered by
|
PTH SECRETION
UPREGULATES OSTEOCLASTIC ACTIVITY need vit D (calcitriol) too but not as efficient because there is a deficiency. |
|
|
plasma PTH levels low in _______destruction
|
gland
(most common) |
|
|
slightly reduced plasma Ca+
greatly reduced plasma Phosphate elevated levels of PTH diagnostic profile of? |
VIT D DEFICIENCY
~ Rickets (children) ~Osteomalacia (adults) |
|
|
What are the 2 sources of vit. D and how are they different?
|
D3 - produced in skin via UV radiation
D2 - Plant steroid ingested in diet; difference is D2 has more double bonds than D3 action in body IDENTICAL |
|
|
in vit D deficiency, why lose phosphate?
|
because PTH is telling kidney to DUMP PHOSPHATE AND HOLD ON TO CALCIUM
|
|
|
If I have patient w/ gland atrophy and another with end organ block
|
patient who does not have parathyroid glands intact will respond to PTH but someone whose organs don't recognize PTH will not respond
|
|
|
WHAT role does vit D play in absorbing Ca+ from gut?
|
CALBINDIN
kicked out, goes to gut and helps facilitate Ca+ w/ phosphate |
|
|
What does PTH's effect on the KIDNEY do to vitamin D metabolite formation, what is made w/o PTH?
|
With PTH the 1,25-(OH)2 metabolite is made -> bone resorption;
/o PTH the 24,25-(OH)2-D3 metabolite is formed does NOT -> bone resorption |
|
|
Vit D is necessary for bone ________
|
MINERALIZATION
|
|
|
Why do we see increased plasma AND urinary levels of Calcium in VITAMIN D EXCESSIVE INTAKE?
|
IF YOU PUT TOO MUCH OF SOMETHING INTO YOUR BODY, YOUR BRAIN SAYS, "COOL. NOW WE CAN STOP WASTING ENERGY MAKING THAT SHIT!" AND DOES EXACTLY THAT. RESULTS? NOT GOOD.
too much vit D drives Ca up so GLANDS STOP SECRETING PARATHYROID HORMONE and no signal to kidney to hang on to calcium and dump phosphate so we can LOSE CALCIUM thru urine too. |
|
|
What are the actions of the 1-25 (D) metabolite?
|
In kidney, binds w/ cell receptor and enters nucleus; stim.s protein synth. of product: CALBINDIN which helps Ca & PO4 absorption from gut; Stim. bone resorption, receptor found in bone cells; works synergistically w/ PTH at bone level to stim. breakdown
|
|
|
if hyperparathyroidism and vit D toxcity both presnt w/ HYPERCALCEMIA, then ....
**************************************** |
********CHECK PTH LEVELS VIA BLOOD ANALYSIS
Hyperparathyroid pt: high PTH, high CA++, Kidney dumps PO4 Vit D toxic pt: LOW PTH because normal gland response to elevated Ca++, high CA++, kidney not getting strong PTH signal so it does not dump it so PO4 levels could be NORMA to ELEVATED |
|
|
What are actions of Vitamin D?
|
Normal mineralization of bone is dependent on Vit D (not 1,25); Major storage site is muscle, profound m. weakness seen in deficiency; 25-OH may play role in m. metabolism and function
|
|
|
The 1-25 metabolite is created in the kidney from the 25-OH-D3 precursor IS UNDER THE INFLUENCE OF PTH!
This 1-25 metabolite (_______) can then initiate? |
his 1-25 metabolite (calcitriol) can then initiate the formation of CALBINDIN in the kidney or go into the systemic circulation.
|
|
|
What is Vit D toxicity d/t, where is Ca absorption enhanced and where are increased Ca levels found?
