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Pathophysiology > Patho Exam 1 > Flashcards

Patho Exam 1 Flashcards

1
Q

Hemostasis is…

A

Blood’s ability to clot blood (clot formation at the site of injury)

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2
Q

Clotting depends on 3 factors… (3 steps to clotting success!)

A

Vascular - local vasoconstriction
Platelet - formation of platelet plug, platelet adhesion, & aggregation (white clot)
Coagulation factors - formation of blood clot (red clot); helps form a stronger clot to promote healing and prevent reopening of injury site

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3
Q

What are the 4 steps in the functional response of activated platelets?

A

Adhesion
Aggregation
Secretion
Procoagulant activity

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4
Q

Describe the adhesion phase in the functional response of platelets.

A

Deposition of platelets on subendothelial matrix in the area of the wound. Adhesion occurs on the edges of the wound

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5
Q

Describe the aggregation phase in the functional response of platelets.

A

Platelet-platelet cohesion. Platelets come together and stick together after they influx to the area to form the clot.

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6
Q

Describe the secretion phase in the functional response of platelets.

A

Release of platelet granule proteins. This protein secretion helps to start the procoagulant activity phase

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7
Q

Describe the procoagulant activity phase in the functional response of platelets.

A

Enhancement of thrombin (protein) generation

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8
Q

Give a cursory summary of the process of clot formation.

A
  • Tissue damage
  • Vascular Spasm
  • Exposed collagen attracts platelets
  • Platelet plug formation
  • Blood coagulation: Damaged cells and platelets cause reaction that yields prothrombin activator. This activates the common pathway [Prothrombin → Thrombin; Fibrinogen → Fibrin]
  • Blood cells trapped in fibrin threads → Clot formed!
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9
Q

Describe the difference between intrinsic and extrinsic pathways in the clotting response.

A

BOTH respond to injury

  1. Intrinsic: Responds to the Endothelial wall injury
  2. Extrinsic: Responds to the skin wound
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10
Q

Clotting Degradation:
____ (abbreviation: __) is a normally-secreted protease that along with ___ helps to break down plasminogen into ___. This conversion can also be done pharmacologically to break down clots, e.g. in the ___ to stop the effects of a ____.

A 
Clotting Degradation:
PLASMINIOGEN ACTIVATOR (abbreviation: tPA) is a normally-secreted protease that along with PA1 helps to break down plasminogen into PLAMSIN.   This conversion can also be done pharmacologically to break down clots, e.g. in the BRAIN to stop the effects of a STROKE.
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11
Q

___ is an enzyme that breaks down the clot matrix.

A

PLASMIN

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12
Q

What happens if you have an excess of tPA?

A

tPA = Plasminogen Activator
Clots struggle to form, and you’d keep bleeding. An adverse effect of pharmacological tPA can cause increased bleeding, but the benefit of breaking up a dangerous clot outweighs the risk

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13
Q

Hemopheliacs lack clotting factor ___ in the clotting cascade.

A

Factor VII. Puts them at risk for bleeds

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14
Q

Prothrombin time (PT) is a measure of ___. Its reference value is __-___ seconds. Therapeutic Range: __-___x Normal. If this value is HIGH, you’re concerned about ___. This is done in [inpatient/outpatient] settings.

A 
Prothrombin time (PT) is a measure of HOW LONG IT TAKES FOR BLOOD TO CLOT. 
Reference value is 12-15 SECONDS.
Therapeutic Range: 1.5-2.5x Normal.  If this value is HIGH, you're concerned about BLEEDING.  This is done in INPATIENT settings, but is NOT comparable between institutions.
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15
Q

Partial Thromboplastin Time (PTT) is a monitor of ___. Its reference value is __-___ seconds. Therapeutic Range: __-___ seconds. If this value is HIGH, you’re concerned about ___. This is done in [inpatient/outpatient] settings.

A

Partial Thromboplastin Time (PTT) is a monitor of LOW MOLECULARWEIGHT HEPARIN (LMWH) - measures how quickly your blood clots. Its reference value is 30-40 seconds. Therapeutic Range: 50-80 seconds. If this value is HIGH, you’re concerned about BLEEDING. This is done in INPATIENT settings, but is NOT comparable between institutions.

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16
Q

International Normalized Ratio (INR) is used only in [outpatient/inpatient] settings. Its reference value is ___-___; therapeutic range: __-__. It takes [how long?] to test and [is/is not] standardized across institutions. A high INR means ___

A

International Normalized Ratio (INR) is used only in OUTPATIENT settings. Its reference value is 0.9-1.1; therapeutic range: 2-3. It takes A FEW DAYS to test [TESTED WEEKLY] and IS standardized across institutions. High INR = blood takes longer to clot (increased bleeding risk)

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17
Q

Which two coagulation measures give instant results? Used in ___ settings. [Comparable/not comparable] between hospitals. High values for these mean ___.

A

PT & PTT (Prothrombin Time & Partial Thromboplastin Time)

INPATIENT settings, can’t compare between hospitals

High values = at risk for bleeding

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18
Q

Of the coagulation measures, which measures the EXTRINSIC pathway? What chemical is measured?

A

PT (Prothrombin time). Measures Coumadin

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19
Q

Which coagulation measure measures the INTRINSIC pathway? What chemical is measured?

A

PTT (Partial thromboplastin time). Measures Heparin

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20
Q

Which coagulation measure measures the COMMON clotting pathway? What chemical is measured?

A

PTT (Partial thromboplastin time). Measures Heparin

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21
Q

The International Normalized Ratio (INR) measures what chemical? What other coagulation test also measures this chemical?

A

COUMADIN. Also measured by PT

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22
Q

__ is a straw-colored liquid that acts as a transportation system in blood. It accounts for __% of blood volume. ___% of this stuff is made up of water.

A

PLASMA is a straw-colored liquid that acts as a transportation system in blood. It accounts for 55% of blood volume. 90% of PLASMA is made up of water.

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23
Q

Other than water, what constitutes the other 10% of plasma? (Go for 6…)

A 
Dissolved proteins
Glucose
Clotting factors, Electrolytes/mineral ions (Mg, Ca, K, Na)
Hormones
CO2
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24
Q

Of the dissolved proteins in plasma, ___ makes up 60%. It is involved with ___ pressure and acts as transport molecules. Other proteins include ___ (37%), ___ (4%), alpha 1-antitrypsin, and regulatory proteins (gene expression).

A

Of the dissolved proteins in plasma, ALBUMIN makes up 60%. It is involved with OSMOTIC pressure and acts as transport molecules. Other proteins include IMMUNO-GLOBULINS [immune sys] (37%), FIBRINOGEN (4%), alpha 1-antitrypsin, and regulatory proteins (gene expression).

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25
Q

Term that means “making of new RBCs”

A

Erythropoeisis

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26
Q

Average lifespan of RBCs

A

120 days (~3 months)

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27
Q

What stimulates the making of new RBCs?

