Exam 2 Flashcards
Soft callus - what is the role of the hematoma?
Hematoma serves as the basis for the fibrin network for granulation tissue
Soft callus - what does granulation tissue contain?
Blood vessels, phagocytic cells, fibroblasts lay down new collagen, susceptible to fix again because there is no bony material
What is a soft callus?
Fibrin, granulation tissue, collagen - still in healing process, not able to withstand weight bearing
Hard callus - chondroblasts role? Osteoblasts?
Chondroblasts start to lay down cartilage - forms a fibrocartilaginous callus (collar)
** still not strong enough to bear weight
Osteoblasts form new bone & replaces the cartilage callus, forms bony/hard callus
Why are there restrictions on weight bearing after an extremity fracture?
Patients can severely inhibit or stop healing process by putting weight on fx’d area too soon, bone needs to stay aligned for soft callus to form around it and progress to hard callus
Stress fracture meaning/difference from pathological fracture?
Stress fracture = low load/high dose
Pathological = break in bone that is caused by an underlying disease such as avascular necrosis
Modifiable risk factors for atherosclerosis (7)
*Lipid metabolism - chylomicrons, VLDL, LDL (want these to be low) HDL (want this to be high)
*HTN - damages endothelial cells and causes hyperplasia of smooth muscles
*Smoking - accelerated atherosclerosis, increases CO2, increases HTN damage to endothelial cells, hyperplasia, increases hyperlipidemia
*Diabetes - too much glucose in bloodstream, attach to proteins causing a glycosylation of proteins which stiffens blood vessels
*Lack of exercise - obesity, diabetes, hyperlipidemia, low HDL levels
*personality - anxious, type a increases MI risk
*genetics
Nonmodifiable risk factors for atherosclerosis
Age and sex
Difference between primary and secondary hypertension
Primary - 90-95%, dont know the cause
Secondary 5-10%, know the cause - most commonly renal hypertension (renal artery narrowed)
Pathogenesis is the same for both = vessels thicken, arteriolorsclerosis leading to L ventricular enlargement, possibly leading to CVA or MI
Most likely areas for atherosclerosis and why
- Abdominal aorta and iliac arteries
- Thoracic aorta, femoral and popliteal arteries
*Proximal coronary arteries (has curvature - perfect place for plaque to form/get stuck) - Internal carotid arteries
Vertebral, basilar and middle cerebral arteries (90 angles - good place for thrombus to form/embolus to get stuck) - Narrowed lumen - perform stress test
- Weakened arterial walls
- Thrombosis
How to reverse atherosclerosis
Remove stressors, add exercise and healthy diet/dietary restrictions and lipid meds
S&S for MI
Severe substernal chest pain/squeezing pressure
Pain radiating down arms
Feeling of indigestion
Angina lasting for 30mins or more
Angina unrelieved by rest
Nausea
Pallor
Pain of infarct unrelieved by positional change
Diaphoresis
SOB
Weakness and feeling of faintness
ST segment elevation
T wave inversion
S&S for MI that PT ‘s need to act on immediately (emergencies; 4)
Severe substernal chest pain or squeezing pressure
Pain radiating down arms
Angina lasting 30 mins or more
Angina unrelieved by rest/positional change
S&S for MI - non-emergency action
Nausea - rest, hydrate, etc.
SOB - rest, pulse ox
Weakness and feeling of faintness - rest, hydrate, pulse ox
Parts of the movement system - how do we measure?
Lungs - respiratory rate
Heart - HR
Muscle - anaerobic and aerobic metabolism
Pathway of RBC
RA, RV, pulmonary arteries, pulmonary capillaries, pulmonary veins, LA, LV, aorta, arteries, arterioles, capillaries, venuoles, veins, RA
S&S of CV disease - dependent edema
Hallmark of R ventricular failure - usually bilateral and peripheral, may be accompanied by jugular venous distension (JVD), cyanosis, and abdominal distension (ascites), bilateral swelling in extremities
S&S of CV disease - claudication
PVD along w CAD - ex. Pain in legs when walking - what to do? Walk in small bouts to 8/10 pain, take rest, then repeat. Continue to build tolerance/make adaptations
Layers of the heart
Fibrous pericardium
Parietal layer of serous pericardium
Pericardial space (fluid)
Viscous serous pericardium
Epicardium
Myocardium
Endocardium
Coronary arteries begin and end?
Begin outermost layer (fibrous pericardium) and end innermost (endocardium) —> ischemia, hypoxia starting at innermost layer, irreparable damage
HTN increases size of what layer of the heart?
Myocardium - increases size without increasing vascularization (as it would w/ adaptation from aerobic exercise)
Structural heart failure
Historic approach of describing heart failure - L v R sided
Functional heart failure
Ejection fraction - amount of blood pumped out of L ventricle. In heart failure, this is either preserved ejection fraction (higher pressure in LV than normal with normal ejection fraction) or reduced ejection fraction
EKG and atrium
P wave - atrial depolarization
P-R interval - time it takes for signal to travel from Sinoatrial (SA) node to atriaventricular (AV) node
**artial fibrillation can present in P wave or P-R interval
QRS - artial repolarization, ventricular depolarization