Vit D works synergystically with parathyroid hormone |
d/t excessive administration or abnormal sensitivity to ordinary amounts of vit D;
Absorption from gut and resorption from bone enhanced DUE TO PUSHING THE SYSTEM; See increased plasma AND urinary levels of Ca. |
|
|
Why do you see increased plasma and urinary levels of Ca in vit D toxicity?
|
PTH responds to raising levels of Ca, toxic amts of vit D facilitate PTH response, nothing to do w/ parathyroid glands.
|
|
|
What are the s/s of Vit D toxicity?
|
Same as hypercalcemia: dulled mentation, m. weakness and hyporeflexia, lethargy, anorexia and constipation
|
|
|
How do you differentiate b/w hyperparathyroidism and Vit D toxicity since have same HYPERCALCEMIC clinical presentation?
|
BLOOD DRAW
|
|
|
How is Vit D toxicity treated?
|
Block effects of Vit D by administering calcitonin or cortisol and wait for excess Vit D to clear.
|
|
|
What could Vit D deficiency be d/t?
|
Inadequate sun,
dietary intake, decreased absorption, DEFECTIVE HYDROXYLATION in liver or kidney |
|
|
What does Vit D deficiency lead to?
|
DECREASED GI absorption of CALCIUM and PO4;
Plasma Ca levels fall buffered by INCREASED PTH secretion; PO4 lost in urine and Ca retained DUE TO PTH |
|
|
What does the negative phosphate balance from Vit D deficiency cause?
|
W/ decrease in Ca levels together causes a decrease in the RATE of bone mineralization, further aggravated by lack of Vit D needed for mineralizaiton and
excessive OSTEOID accumulates. |
|
|
What are the results, diagnostic profile and treatment of Vit D deficiency?
|
Rickets or Osteomalacia patient profile:
~slightly reduced plasma Ca, ~greatly reduced plasma PO4 and ~elevated levels of PTH; Replacement doses of Vit D and supplemental Ca. |
|
|
OSTEOMALACIA
|
SOFT bone that has DEFECTIVE MINERALIZATION of OSTEOID in adults
Excess OSTEOID accumulation over time ****REVERSIBLE****** in skeletaly mature individuals w/ minimal bone deformation |
|
|
What are s/s of osteomalacia?
|
~Bone pain
~Muscle weakness ~Pseudo Fx (seam of demineralization looks radiolucent and body perceives as Fx -> Fx repair process but can't form procallus to callus; can't tell diff. on film. |
|
|
What is Rickets?
|
Osteomalacia in a person w/ OPEN GROWTH plates;
RICKETS IN CHILDREN IS WORSE THAN OSTEOMALACIA IN ADULTS |
|
|
Where does Rickets lack control and what is seen radiographically?
|
GETS wider and wider because NOT REPLACING / CONVERTING H to BONE
Lack control over EPIPHYSEAL CARTILAGE MINERALIZATION and over ENDPLATE growth; fuzzy growth plates, bowing bones, "PAINTBRUSH metaphysis" |
|
|
OSTEOPOROSIS
|
RESORPTION EXCEEDS DEPOSITION
A condition of BONE MASS not being enough, the bone is otherwise normal and healthy (ratio of organic to inorganic OK) |
|
|
WHAT'S THE OVERRIDING FACTOR ABOUT BONE MASS?
|
Bone mass will RETURN TO ITS NORMAL SET POINT, no matter what the hell you do...you will never be young again.
|
|
|
variation on implantation (means of organism getting into bone) besides a PUNCTURE:
|
SURGERY
|
|
|
What factors affect loss of bone?
|
GENETICS
diet, lifestyle, gender, race, Rx (steroids, heparin, chemo), etc. |
|
|
MOST common way acute pyogenic osteomyelitis is spread
(of the 3: hematogenous, direct implantation, lymphatic) |
HEMATOGENOUS spread due to metaphyseal growth plate vascular concentration (anastomoses)
CHILDREN CHILDREN CHILDREN CHILDREN fever, dull, throbbing with every heartbeat kind of pain due to vascularity |
|
|
OSTEOPOROSIS is the most common cause of:
|
PATHOLOGICAL FRACTURE
$20 billion/year; dramatically changes life, fear; *****hip Fx 50% mortality rate |
|
|
Why are children susceptible to acute pyogenic osteomyelitis?