A

Primarily HYPOXIA: decrease in the pO2 of arterial blood. Erythropoietin is a hormone (mostly from the kidney, some from liver) that stimulates bone marrow to produce RBC

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28
Q

What does Erythropoietin do?

A
  • Hormone that stimulates bone marrow to produce RBC

- Comes mostly from kidney, some from liver

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29
Q

What is COPD?

A

Chronic obstructive pulmonary disease = damage to lungs that decreases ability to diffuse O2 from lungs into blood stream, so level of O2 in blood is always low. You start to produce more RBC to help get more O2 to your tissues; this is common in multiple types of lung disease

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30
Q

It takes __ days to produce new RBC

A

5 days to produce new RBC

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31
Q

RBCs have [flexible/inflexible] plasma membranes that allow them to get through small capillary beds.

A

RBCs = FLEXIBLE plasma membranes

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32
Q

On what types of cells is hemoglobin found?

A

Hemoglobin is a protein that is the primary component of RBC (Erythrocytes)

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33
Q

___ is an iron-containing oxygen transport protein in the red blood cell. It composes __% of RBC and is a good indicator of ___.

A

HEMOGLOBIN (Hgb). 35% of RBC; good indicator of O2 carrying capacity

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34
Q

Fetal hemoglobin has a [higher/lower] affinity for O2 than adults, meaning you need a [higher/lower] partial pressure of O2 to allow it to bind to hemoglobin

A

Fetal hemoglobin has a HIGHER affinity for O2 than adults, meaning you need a LOWER partial pressure of O2 to allow it to bind to hemoglobin

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35
Q

__ and __ have MUCH higher affinity for hemoglobin than O2, meaning they need much [more/less] to be available in order to bind.

A

CO2 and CO have 230x stronger bonding affinity to hemoglobin!

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36
Q

When CO binds to hemoglobin, it [increases/decreases] O2 affinity for hemoglobin. Why?

A

CO binding to hemoglobin INCREASES O2 affinity for hemoglobin so it doesn’t let it off the bus at the tissue level!

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37
Q

CO2 binds at [the same/ a different] site than O2. This [increases/decreases] the amount of O2 that can be bound for a given partial pressure of O2.

A

CO2 binds at A DIFFERENT site than O2. This DECREASES the amount of O2 that can be bound for a given partial pressure of O2.

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38
Q

Describe the Haldane effect.

A

Deoxygenated blood increases ability to carry CO2

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39
Q

Describe the Bohr effect.

A

In the presence of CO2, hemoglobin’s affinity for O2 decreases

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40
Q

Levels of [CO2/ O2 / CO] in blood regulate respiratory levels and breathing pattern!

A

Levels of CO2 in blood regulate respiratory levels and breathing pattern!

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41
Q

RBCs are shaped as __. This increases the ___-to-____ ratio and increases the diffusion of __ and __ into and out of cell.

A

RBCs are shaped as BICONCAVE DISCS. This increases the SURFACE AREA-to-VOLUME ratio and increases the diffusion of O2 and CO2 into and out of cell.

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42
Q

Clinical concerns for a pt with low HCT/Hbg/RBC?

A

FATIGUED! Consider the energy cost of the activity and the patient’s response if their values are low. You may need to reduce the intensity of an activity in the short-term while these values are repleted (either via transfusion or by their body).

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43
Q

___ is the fraction of blood volume composed of RBC, expressed as a percentage

A

HEMATOCRIT

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44
Q

What blood values do you look at to see if O2 is low?

A

Hematocrit or hemoglobin

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45
Q

What conditions would yield a high hematocrit?

A

Dehydration (less H20, so higher RBC%), blood doping (increases #RBC)

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46
Q

What conditions would yield a low hematocrit?

A

Following excessive fluids (given via IV)
Anemia (pathologic anemia)
Blood loss (b/c it takes ~5 days to replace RBC but you replace the other blood components much quicker → lower RBC %)

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47
Q

Platelets are AKA __

A

Thrombocytes

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48
Q

What’s the function of platelets?

A

HEMOSTASIS: A blood clot is formed as platelets become trapped in a network of protein fibers

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49
Q

What’s the life span of platelets?

A

8-10 days in circulation (continuously regenerated by body)

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50
Q

What are the clinical implications for a patient with low platelets?

A

AT RISK FOR BLEEDING

  • Bruising
  • Chronic bleeding, spontaneous nosebleeds, blood in urine
  • Seen as a side effect of chemo (chemo pts are at high risk for bleeding)
  • Decrease in platelets in bone marrow disease (leukemias, myelomas, CA of bone)
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51
Q 
Platelet count = <5,000 - 10,000 cells/mm3
Activity restriction?
A

BEDREST, especially with signs of active bleeding

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52
Q 
Platelet count = 10,000 - 20,000 cells/mm3
Activity restriction?
A

ADLs
Mobility to complete ADLs
Discussion w/medical team

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53
Q 
Platelet count = 20,000 - 30,000 cells/mm3
Activity restriction?
A 
AROM activity
LIGHT exercise (walking, biking)
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54
Q 
Platelet count = 30,000 - 50,000 cells/mm3
Activity restriction?
A 
AROM (no resistance)
Moderate exercise (walking, biking, swimming)

NO strength training [60-80% max] (leads to microtears in tissue –> bleeding)

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55
Q

Platelet count > or equal to 50,000 cells/mm3

Activity restriction?

A

UNRESTRICTED activity

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56
Q

Generally, you don’t want to do MMT with a platelet count <_____ cells/mm3 due to increased risk of bleeding (though some exceptions exist).

A

Avoid MMT with platelet count <50,000 cells/mm3

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57
Q

WBCs aka ___ provide the primary ___ response and fight ___.

A

WBC aka LEUKOCYTES provide primary IMMUNE response and fight INFECTION

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58
Q

WBC count = ____

Low WBC count = ____

A

WBC count = INFECTION (e.g. pnemonia)

Low WBC count = at RISK for infection (cancer, HIV, impaired immune sys)

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59
Q

WBCs can be generally dicotimized into ___ and ___

A

GRANULAR and AGRANULAR leukocytes

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60
Q

3 types of granular leukocytes

A

Basophils
Neutrophils
Eosinophils

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61
Q

2 types of agranular leukocytes

A
  • Lymphocytes (T Cell, B Cell, Natural Killer [NK] Cell)

- Monocytes

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62
Q

Lymphocytes are [granular/agranular] and make up ___% of WBC. They play a large role in ___. Their subtypes include __, __, and ___. How long does each subtype live?

A

Lymphocytes are AGRANULAR and make up 20-40% of WBC. They play a large role in DEFENDING body against DISEASE.
T Cell - last a few days, months, or years
B Cell - last 2-3 days
Natural Killer (NK) Cell - live variable length of time

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63
Q

Monocytes are [granular/agranular] and make up ___% of WBC. They are increased during ___ and live __-___x longer than granulocytes. They’re called ___ at the tissue level; this cell lives from ___ to ___.

