Exam 2 Flashcards

1
Q

Soft callus - what is the role of the hematoma?

A

Hematoma serves as the basis for the fibrin network for granulation tissue

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2
Q

Soft callus - what does granulation tissue contain?

A

Blood vessels, phagocytic cells, fibroblasts lay down new collagen, susceptible to fix again because there is no bony material

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3
Q

What is a soft callus?

A

Fibrin, granulation tissue, collagen - still in healing process, not able to withstand weight bearing

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4
Q

Hard callus - chondroblasts role? Osteoblasts?

A

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

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5
Q

Why are there restrictions on weight bearing after an extremity fracture?

A

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

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6
Q

Stress fracture meaning/difference from pathological fracture?

A

Stress fracture = low load/high dose

Pathological = break in bone that is caused by an underlying disease such as avascular necrosis

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7
Q

Modifiable risk factors for atherosclerosis (7)

A

*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

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8
Q

Nonmodifiable risk factors for atherosclerosis

A

Age and sex

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9
Q

Difference between primary and secondary hypertension

A

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

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10
Q

Most likely areas for atherosclerosis and why

A
  • 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
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11
Q

How to reverse atherosclerosis

A

Remove stressors, add exercise and healthy diet/dietary restrictions and lipid meds

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12
Q

S&S for MI

A

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

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13
Q

S&S for MI that PT ‘s need to act on immediately (emergencies; 4)

A

Severe substernal chest pain or squeezing pressure
Pain radiating down arms
Angina lasting 30 mins or more
Angina unrelieved by rest/positional change

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14
Q

S&S for MI - non-emergency action

A

Nausea - rest, hydrate, etc.
SOB - rest, pulse ox
Weakness and feeling of faintness - rest, hydrate, pulse ox

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15
Q

Parts of the movement system - how do we measure?

A

Lungs - respiratory rate
Heart - HR
Muscle - anaerobic and aerobic metabolism

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16
Q

Pathway of RBC

A

RA, RV, pulmonary arteries, pulmonary capillaries, pulmonary veins, LA, LV, aorta, arteries, arterioles, capillaries, venuoles, veins, RA

17
Q

S&S of CV disease - dependent edema

A

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

18
Q

S&S of CV disease - claudication

A

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

19
Q

Layers of the heart

A

Fibrous pericardium
Parietal layer of serous pericardium
Pericardial space (fluid)
Viscous serous pericardium
Epicardium
Myocardium
Endocardium

20
Q

Coronary arteries begin and end?

A

Begin outermost layer (fibrous pericardium) and end innermost (endocardium) —> ischemia, hypoxia starting at innermost layer, irreparable damage

21
Q

HTN increases size of what layer of the heart?

A

Myocardium - increases size without increasing vascularization (as it would w/ adaptation from aerobic exercise)

22
Q

Structural heart failure

A

Historic approach of describing heart failure - L v R sided

23
Q

Functional heart failure

A

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

24
Q

EKG and atrium

A

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

25
Q

EKG and ventricles

A

QRS - artial repolarization, ventricular depolarization
S wave - ventricular repolarization
ST segment - depressed = angina

ST segment elevated = MI

26
Q

S&S for angina (8)

A

Pressure behind breast bone
Pain radiation to neck, jaw, back, shoulder, arms
Toothache
Burning indigestion
Dyspnea
Nausea
Belching
ST segment depression

27
Q

Angina treatment (5)

A

CABG
Angioplasty
Meds
Exercise
Diet

28
Q

Stable angina

A

Hearty working hardy

29
Q

Unstable angina + variant angina

A

Most dangerous - can happen w/o physical exertion, doesn’t follow a pattern

Variant - Happens when resting

30
Q

CK MB

A

Marker in blood (serum enzymes) to tell if someone has had MI, highest 24 hrs post

31
Q

CK MM, CK BB

A

Serum enzyme/marker released by skeletal muscle, indicator of rhabdomylosis

Stroke - BB

32
Q

Left sided heart failure

A

Caused by MI, fluid backs up into lungs - can be indicated by heart sounds (S3) - heart murmur, swish, etc

33
Q

Right sided heart failure

A

Caused from L sided heart failure, —> dependent edema, JVD

34
Q

Valvular disease S&S (7)

A

Easy fatigue
Dyspnea
Palpations
Chest pain
Pitting edema
Orthopnea - sensation of breathlessness in recumbent position (lying down flat) and is relieved by sitting or standing
Dizziness and fainting

35
Q

Orthopnea

A

Orthopnea - sensation of breathlessness in recumbent position (lying down flat) and is relieved by sitting or standing

36
Q

3 functions of lymphatic system

A

Transports interstitial fluid back to cardiovascular system
Filters and destroys foreign material - initiates immune response
Absorbs lipids from GI tract

37
Q

9 structures of lymph system

A

Red bone marrow
Red bone marrow
Spleen
GI tract
Thymus gland
Tonsils
Lymph vessels
Lymph tissue
Lymph nodules
Lymph ducts
Lymph nodes

38
Q

Pressure gradient for lymph

A

Blood capillaries, interstitial fluid, lymph capillaries, lymph veins, lymph ducts, large circulatory veins