|
WEAK IMMUNE SYSTEM:
'Boys! 'Metaphyses of all bones 'Strep, E. coli and S. aureus |
|
|
ACUTE PYOGENIC SPONDYLODISCITIS describe x-ray:
"Osteo" = BONE "Myelo" = MARROW A sequestrum is a piece of dead bone that has become separated during the process of necrosis from normal/sound bone. It is a complication (sequela) of osteomyelitis. |
VERTEBRAL COLLAPSE
HEMATOGENOUS SPREAD PATHOLOGICAL FRACTURE due to HOLES from bacteria **If it crosses tissue types, then it is a BACTERIAL INFECTION** |
|
|
PATIENT presentation of OSTEOPOROSIS
|
Vertebral BODY fracture
Height LOSS COLLES's fracture Loss of TEETH |
|
|
How does bacterial infection patient present and what does x-ray look like?
|
LOCAL EDEMA creates a THROBBING PAIN due to vascular compression (w/ every beat of my heart)
RAPID FEVER X-ray reveals lesion CROSSES MORE THAN ONE TISSUE TYPE = BACTERIAL infection (osteomyelitis) |
|
|
What's the worst part of acute pyogenic osteomyelitis pain-wise?
|
PERIOSTEAL LIFTING
oozing underneath and necrosis |
|
|
What kind of osteomyelitis (10%) goes on to become
CHRONIC PYOGENIC OSTEOMYELITIS? |
1. PATHOLOGIC FRACTURE
2. DRAINING SINUS or CLOACA (hole) = granulomatous tissue has been walled off to protect from foreign substance like stitches 3. SQUAMOUS CELL CARCINOMA (rare) 4. BONE SARCOMA (rare) |
|
|
LAB VALUES for osteoporosis?
|
NORMAL
Osteoporosis lab values are all normal. |
|
|
GRANULOMATOUS tissue?
(chronic pyogenic osteomyelitis) A Mexican stand-off |
chronic pyogenic osteomyelitis: sinus and ulcer formation
WHITE BLOOD CELLS/LEUKOCYTES HAVE WALLED OFF A FOREIGN SUBSTANCE (stitches, etc.) |
|
|
ACUTE pyogenic osteomyelitis
boys, metaphyses of all bones, staph, strep, s. aureus |
~~~periostieum, cortical bone and medullary cavity are all INFECTED~~~
LESS THAN 6 MO. OLD = acute `edema (throbbing pain! feel pain with every heartbeat due to vascular distention) `mechanical compression of vessels `hyperemia OSTEOCLASTIC activity (focal) REGIONAL/GEOGRAPHIC OSTEOPENIA KILLING/LYSING of osteocytes |
|
|
describe CHRONIC pyogenic osteomyelitic bone SPECIMEN
|
ROUGHENED & IRREGULAR CORTEX due to lifting and filling of periosteum
POROUS REACTIVE BONE lacks medullary cavity space |
|
|
What are some non-drug treatments of osteoporosis?
|
Exercise - Wolff's Law
Diet Fall prevention |
|
|
ACUTE pyogenic osteomyelitis X-RAY
|
dark spots (lucency)
tissue (periosteal lifting) = INFECTION |
|
|
What are some prescriptions for osteoporosis?
|
CALCITONIN puts the bone in ($$$$)
HORMONE REPLACEMENT (high CA rates) FOSAMAX (Boniva is improvement; both DOWNREGULATE osteoclasts) - nasty drug fucks up your GI system, can't take if bedridden or not upright due to GI & esosophageal erosion |
|
|
What are the likelihoods of suffering osteoporotic Fx?