A

Monocytes are AGRANULAR and make up 4-8% of WBC. They are increased during CHRONIC INFLAMMATION [e.g. tendinosis] and live 3-4x longer than granulocytes. They’re called MACROPHAGES at the tissue level; this cell lives from MONTHS to YEARS.

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64
Q

In general, granulocytes are involved with __ and ___. Their life span is __ in blood and __ in tissue.

A

In general, granulocytes are involved with IMMUNE RESPONSE and INFECTION CONTROL. Their life span is 12 HOURS in blood and 4 DAYS in tissue.

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65
Q

Basophils are [granular/agranular] and make up ___% of WBC. They are increased during ___ and resolve a bit quicker than ___.

A

Basophils are GRANULAR and make up 1% of WBC. They are increased during ALLERGIC REACTION OR TISSUE INJURY and resolve a bit quicker than EOSINOPHILS.

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66
Q

Neutrophils are [granular/agranular] and make up ___% of WBC. They are crucial in the ___ response and are the ___ after injury.

A

Neutrophils are GRANULAR and make up 60-70% of WBC. They are crucial in the ACUTE INFLAMMATORY response and are the FIRST RESPONDERS after injury.

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67
Q

Eosinophils are [granular/agranular] and make up ___% of WBC. They are increased with ___ or ___.

A

Eosinophils are GRANULAR and make up 1-3% of WBC. They are increased with ALLERGIC REACTION or PARASITIC INFECTION.

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68
Q

Reference range for WBC

A

WBC: 4,500-11,000 cells/mm3

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69
Q

Reference range for RBC

A

Males: 4.5-5.3 x 10^6 /mm3
Females: 4.1-5.1 x 10^6 /mm3

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70
Q

Reference range for Hgb

A

Males: 13-18 g/dl
Females: 12-16 g/dl

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71
Q

Reference range for Hct

A

Males: 37-49%
Females: 36-46%

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72
Q

Reference range for Plts

A

150,000 - 450,000 cells/mm3

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73
Q

WBC Count counts the actual number of ____ per ___. WBCs fight ___ and react against ___.. Increases and decreases are [normal/abnormal]

A

WBC Count counts the actual number of WBC per VOLUME OF BLOOD. WBCs fight INFECTION and react against FOREIGN BODIES OR TISSUES. Increases and decreases are ABNORMAL

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74
Q

RBC count counts the actual # of __ /volume blood. Increase and decreases point to ___.

A

RBC count counts the actual # of RBC /volume blood. Increase and decreases point to ABNORMAL CONDITIONS.

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75
Q

Hemoglobin (Hgb) measures the amount of ____ in blood.

A

Hgb measures AMOUNT OF O2 CARRYING CAPACITY in blood

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76
Q

Hematocrit (Hct) measures ____ in given volume of whole blood.

A

Hct measures % RBC in given volume whole blood

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77
Q

Platelet (Plt) count gives ___ in a given volume of blood. Indicates ___ of the blood.

A

Plt count = # platelets in volume blood. Indicates CLOTTING POTENTIAL

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78
Q

Mean Corpuscle Volume (MCV) is a measurement of the average ___. MCV is elevated when ___ are ____. MCV decreased when ___. Give an example of each.

A

Mean Corpuscle Volume (MCV) is a measurement of the average SIZE OF RBCs. MCV is elevated when RBC ARE LARGER THAN NORMAL (macrocytic). MCV decreased when RBCs ARE SMALLER THAN NORMAL

High MCV: anemia from vitamin B12 deficiency

Low MCV: iron deficiency anemia, thalassemias

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79
Q

Mean Corpuscle Hemaglobin (MCH) is a calculation of the average amount of ___. [Macrocytic/microcytic] RBCs are large and have a HIGHER MCH, and vice versa.

A

Mean Corpuscle Hemaglobin (MCH) is a calculation of the average amount of O2 CARRYING HEMOGLOBIN IN A RBC. MACROCYTIC RBCs are large and have a HIGHER MCH, and vice versa.

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80
Q

Mean Corpuscle Hemaglobin Concentration (MCHC) is a calculation of the average ___. Decreased MCHC is called ___ and is seen when ___. Increased MCHC values are called ___ and are seen when __.

A

Mean Corpuscle Hemaglobin Concentration (MCHC) is a calculation of the average CONCENTRATION OF Hgb INSIDE RBC. Decreased MCHC is called HYPOCHROMIA and is seen when HEMOGLOBIN IS ABNORMALLY DILUTED IN RBC, e.g. iron deficiency anemia. Increased MCHC values are called HYPERCHROMIA and are seen when hemoglobin concentration is high in cells, e.g. burn patients.

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81
Q

Red Cell Distribution Width (RDW) is a calculation of the ___. This may be high in ___.

A

RDW calculation of VARIATION OF SIZE OF RBCs. May b ehigh in some ANEMIAS in which the variation (anisocytosis) in RBC size causes increase in RDW.

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82
Q

Make an X. What values go where on a hand written chart?

A 
Top of X going clockwise:
Hgb (top)
Plt (right)
Hct (bottom)
WBC (left)
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83
Q

A CBC with Differential looks at the ____ that are present.

A

CBC with differential looks at the TYPES of WBC that are present.

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84
Q

Role of Neutrophils

A

Target bacteria and fungal infections

- Most abundant type of WBC blood cell (60-70% of WBC)

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85
Q

Role of Lymphocytes

A

Produce antibodies, fight tumor cells, respond to viral infection
- 25% of WBC count, but varies

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86
Q

Role of B Cells

A

Produce antibodies

Type of lymphocyte.

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87
Q

Role of T Cells

A

Recognize foreign substances and process them for removal

Type of lymphocyte.

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88
Q

Role of Monocytes

A

Ingestion of bacteria and other foreign particles. Clean up debris after neutrophils have done their job
- 5-10% total WBC

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89
Q

Role of Eosinophils

A

Attack parasites and play a role in asthma and allergy. Stain red
- 1-3% WBC count

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90
Q

Role of Basophils

A

Release histamines during allergic reactions. Stain blue.

- 1% or less of total WBC count, but may increase/decrease in certain disease states

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91
Q

Fresh Frozen Plasma (FFP) involves ___ being removed via ___ and frozen for later use. Contains ___ from the original blood. Can be stored for ___ (how long?). Used to treat ___.

A

Fresh Frozen Plasma (FFP) involves PLASMA being removed via PHARESIS and frozen for later use. Contains ALL COAGULATION FACTORS AND PROTEINS from the original blood. Can be stored for 10 YEARS (how long?). Used to treat LIVER DISEASE, COAGULOPATHIES.

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92
Q

Transfusions can give ___ or ___. Negative reactions to a transfusion = (go for 4!)