|
Women: 1 in 2 over 50 y/o
Men: 1 in 4 over 50 y/o Juvenile osteoporosis: late teens early 20s, bone breaking Disuse osteoporosis |
|
|
ACROMEGALY
Osseous enlargement: phalangeal tufts, vertebrae, flared ends of long bones, SPADE-LIKE HAND |
growth hormone abnormality in SKELETALLY MATURE individuals;
3:1 million births, more common in FEMALES 3:2 |
|
|
SX of acromegaly?
|
INCREASE in SOFT tissues ->
FACIAL changes Small increase in skeleton Bigger ears and nose Thickened coursened jaw (LANTERN JAW) underbite dev. Frontal bone enlargement (supraorbital ridges) |
|
|
What are treatments of acromegaly?
|
Removal of pituitary gland,
radiation therapy, somatostatin therapy |
|
|
What is gigantism?
|
Effect of excessive growth hormone on IMMATURE skeleton; symmetric and proportional overgrowth of all tissues.
|
|
|
What does OCCULT fracture mean?
|
INVISIBLE
SCAPHOID & RIBS X-RAY AGAIN IN 7-10 DAYS |
|
|
PAGET'S DISEASE and synonym
|
A thickening and disturbance of the architecture of bone; Remodeling problem, INITIALLY EXCESSIVE RESORPTION of bone THEN EXCESSIVE REMODELING of bone;
aka: OSTEITIS DEFORMANS |
|
|
Paget's "banana" fx
|
TRANSVERSE rare
|
|
|
What is the frequency of Paget's Disease and who commonly/uncommonly has it?
|
5-11% of population over age 60, more common in males; found in western Europe, Australia, U.S.; Rare in come ethnic groups Scandinavians, Asians, Middle Eastern
|
|
|
How can Paget's be classified and where are common locations?
|
Monostotic or Polyostotic; pelvis, skull, spine, tibia, femur
|
|
|
OSTEOID constitution
|
precursor to mineralized bone
* accumulates w/ vit D deficiency and the shift from mostly inorganic in adults to more organic (soft) |
|
|
CAN you see osteomalacia on a film?
|
Yes, as a PSEUDOFRACTURE but it is not! IT is a radiolucent discontinuity through the bone but osteoid is not being converted to mineral at the osteoid seam due to OSTEOMALACIA. HIGH CONCENTRATION OF VASCULAR AREAS WILL BE PRONE TO SHOW THE SEAMS OF MINERALS BEING SUCKED OUT = LOOKS LIKE A FRACTURE
|
|
|
PAGET'S clinical 6:
|
1. 95% ASYMPTOMATIC
2. Enlarged HAT SIZE 3. SABRE SHIN (ant. bowing) 4. Pathologic FRACTURES 5. PAGETIC STEAL (high vasculature present, orthostatic hypotension) 6. Heart failure d/t CARDIOMEGALY |
|
|
What are the 3 stages of Paget's?
|
1. OsteoLYTIC (odds of picking it up on radiograph is LOW)
BONE RESORPTION compromising structural integrity 2. MIXED lytic and blastic 3. SCLEROTIC (burnout) bone looks WHITE |
|
|
pseudofractures
|
osteomalacia
discontinuity of the bone due to osteoid seam demineralization/lack of hardening of osteoid |
|
|
What is malignant degeneration in reference to Paget's?
|
Yochum's stage 4,
very rare 1-2% polyostotic disease; Aberrant bone cells can be predisposed to osteosarcoma (more often) and chondrosarcoma |
|
|
film of OSTEOMALACIA
|
areas of DE-MINERALIZATION
called PSEUDOFRACTURES |
|
|
What are 4 hereditary diseases of bone?
|
1. Achondroplasia 2. Marfan's Syndrome 3. Osteogenesis Imperfecta 4. Osteopetrosis
|
|
|
common place to look for RICKETS in children?
|
KNEES because of femur and tibia growth of endplates
*Look for PAINTBRUSH METAPHYSES |
|
|
What is Achondroplasia?