A

Transfusions can give a UNIT OF PACKED RED BLOOD CELLS (uprbc) or PLATELETS.

Bad reactions include:

(1) Fever
(2) Acute hemolytic transfusion rxn: cells clump together
(3) Allergic rxn
(4) Acute pulmonary edema

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93
Q

What goes where on a Basic Metabolic Panel (BMP) (handwritten chart)? There are 3 spots on top, 3 on bottom, and a < to the right.

A

Na | Cl | BUN
————————–< Glu
K | HCO3 | Cr

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94
Q

Which tests from the Basic Metabolic Panel are measures of kidney function?

A

BUN (Blood, Urea, Nitrogen)

Creatinine

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95
Q

What is the clinical relevance of Sodium on the BMP?

A

Important in muscle activity (contractions) and brain function

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96
Q

What is HCO3?

A

Bicarbonate. Critical in acid-base relationship (buffer)

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97
Q

What might a high or low Potassium (K) indicate?

A

Risk for sudden cardiac death

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98
Q

What are 2 measures to look at glucose?

A
  • Plasma glucose (short term, changes based on intake)

- Hemaglobin A1c (HA1c) (measures glucose in blood over life span of RBC [3 months])

99
Q

Normal PLASMA GLUCOSE ranges:
Child
Adult
Adult >60yo

A

Child: 60-100 mg/dl
Adult: 70-100 mg/dl
Adult > 60: 80-110 mg/dl

100
Q

Plasma glucose is taken from [arterial/venous] blood via a ___. It reflects [long term/instantaneous] glucose levels.

A

Plasma glucose - from VENOUS blood via FINGER PRICK

Tells INSTANTANEOUS glucose levels.

101
Q 
Hemoglobin A1c ranges fro Blood Sugar Control
Normal
Good
Fair
Poor
A 
HA1c Range
Normal: 4.0-6.0%
Good: 2.5-5.9%
Fair: 6.0-7.0 %
Poor: > 7.0%
102
Q

Hemoglobin A1c is taken from [arterial/venous] blood and indicates control of blood sugars over ___. As HA1c goes up, blood sugar goes ___.

A

Hemoglobin A1c is taken from VENOUS blood and indicates control of blood sugars over 3 month time frame [LONG term!]. As HA1c goes up, blood sugar goes UP

103
Q

Patient is in a state of hypoglycemia. What will physical exercise/activity do?

A

Physical activity requires glucose, so increased activity –> decrease in glucose (from already low state)

104
Q

Patient is in a state of hypERglycemia. What will physical exercise/activity do?

A

If blood sugar is HIGH, there is no available insulin to assist with metabolism. Exercise if already dangerously hyperglycemic will INCREASE glucose levels, progressing toward KETOACIDOSIS due to metabolism that occurs with activity.

105
Q

What are specific tests for myocardial infarction (MI)?

A

Troponin (I or T) (cardiac specific proteins that regulate muscle contractions) (Elevate within 3-4 hrs of injury, stay elevated for 10-14 days)

Creatine Kinase (CK) (Enzyme in heart, brain, and skel muscle that assists with muscle contraction. Rises 4-6 hrs post injury, peaks in 18-24 h, normalizes in 2-3 days)

CK-MB (MB is cardiac muscle specific form of CK. CK-MB is ratio of total muscle damage to cardiac muscle. Rises at 3-4 hrs, peaks 18-24 hrs, normal within 24 hrs)

106
Q

Cholesterol levels identify risk for __. Total cholesterol should be <___.

A

Cholesterol: ID risk for cardiac disease. Total should be <200

107
Q

Brain nateuretic peptide (BNP or NT-proBNP) assists with regulating ___, and therefore the work that the ___ [organ part] must do. It increases as ___.

A

BNP assists with regulating BLOOD VOLUME Increases as the left ventricle is stretched and has to work harder (increased demand).

108
Q

D-Dimer detects __ as degredation products and is used to diagnose __ and __.

A

D-Dimer detects FIBRIN as degredation products and is used to diagnose PULMONARY EFFUSION and DVT.

109
Q

Erythrocyte Sedimentation Rate (ESR) is a non-specific test for ____. Measures degree of ___ of RBC.

A

ESR = non specific test for INFLAMMATORY disorders. Measrues RBC clumping which indicates inflammation

110
Q

What are 6 tests of liver function?

A

Ammonia (liver disease can’t convert ammonia –> urea)
Albumin (ability of liver to syn. proteins)
Bilirubin
Alanine Amino Transferase (ALT)
Alkaline Phosphatase (ALP)
Aspartrate Aminotransferase (AST)

111
Q

What tests would come from arterial blood?

A

pH
partial pressure O2
pCO2 (acid)
Bicarbonate (HCO3) (base)

112
Q

What is pathology?

A

Study of changes in cells and tissues as a result of disease

113
Q

What is disease?

A

Impairment of cell, tissue, organ, or system functioning

114
Q

What is illness?

A

State that results in suffering or distress

115
Q

What is health?

A

Condition of being sound in body, mind, and spirit

116
Q

What’s the difference between etiology and Pathogenesis?

A

Etiology - cause

Pathogenesis - mechanism of development

117
Q

Health exists on a ___ from wellness (optimal functioning) to illness (death)

A

Health = CONTINUUM

118
Q

What is the difference between a sequela and a complication?

A

Sequela - outcome of the disease; condition following and resulting from the disease; often normal after disease

Complication - a NEW or separate process that may arise SECONDARILY to original process

119
Q

Acute illness has a [rapid/slow] onset and [long/short] duration. Stages include (5!)

A

Acute illness = RAPID onset, SHORT duration

Physical symptoms (SOB, fever...)
Cognitive awareness (it has meaning to pt)
Emotional Repsonse (denial, fear)
Sick role (person realizes they need medical attn)
Dependency (Receives and accepts dx and treatment plan)
120
Q

Sub acute illness is between __ and ___. It’s longer than __ and less than ___.

A

Between acute and chronic.

Longer than a few days, less than a few months.

121
Q

Chronic illness includes illnesses that involve permanent _ or ___; residual physical or cognitive ___, need for special __ or long-term __. May fluctuate in intensity as ___ occur.

A

Chronic =
- Permanent impairment/disability
- Residual physical or cognitive disability
- Need for special rehab or long-term medical management
May fluctuate in intensity as ACUTE EXACERBATIONS occur

122
Q

Differentiate between primary, secondary, and tertiary disease prevention.

A

Primary - PREVENTION. Exercise to prevent heart disease, helmets

Secondary: disease occurred, and you’re intervening but before person notes anything is wrong

Tertiary: preventing complications and progressions

123
Q

Low Mg or High or Low K can lead to…

A

Myocardial event, sudden death. WAIT until patient is stable to treat!

124
Q

CK, MB, Troponin, and CK-MB must [be high/low/have peaked] before you treat. Why?