|
No cartilage growth; most common form of dwarfism; 1/4,000 births; most common disorder of growth plates
|
|
|
What would be the radiographic appearance of a child w/ RICKETS?
|
less dense SYSTEMICALLY - OSTEOPENIA
|
|
|
How would someone with achondroplasia look and what are some changes visible on radiographs?
|
Small arms and legs w/ normal size torso; premature closure @ growth plates; O & I shrinks too w/ change in orientation of sacrum, almost parallel to floor; obturator foramen rotate to champagne glass deformity.
|
|
|
What would be the radiographic appearance of an adult w/ OSTEOMALACIA
|
OSTEOPENIA
|
|
|
What is Marfan's Syndrome and what does it involve?
|
A connective tissue (type I collagen) disorder that involves the skeleton, lens of the eye, mitral valve prolapse, vascular system
|
|
|
Is osteoporosis a pathology?
|
DEPENDS on if it causes a fracture or not (from our clinical perspective) but it is more of a COMPLICATION of pathologies.
|
|
|
How common is Marfan's and what is seen on radiographs?
|
1/10K births;
long slender extremities, arachnodactyly SPIDER-LIKE, hypermobility ("double jointed"), KHYPHOscoliosis DUE TO HYPERMOBILE CONNECTIVE TISSUE everywhere; life expectancy altered d/t dissecting aneurysms |
|
|
bone resorption EXCEEDS deposition
|
osteoMALACIA
*demonstrate osteopenia |
|
|
What is Osteogenesis Imperfecta?
|
AKA brittle bone disease; 4 types (I-IV); defect in type I collagen synthesis
|
|
|
the ratio of organic to inorganic is fine, there is just NOT enough BONE
|
osteoPOROSIS
*demonstrate osteopenia |
|
|
What is the worst case scenario with osteogenesis imperfecta?
|
Type II - O. I. Congenita; Fatal condition; extremely brittle bones.
|
|
|
Both ___________ and ___________ would appear radiographically the SAME but for completely different reasons.
|
OsteoPOROSIS and OsteoMALACIA
both appear OSTEOPENIC due to systemic bone loss but Malacia is resorption exceeding deposition and Penia is not enough bone altogether |
|
|
Describe a Type I Osteogenesis Imperfecta Tarda.
|
Abnormal skeletal fragility, decreased bone density, Fx.s, bowing deformities, eye sclera appears blue; hearing loss d/t bony deformities; dental imperfections.
|
|
|
Loss of MASS
|
osteoPOROSIS
|
|
|
What is Osteopetrosis and what are the two forms?
|
Marble bone disease or Albers - Schonberg disease; Mild - autosomal dominant, Lethal - autosomal recessive
|
|
|
blood work in someone with osteoPOROSIS is
|
NORMAL
|
|
|
At what age do we reach peak bone mass
|
late 20's-early 30's
|
|
|
osteoporosis diagnosed in teens and 20's
|
JUVENILE OSTEOPOROSIS
|
|
|
How is osteopetrosis characterized and how would it appear on a radiograph?
|
Hypofuctioning of osteoclasts, too much bone, very brittle in nature; Radiopaque and wider, difficult to find medullary cavity and cortex.
|
|
|
osteoporosis seen with long term immobilization
|
DISUSE OSTEOPOROSIS
casting, paraplegia, quadriplegia |
|
|
Is bone mass different between men and women?
|
Yes, depending on what you do (ie, football player vs. office worker)
|
|
|
ORGANIC TO INORGANIC RATIO as we age
|
1:1 (child)
1:4 (peak 20's to geriatric) 1:7 (decline) |
|
|
Why would someone with osteopetrosis have a shortened lifespan and what would their PTH levels be?
|
Hematopoiesis decreased b/c medullary cavity small -> anemia, infection; PTH elevated body works harder to mobilize Ca, must get it from gut since osteoclasts not functioning.
|
|
|
ACROMEGALY
vs GIGANTISM |
acromegaly is MATURE skeleton affects of pituitary adenoma so not proportional growth of tissues
gigantism is IMMATURE due to same reason skeleton growth but all growth is SYMMETRICALLY large |
|
|
Factors contributing to reaching OPTIMAL BONE MASS
|
HORMONES!
DIET/NUTRITION ACTIVITY GENETICS/FRAME SIZE/FAMILY ETHNIC DRUGS USE/ABUSE EATING DISORDERS LONGITUDINAL/COMPRESSION STRESS 3 HR. MIN. A DAY |
|
|
ACRO + MEGALY
|
DISTAL + ENLARGEMENT
(acromegaly is often hands and feet that you can see) |
|
|
What are 3 classifications of osteomyelitis?
|
1. Acute: sudden onset or <6 months duration 2. Chronic: >6 months duration can go on for years 3. Subacute (Brodie's Abscess): Inflammation, pus, abscess in bone, Sx don't occur until pathological Fx occurs
|
|
|
excessive growth hormone causes ? with acromegaly
|
organ hypertrophy
enlargement of soft tissue coarsening of facial features (nose and ears) cranial bosses enlarge |
|
|
It is often assumed intervention during childhood that increases mass will persist throughout life but why may this not be true?
|
because we turn over our skeleton every 7 years
The effects of early athletics may disappear as homeostatic mechanisms bring bone mass BACK TO SET POINT |
|
|
How to find acromegaly?
|
elevated growth hormone detection! then remove the pituitary
|
|
|
What 3 ways can an infectious organism get into bone?
|
1. Hematogenous (includes lymphatics)
2. Direct Extension 3. Implantation from foreign object |
|
|
Even though gigantism is proportional, they will continue to develop the pituitary giant growth of __________ later.
|
acromegaly
|
|
|
WOLFF'S LAW
EXERCISE DIET GENETICS ENVIRONMENTAL *do these factors hold as we age or do we always return to set point |
who knows -the answer is fluid because the body is plastic. Peak bone mass is relative.
Now we all take drug therapies for chronic conditions and we blow our bone mass no matter what we do |
|
|
Primary cause of EITHER acromegaly or giantism:
|
PITUITARY ADENOMA
|
|
|
Describe Acute pyogenic osteomyelitis, who commonly affected, how spread and what organism causes?
|
A pus producing infection; usually bacterial in origin = S. aureus 80-90%/cases; hematogenous spread in metaphyseal area of bone (very active in children); can be very aggressive depending on virulence
|
|
|
why is PAGET'S disease different?
|
Has it's own category of pathology - has it's own ballpark
THICKENING OF BONE W/ ERRATIC ARCHITECTURE |
|
|
Factors that affect bone loss (ie, what are contributing factors to osteoporosis)?
|
white
small frame thin family history then...diet (carbonated beverages) |
|
|
DISEASE of REMODELING problem of bone in skeletally mature people
|
PAGET'S DISEASE (Osteitis Deformans) "bone deformation"
remodeling errata |
|
|
Who is at high risk for Osteomyelitis? (7)
|
1. Children 2. Diabetics 3. Elderly 4. Immunocompromised 5. IV drug abusers 6. Homeless 7. Post-surgical patients
|
|
|
IF 5-11% of the population has Paget's after 60, what does this tell you?
|
It's ASYMPTOMATIC!
an incidental finding |
|
|
fracture presentation of Paget's
|
pathologic because bone is being laid down eclectically
(similar to osteopetrosis) |
|
|
MOST COMMON cause of PATHO-LOGIC FRACTURE
|
osteoPOROSIS
(not pathology, but pathological) |
|
|
Stealing of Paget's
|
STEALING of VASCULAR SUPPLY due to vascular overgrowth in Paget's so ORTHOSTATIC HYPOTENSION
|
|
|
prevailing hypothesis of Paget's?