A

These measure cardiac function. Elevated values indicate myocardial death. Don’t want to treat during active cardiac death

125
Q

What are common mechanisms of cell injury? (8 total)

A
  • Ischemia (decrease BF)
  • Infectious Agent (bacterial, viral, fungal and parasitic)
  • Immune Rxn
  • Genetic Factors
  • Nutritional factors
  • Physical factors (trauma, physical agents)
  • Mechanical Factors (tissue failure b/c stress/load)
  • Psychosocial factors (influence injury threshold)
126
Q

A stress on a cell can lead to ___ or ___. A persistent stress leads to cellular ___.

A

Stress can lead to:

  • Increased functional demand OR
  • Reversible cell injury

Persistent stress –> ADAPTATION

127
Q

Hypertrophy

A

Increase size of cell and organ → no new cells; growth caused by increased size

128
Q

Hyperplasia

A

Increase NUBMER of cells leads to increased organ size

129
Q

Atrophy

A

Reduced size of organ (decrease in cell size and number)

130
Q

Metaplasia

A

Change in cell morphology and fxn resulting from conversion of one cell to another

131
Q

Irreversible cell injury –> ___, aka Cell death. Cells are degraded by ___. Dead cell contents is released into circulatory system where they can be measured (e.g. __ or ___)

A

Irreversible cell injury –> NECROSIS, aka Cell death. Cells are degraded by LYSOSOMES. Dead cell contents is released into circulatory system where they can be measured (e.g. CK or CKMB)

132
Q

Stages of Healing: name all 3 and tell how long each one lasts.

A

Inflammation: Days 1-6
Proliferation: Days 3-20
Maturation: Days 9+

133
Q

What is the cause of erythema and heat with the inflammatory response? What is the cause of edema? Cause of pain? Cause of loss of function?

A 
CAUSES:
Erythema - increased vascularity
Heat - increased vascularity
Edema - blocked lymphatic drain
Pain - physical pressure or chemical irritation of pain sensitive structure
Loss of fxn - pain & Swelling
134
Q

Inflammatory phase responses can be summed in 4 response types. Name them.

A

Vascular, Hemostatic, Cellular, Immune

135
Q

Inflammatory Vascular response

A
  • Vasoconstriction then vasodilation (mediated by chemical mediators) (brings in phagocytitic cells)
  • Slowing of BF
  • Margination, pavementing, emigration of leukocytes
  • Accumulation of fluid in interstitial tissues (edema)
136
Q

Inflammatory hemostatic responses

A
  • Retract and seal off vessels

- Plts form clots and assist with building fibrin lattice –> tensile strength

137
Q

Inflammatory Cellular response

A
  • Clot formation
  • Delivery of leukocytes to injury to rid area of bacteria and debris (Phagocytosis)
  • Monocytes most important and develop into macrophages which produce products needed for healing
138
Q

Inflammatory immune response

A
  • Mediated by cellular and humeral factors
  • Activation of compliment system, resulting in components that increase vasc. permeability, stimulate phagocytosis, and are chemotaxic stimuli for leukocytes
139
Q

The clotting cascade activation is part of the ___ response. Cell damage causes release and activation of __ and ___. Platelets attach to ___, release ___, and start the clotting cascade. 2 pathways and both lead to making ___, which converts to ___ and then converts __ to __.

A

Clotting cascade = vascular response

Cell damage –> release and activation of PROTHROMBIN and PLATELETS

Platelets attach to exposed collagen, release PDGF –> Start clotting cascade

2 pathways lead to making prothrombin convert to thrombin, then fibrinogen to fibrin.

140
Q

Chemical mediators of vasodilation

A

Histamine, serotonin, Prostaglandins

141
Q

Mediators of Increased vascular permeability

A

Bradykinin, C3a, C5a, platelet activating factor (PAF), histamine, serotonin, Prostaglandins

142
Q

Mediators of chemotaxis

A

Histamine, C5a, monokines, kallicrein, lymphokines

143
Q

Mediators of fever

A

Prostaglandins

144
Q

Mediators of pain

A

Prostaglandins, Hageman factor, bradykinin

145
Q

___ are an acute responder. Describe how these cells get from inside the blood vessel to tissue outside.

A

NEUTROPHILS

  • Margination: line the walls of blood vessels. Usually takes ~1 hr
  • Pavementing: leukocytes lay down in layers
  • Diapedesis - leukocytes squeeze through intact blood vessel walls
  • Emigration - leukocytes migrate from blood vessels into perivascular tissues
146
Q

Describe transudate

A

Type of edema (increase in interstitial fluid) composed of very LITTLE protein and cells. Made up of dissolved electrolytes and water.

147
Q

Describe exudate

A 
Type of edema
Cloudy viscous fluid
Increased # of cells and plasma proteins
High content of lipids & cellular debris
Usually generated early in inflammatory process
148
Q

What is pus?

A

Type of exudate consisting of neutrophils, liquified digestion products of underlying tissue, fluid exudate, and bacteria (if infection)

149
Q

Neutrophils are a(n) ____ responder in ___ inflammation. Migrate to area within __ of the injury. Function in ___ to clear site of debris to set up tissue repair.

A

Neutrophils are a(n) INITIAL responder in ACUTE inflammation. Migrate to area within HOURS of the injury. Function in PHAGOCYTOSIS to clear site of debris to set up tissue repair.

150
Q

Basophils contribute to an [early/late] increase in vascular ___. They release ____ and are precursors to ___. They [are/are not] phagocytitic.

A

Basophils contribute to an EARLY increase in vascular PERMEABILITY. They release HISTAMINE and are precursors to MAST CELLS. They ARE NOT phagocytitic. (usually involved in allergic rxn)

151
Q

Eosinophils act ___ [time frame] after neutrophils. They are involved in __ and are present in ___ and ___.

A

Eosinophils act 2-3 DAYS after neutrophils. They are involved in PHAGOCYTOSIS and are present in CHRONIC INFLAMMATION and ALLERGIC OR PARASITIC RXN.

152
Q

Monocytes are active __-___ after injury. They’re involved in [acute/chronic] inflammatory conditions and convert into __.

A

Monocytes are active 24-48 HOURS after injury. They’re involved in CHRONIC inflammatory conditions and convert into MACROPHAGES.

153
Q

Macrophages develop from ___ after those cells are activated in the ____-___ range. These produce ___ that facilitate the removal of tissue and bacteria. They localize the inflammatory process and attract __ to the injured area.

A

Macrophages develop from MONOCYTES after those cells are activated in the 24-48 HOUR range. These produce ENZYMES that facilitate the removal of tissue and bacteria. They localize the inflammatory process and attract FIBROBLASTS to the injured area.

154
Q

Lymphocytes are involved with [acute/chronic] inflammation. They supply ___ to mediate immune respnose

A

Lymphocytes are involved with CHRONIC inflammation. They supply ANTIBODIES to mediate immune respnose

155
Q

Acute inflammation WBC

A

Neutrophils, Basophils

156
Q

Chronic inflammation WBC

A

Eosinophils
Monocytes/Macrophages
Lymphocytes

157
Q

In the Immune response, ___ activate T lymphocytes by presenting antigens. The T cells activate inflammatory mediators to activate ___. These evolve into ___ that make antibodies specific to foreign antibodies. Antibodies coat ___, ___, an d___ so they’re easily ingested via ___. This activates the ___ system.

A

In the Immune response, MACROPHAGES activate T lymphocytes by presenting antigens. The T cells activate inflammatory mediators to activate B CELLS. These evolve into PLASMA CELLS that make antibodies specific to foreign antibodies. Antibodies coat VIRUSES, BACTERIA, and ANTIGENS so they’re easily ingested via PHAGOCYTOSIS. This activates the COMPLEMENT system.

158
Q

The compliment system is a series of ___ plasma proteins that result in 1 of 2 cascades. These enhance the ___ response and optimize ___.

A

The compliment system is a series of ENZYMATIC plasma proteins that result in 1 of 2 cascades. These enhance the INFLAMMATORY response and optimize PHAGOCYTOSIS.

159
Q

In the hemostatic response, blood vessels are __ and ___. Platelets form clots and assist in building of ___ which provides tensile strength in the inflammatory phase.

A

In the hemostatic response, blood vessels are RETRACTED and SEALED OFF. Platelets form clots and assist in building of FIBRIN LATTICE which provides tensile strength in the inflammatory phase.

160
Q

The proliferation phase consists of 4 subphases:

A

Epitheliazation
Collagen production
Wound Contracture
Neovascularization

161
Q

Maturation Phase involves 7 main characteristic changes

A
  • Changes occur in size, form, and shape of scar tissue
  • Orientation and cross linking of collagen fibers
  • Maximize the strength of the healing tissue
  • Longest phase of healing
  • Decreased edema
  • Scar becomes whiter
  • Vascularity decreases
162
Q

Epithelializlation is initiated within a few __ of injury and takes __ total for small wounds. ___ cells detach from the ___ and migrate to beet and close the wound.

A

Epithelializlation is initiated within a few HOURS of injury and takes 48 HOURS total for small wounds. BASAL cells detach from the BASEMENT MEMBRANE and migrate to meet and close the wound.

163
Q

Collagen production first involves the migration of ___ to the injury site due to __ mediators. These align [parallel/perpendicular] to capillaries. These cells synthesize collagen which is cleaved by ___ to form ____. Those then coil together to form collagen ___ which combine to form collagen ___. Must occur in presence of ___ (chemicals/elements)

A

Collagen production first involves the migration of FIBROBLASTS to the injury site due to CHEMOTAXIC mediators. These align PERPENDICULAR to capillaries. These cells synthesize collagen which is cleaved by PROCOLLAGENASE to form TROPOCOLLAGEN. Those then coil together to form collagen FIBRILS which combine to form collagen FIBERS. Needs O2, zinc, iron, manganese, copper, and asorbic acid

164
Q

Granulation tissue formation is marked by the presence of the greatest amount of type ___ collagen and tensile strength that is __ % of normal tissue. As granulation tissue increases, ___ decreases. In general, granulation tissue contains new __, __, and __.

A

Granulation tissue formation is marked by the presence of the greatest amount of type III collagen and tensile strength that is 15 % of normal tissue. As granulation tissue increases, FIBRIN decreases. In general, granulation tissue contains new NEW CAPILLARIES, FIBROBLASTS, and MYOBLASTS.

165
Q

Wound contracture begins around __ days post injury and peaks at __. ____ are primarily responsible for wound closure. Contractile speed is fastest in __ wounds, slowest in __.

A

Wound contracture begins around 5 days post injury and peaks at 2 WEEKS POST INJURY. MYOFIBROBLASTS are primarily responsible for wound closure. Contractile speed is fastest in 1 DIMENSION wounds, slowest in CIRCULAR WOUNDS.

166
Q

Neovascularization involves ___ to supply the area. Vessels grow via small __ that ____ with existing vessels.

A

Neovascularization involves ANGIOGENESIS to supply the area. Vessels grow via small BUDS that ANASATOMOSE with existing vessels.

167
Q

Collagen syntheseis ca be managed with ___, decreasing the amount of local ___, and facilitating conditions that favor [lysis/synthesis] over [lysis/synthesis].

A

Manage synthesis with PRESSURE to decrease O2 and favor LYSIS

168
Q

Collagen [lysis/synthesis] is O2 dependent but [lysis/synthesis] is not. Type __ of collagen is primarily synthesized. Collagen formation in excess of lysis can result in __ or __ scarring. Describe each. Collagen synthesis can last __ months post injury.

A

Collagen SYNTHESIS is O2 dependent but LYSIS is not. Type I of collagen is primarily synthesized. Collagen formation in excess of lysis can result in KELOID or HYPERTROPHIC scarring. Describe each.
Hypertrophic: raised red lump that DOES NOT grow beyond borders of original wound. Keloid grows way beyond, minimal treatment options once it forms. Collagen synthesis can last 12-24 months post injury.

169
Q

Collagen in scars is [elastic/inelastic]

A

INELASTIC

170
Q

Complications of healing/tissue repair (5)

A 
Infection
Ulceration
Dehiscense
Keloid Development
Adhesions
171
Q

Acute inflammation resolves within ___. Chief phagocyticic cell = ____. [Minimal/max] scarring.

A

Acute inflammation resolves within A FEW WEEKS (2-4 wks). Chief phagocyticic cell = NEUTROPHILS. MINIMAL scarring.

172
Q

Chronic inflammation is present for a prolonged period of time, usually > ____. Chief phagocyticic cells = __, __, and __. Marked by __, __, or __ formation.

A

Chronic inflammation is present for a prolonged period of time, usually > 6 MONTHS (to years). Chief phagocyticic cells = LYMPHOCYTES, MONOCYTES, MACROPHAGES. Marked by FIBROSIS, SCARRING, or GRANULOMA formation.

173
Q

According to the induction theory, scar mimics the tissue ___.

A

Induction Theory: scar mimics tissue it is healing

174
Q

According to the tension theory, internal and external stresses on tissue during __ phase give structure. These include __, __, __, __, and __. They involve [high/low] load and [brief/sustained] stretch. __ and __ decrease tensile strength

A

According to the tension theory, internal and external stresses on tissue during MATURATION phase give structure. These include MUSCLE TENSION, JOINT MOVEMENT, SOFT TISSUE LOADING, FASCIAL SLIDES, TEMPERATURE, and MOBILIZATION. They involve LOW load and SUSTAINED stretch. IMMOBILIZATION and STRESS DEPRIVATION decrease tensile strength

175
Q

Possible etiologies of chronic inflammation?