|
VIRUS that behaves similar to chicken pox that recurs as shingles
|
|
|
Paget's STEAL
|
orthostatic hypotension due to more blood vessels in bone hoarding the blood (neovascularization) so heart has to work harder in POLYOSTOTIC paget's
|
|
|
What are s/s of acute pyogenic osteomyelitis?
|
Rapid, high fever; severe throbbing pain that worsens rapidly; pathologic Fx
|
|
|
Treatment for Paget's
|
usually NONE
polyostotic paget's heart monitor use fosamax (bone builder) calcitonin stabilizes normal bone loss but very expensive |
|
|
MONOSTOTIC
vs POLYOSTOTIC |
one bone expression
vs many bone expression |
|
|
CLINICAL PRESENTATION as MALIGNANT DEGENERATION of POLYOSTOTIC PAGET'S
|
nasty NEOPLASIA
rare; only 1-2% of polyostotic osteosarcoma chondrosarcoma |
|
|
How fast does a VERTEBRAL BODY fx happen?
|
SLOWLY
|
|
|
collagen problem w/ Marfan's
|
procollagen peptidase and crosslinking collagen problems
|
|
|
common bones of PAGET's
|
pelvis skull spine tibia femur
|
|
|
Osteogenesis Type II ________
|
CONGENITA
|
|
|
Briefly describe the cellular events in bone infection.
|
Inflam cascade: vasodilation, PMNs, bacteria contacts bone cells which lyse and die, necrosis, WBCs in area continues to next cell and moves on, pus prod'n through cortex, bores thru periosteum, lifted w/ all pus/crud (OW!), reactive bone form'n...
|
|
|
Osteogenesis type 1 _______
|
TARDA
|
|
|
3 things that make bone whiter
vs. whiter and bigger? |
Only PAGET'S makes bone both whiter and bigger
Hodgkin's lymphoma and Blastic metastases and Paget's all make bones white, only Paget's makes whiter AND bigger |
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what is the defect in osteogenesis imperfecta
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TYPE 1 collagen problem
'extremely brittle bones' |
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How is height lost?
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compression of IVD's and VERTEBRAL BODIES
*loss of anterior and posterior height w/ low bone density and osteophytic changes |
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which type of OSTEOGENESIS IMPERFECTA is UNIFORMLY FATAL?
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OI CONGENITA (type II)
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there is a high degree of ______________ in affected bone of Paget's patient
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VASCULARIZATION
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less severe Osteogenesis Imperfecta
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TARDA Type 1
not as fragile prone to fx decreased bone density bowing deformities can of hereditary nature (not metabolic like Rickets) sclera appears BLUE due to abnormal density hearing loss due to 3 bones deformed yellowy-brown teeth due to lack of enamel |
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What can occur d/t pyogenic osteomyelitis?
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10% go on to become chronic bone infections; pathologic Fx; Draining sinus; Squamous cell carcinoma and bone sarcomas are rare but d/t chronic irritations
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Marble bone disease or Albers-Schonberg disease
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OSTEOPETROSIS
(stone bone) |
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skull of Paget's x-ray appearance and effect of bone
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COTTON WOOL SKULL and basalar thickening as well as settling of skull down and around foraminal vertebrae. Possible brainstem and cranial nerve involvement.
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what causes osteopetrosis
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Osteoclasts are too petrified to go to work!
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LAB VALUES of OSTEOPOROSIS
*this is on the test |
ESR is NORMAL
CALCIUM levels NORMAL PHOSPHATE levels NORMAL ALKALINE PHOSPHATASE is NORMAL |
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OSTEOCLASTS BOTH
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break down and remodel bone. From a bone architectural structure, MAKE THE MEDULLARY CAVITY as UNIFORM DENSITY (with the blasts). Medullary cavity won't be created as bone widens (appositional bone growth)
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spine of Paget's x-ray
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cortical outline of vertebra BIGGER AND WHITER - look like a white frame
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If we aren't making medullary cavity and tight due to osteopetrosis, what does the medullary cavity look like?