A
  • Persistence of injurious agent
  • Interference with healing process
  • Immune response
176
Q

3 phases of bone healing

A
  • Reactive phase (Impaction, Induction, Inflammatory)
  • Reparative phase (Soft & Hard Callus)
  • Remodeling
177
Q

The reactive phase starts with __, or the time of injury. It’s worse with increased __ at impact. Effect is lessened by [increased/decreased] bone volume and [incr./decr] bone elasticity.

A

The reactive phase starts with IMPACTION, or the time of injury. It’s worse with increased FORCE at impact. Effect is lessened by INCREASED bone volume and INCREASED bone elasticity.

178
Q

The second part of the reactive phase, ___, takes place during week __. __ and ___ activity are stimulated at the site of blood supply disruption. A ___ develops.

A

The second part of the reactive phase, INDUCTION, takes place during week 1. OSTEOBLASTIC (make bone) and OSTEOCLASTIC (remove bone tissue) activity are stimulated at the site of blood supply disruption. A HEMATOMA develops.

179
Q

The third part of the reactive phase, ___, takes place in weeks __-___, but usually peaks at ___ weeks. It involves the ___ of necrotic bone and the creation of early ___ or ___ callus. Here, we observe fracture site ___ and the loss of ___. ___ activity removes the hematoma. Clinically involves __, __, and __.

A

The third part of the reactive phase, INFLAMMATORY, takes place in weeks 2-8, but usually peaks at 4-6 weeks. It involves the RESORPTION of necrotic bone and the creation of early FIBROUS or CARTILAGINOUS callus. Here, we observe fracture site GAPPING and the loss of FX LINE VISUALIZATION. PHAGOCYTIC activity removes the hematoma. Clinically involves PAIN, SWELLING, and HEAT.

180
Q

The reparative phase of bone healing starts with the ___ phase in weeks __-__ (usually __-__ weeks). The fracture hematoma is invaded by __ and __ which lay down the matrix for the callus. The early __ is composed mainly of __ tissue and __ with [large/small] amt of bone. [Increased/decreased] vascularity in this phase.

A

The reparative phase of bone healing starts with the SOFT CALLUS phase in weeks 3-12 (usually 3-6 or 8 weeks). The fracture hematoma is invaded by CHONDROBLASTS and FIBROBLASTS which lay down the matrix for the callus. The early SOFT CALLUS is composed mainly of FIBROUS tissue and CARTILAGE with SMALL amt of bone. INCREASED vascularity in this phase.

181
Q

The second part of the reparative phase of bone healing is called the ___ in weeks __-__. ____ mineralize the soft callus (a process known as __) to form a hard callus. Site is still __ and weak at the bridging of the fracture. Phase is complete with fx is __. We see clinical and ___ healing during this phase.

A

The second part of the reparative phase of bone healing is called the HARD CALLUS in weeks 5-12. OSTEOBLASTS mineralize the soft callus (a process known as ENDOCHONDRAL OSSIFICATION) to form a hard callus. Site is still IMMATURE and weak at the bridging of the fracture. Phase is complete with fx is STABLE. We see clinical and RADIOLOGICAL healing during this phase.

182
Q

The final bone healing phase, ___ (wks __ to ___), begins when the fracture is __ and __ healed, and ends when the bone has returned to its normal state. __ and __ activity is balanced. Stability [increases/decreases] and immature bone is replaced by more mature bone.

A

The final bone healing phase, REMODELING (wks 4 - MONTHS), begins when the fracture is CLINICALLY and RADIOLOGICALLY healed, and ends when the bone has returned to its normal state. OSTEOBLASTIC and OSTEOCLASTIC activity is balanced. Stability INCREASES and immature bone is replaced by more mature bone.

183
Q

Healing time frame for bone
Child
Adolescent
Adult

A

Bone healing
Child: 4-6 wks
Adolescent: 6-8 weeks
Adult: 10-18 weeks (closer to 8 wks if healthy, closer to 12 with comorbidities, bad nutrition etc)

184
Q

Tendon healing time frame

A

4-6 weeks

185
Q

Ligament healing time frame at the:
Digit
Knee
Ankle

A

Ligament healing at the:
Digit - 3 weeks
Knee - 3 months
Ankle - >1 year

186
Q

Caspule healing time frame

A

3-5 weeks

187
Q

Positive bone balance e.g.

A

Heterotrophic ossification: extra bone formation in wrong place (eg at joints). Restricted ROM, hard end feel.

188
Q

Negative bone balance e.g.

A

Osteoporosis

189
Q

Wolff’s Law:
If loading on a particular bone [incr/decr], the bone will remodel itself over time to become ___ and ___ that sort of loading.

A

Wolff’s Law: if Loading on a particular bone INCREASES, the bone will remodel itself over time to become STRONGER and RESIST that sort of loading.

190
Q

Describe primary bone healing

A

Direct or intimate contact between fx fragments (well approximated edges). Slow process and can’t bridge fx gaps. May use fixation devices

191
Q

Describe secondary bone healing

A

Casting or external fixation or intermedullary rod.

Most common type of bone healing. Characteristic callus formation evident on radiographs

192
Q

Bone healing is influenced by… (7 things)

A
  • Age
  • Degree of local trauma (swelling/blood)
  • Degree of bone loss (osteopenia v. osteoporosis)
  • Type of bone/location
  • Degree of immobilization
  • Comorbidities
  • WB stress
193
Q

What is the dif. btwn clinical and radiographical healing?

A

Radiograph - Looking for callus formation and disappearance of fx line (at least 2 views). Considered healed when there is progressive callus formation and blurring and disappearance of the fx line

Clinically: presence, absence, or diminution of patient’s pain with fxnl activities. Exam fx site for tenderness to palaption and motion

194
Q

For tendon repair, early immobilization (weeks __-__) facilitates healing. Active contraction before __ weeks can deter healing.

A

For tendon repair, early immobilization (weeks 4-6) facilitates healing. Active contraction before 3 weeks can deter healing.

195
Q

Vascularity is [good/poor] in ligaments. Ligaments along capsule heal [better/poorly] - why?

A

POOR. When they lie along well-vacularized capsules, they heal better, but within a capsule, they dont heal well.

196
Q

Ligamentous healing is affected by… (4 things)

A
  1. Degree of tear
  2. Type of ligament
  3. Length of Immobilization
  4. Amount of loading
197
Q

Vascularity is [good/poor] in complete ligament rupture because ____.

A

Vascularity is POOR in complete ligament rupture because it disrupts the SYNOVIAL SHEATH (where the blood supply is). No blood, no healing!

198
Q

__ and ___ (locations) ligaments have adequate repair response. ___ (location) do not. Why?

A

CAPSULAR and EXTRACAPSULAR ligaments have adequate repair response. INTRACAPSULAR do not (synovial environment, limited neovascularization, fibroblast migration from surrounding tissue)

199
Q

Even post healing, ligaments are __-___% weaker than original ligament.