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WHITE
tons of bone but very BRITTLE not making blood/hematopoiesis so shortened lifespan |
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What is Brodie's Abscess?
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Subacute infection of bone, begins in children, osteolytic lesion gets walled off, sclerotic margin forms around walled off lesion, spontaneous sterilization, commonly in tibia prone to path. Fx
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PTH levels in hypofunctioning osteoclasts due to OSTEOPETROSIS
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elevated to some degree
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upper cervical spine Paget's
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BIGGER AND WHITER
(LOOKS LIKE CONGENITAL BLOCK VERTEBRAE which bones did not separate) |
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naturally occurring fosamax to the nth degree would look like
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OSTEOPETROSIS
no medullary cavities due to osteoclast lask EHRLENMEYER FLASK DEFORMITY (looks like a canoe paddle) |
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How common is TB in bone and how does it appear?
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1-3% of those w/ pulmonary TB can move into bone; general s/s of infection.
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Erlenmeyer FLASK deformity
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OSTEOPETROSIS
(canoe paddle shaped bones that have no visible medullary cavity and are extremely brittle) |
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pelvis of Paget's
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much BIGGER AND WHITER on one side
bone scan show uptake |
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When osteoclasts are petrified!
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OSTEOPETROSIS
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Tuberculosis in bone:
name? progression? likes to go where? Hallmark deformity? |
POTT'S DISEASE
Extremely destructive and difficult to treat; likes areas of bone w/ high O2 content; spine: vertebral body; GIBBOUS DEFORMITY |
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In the real world, patient's have a right to have more than one _______.
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problem
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TB in bone is AKA and what is it prone to?
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Pott's disease; patho. Fx, neurologic involvement (spinal nn.), arthritis.
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red flag of Paget's
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Older man comes in and complains that his hats don't fit anymore
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What are 2 types of syphilis?
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Congenital and acquired
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tibia presentation of Paget's
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SABRE SHIN bowing both anterior and posterior sides due to lytic
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What does congenital syphilis do to bone?
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Destroys epipyseal cartilage (wide growth plates); Reactive bone formation (thick cortex) both sides; May show changes 5th month in utero; Pseudo bowing also called sabre shin but d/t lifting of periosteum.
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What does acquired syphilis do to bone?
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Involves cortical bone and periosteum; Layering of bone on anterior tibia (Sabre shin); Lysis and collapse of nasal bones (infection can get to skull and destroy things); symptoms 2-5 years post. infection
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What is Gumma?
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Scattered radiolucencies;
GRANULOMATOUS mass (gummata are the uclers) of tissue due to SYPHILLIS |
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Brodie's abscess, the 3rd variety of bone infection, is also called a type of ___________ bone infection.
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subacute
lytic phenomenon, bacterial changes but bone walls it off so early on, not much radiolucency (dark areas). Thickness of sclerotic margin varies around the radio |
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why does a BRODIE'S ABCESS result in spontaneous sterilization?
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bone has walled off infection - essentially cutting blood supply and spontaneous sterilization
Lytic center, sclerotic border |
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How big is the sclerotic border, how big is the radiolucent area and where is it?
Brodie's abcess |
determining Brodie's abcess = subacute so no signs and symptoms
1. round hole of sclerotic margin 2. radiolucent punched out area 3. usually at metaphysis |
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can Brodie's abcess be prone to pathologic fx?
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sure! There are no signs and sx but it is an area of weakness pre-exisiting due to pathology
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Why is TB coming back?
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adaptation and resistance to our antibiotics
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Why is TB relative to bone pathology?
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1-3% of TB patients will develop before 3rd decade (0-20's)
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Sclerosis is radio________.
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dense = cortical thickening
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Paget's bowing occurs in anterior of tibia. How is sabre shin different in syphilitic patient?
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there is NO bowing, just bone deposition on anterior side and patient in congenital syphilis is likely a child (whereas Paget's is older person)
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how does gumma present radiographically?
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LUCENCY
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