A

Post injury ligaments are 30-50% weaker

200
Q

Capsule vascularity is [good/poor]. Healing is also affected by __, __, and __.

A

Capsule vascularity is POOR. Healing affected by TIME OF IMMOBILIZATION, COMORBIDITIES, DEGREE/LOCATION OF TEAR

201
Q

__% of skeletal muscle injuries are __ or ___. Usually occurs [mid muscle/myotendinous junction]. Repair with a scar leads to loss of ___.

A

90% of skeletal muscle injury = CONTUSIONS or STRAINS. Usually occur at MYOTENDINOUS JUNCTION. Repair with a scar leasd to loss of MUSCLE POWER/CONTRACTILE CAPABILITIES

202
Q

Regeneration of skeletal muscle requires intact ____ (area between epidermis and dermis)/ ____.

A

Regeneration of skeletal muscle requires intact BASEMENT MEMBRANE/SARCOLEMMA

203
Q

Skeletal muscle can/cannot proliferate. Instead, ____ cells can in some circumstances to form new ___.

A

Skeletal muscle CANNOT proliferate. Instead, stem or reserave cells (SATELLITE cells) can proliferate and differentiate in some circumstances –> new skeletal muscle cells after death of adult muscle fibers

204
Q

Articular cartilage has __ (#) layers. Name them

A 
4 layers:
Zone 1: Superficial Tangential Zone
Zone 2: Middle or Tangential Zone
Zone 3: Deep or Radial Zone
Zone 4: Zone of Calcified Cartilage
205
Q

The outermost layer of articular cartilage, ___, has Type __ collagen fibers that are oriented [parallel/perpendicular] to the joint surface. It acts to [increase/reduce] friction between opposing joint surfaces.

A

The outermost layer of articular cartilage, Superficial Tangential Zone (Zone I), has Type II collagen fibers that are oriented PARALLEL to the joint surface. It acts to REDUCE friction between opposing joint surfaces.

206
Q

In the ___ zone (Zone __) of articular cartilage, collagen fibers are arranged ___ and form and open latticework more [distally/proximally]. It aids in shock absorption

A

In the MIDDLE or TANGENTIAL ZONE (Zone II) of articular cartilage, collagen fibers are arranged RANDOMLY and form and open latticework more PROXIMAL. It aids in shock absorption

207
Q

In the __ zone (Zone ___), some of the fibers lie ____ (orientation) and extend across the interface between the __ and __ portions of the articular cartilage.

A

In the DEEP or RADIAL zone (Zone III), some of the fibers lie PERPENDICULAR and extend across the interfac between the UNCALCIFIED and CALCIFIED portions of the articular cartilage.

208
Q

In the zone of ___ (Zone __) we see a ___ cartilage layer

A

In the zone of CALCIFIED CARTILAGE (Zone IV) we see a CALCIFIED cartilage layer

209
Q

What does the tidemark separate in articular cartilage?

A

Separates articular cartilage from the type of cartilage on the subchondral bone. It divides the superficial UNcalcified cartilage from the deeper CALCIFIED cartilage.

210
Q

The tidemark is only found in ___. Do you see it more in adults or kids?

A

Tidemark is ONLY found in JOINTS. More prominent in adults and non-growing joints.

211
Q

Articular cartilage has [good/bad] healing ability. Why?

A

Articular cartilage: BAD healing ability:
NO lymph
NO blood
NO nerves.

212
Q

If you injure just the articular cartilage, what might you do to improve healing?

A

If you injure cartilage with SUBCHONDRAL bone too, the bone increases vascularization to facilitate healing, which in turn helps the cartilage by giving it access to inflammatory cells and access to fibrin-fibronectingel

213
Q

Edema is an increase in intra___, intra___, or intra___ fluid.

A

Edema = increase in INTERSTITIAL, INTRACELLULAR< or INTRA-ARTICULAR fluid.

  • Interstitial = connective tissue area
  • intra-articular = within joint
214
Q

How do you differentiate between systemic and local edema?

A

Bilateral comparison
Weight (incr. with systemic edema)
Difficulty breathing (backed up fluid from heart will go into lungs, increases lung pressure, and fluid leaks into lung tissue)

215
Q

How do you measure edema?

A

Amount of time takes for skin to return to normal

Measure depth you can push in

216
Q

What are LOCAL manifestations of edema?

A 
Increased girth (of area)
Pitting Edema

(NO lung sounds or weight gain)

217
Q

What are SYSTEMIC manifestations of edema?

A

Increased girth
Pitting edema
Lung sounds
Weight gain

218
Q

What are lymphatic manifestations of edema?

A

Increased girth
May or may not have pitting edema
Weight gain

(NO lung sounds)

219
Q

There is a delicate fluid balance in the body between intracellular and extracellular. Where is each located? What are mediators of each?

A

INTRACELLULAR

  • Located in cytoplasm
  • Mediated by Na, K

EXTRACELLULAR

  • Intravascular (aa or vv) or interstitial (CT space)
  • Mediated by capillary dynamics
220
Q

___ pressure is determined by the concentration of proteins inside and outside of blood vessels. This pressure is generally pushing [into/out of] vessels, leading to a slight [increase/decrease] of fluid in interstitial space.

A

ONCOTIC. This pressure is generally pushing INTO vessels, leading to a slight DECREASE of fluid in interstitial space.

221
Q

___ pressure is exerted by a fluid. This pressure is generally pushing [into/out of] vessels, leading to a slight [increase/decrease] of fluid in interstitial space.

A

HYDROSTATIC. This pressure is generally pushing OUT OF vessels, leading to a slight INCREASE of fluid in interstitial space.

222
Q

To manipulate pressures of intravascular fluid, change the amount of __ OR ___ in the blood stream

A

Change amount of PROTEIN or WATER in blood stream to manipulate pressure

223
Q

Capillary permeability:

  • For water?
  • For proteins?
  • For other solutes (glucose, electrolytes)?
A

Capillary permeability:

  • Water: FREELY PERMEABLE
  • Proteins: LOW PERMEABILITY
  • For other solutes (glucose, electrolytes): VARIABLE PERMEABILITY
224
Q

With what conditions do we see edema?

A 
Kidney dysfunction
Autoimmune disorders
Congestive heart failure
Cancer & lymph node removal
Acute trauma/injury
225
Q

Pathophysiologic categories of edema include (5!)

A
  • Increased hydrostatic pressure
  • Reduced plasma osmotic pressure
  • Lymphatic obstruction
  • Sodium Retention
  • Inflammation
226
Q

What lab value test can help to determine reduced plasma osmotic pressure (hypoproteinemia)?

A

ALBUMIN (it’s a measure over time, not instantaneous)

227
Q

What are clinical examples of increased hydrostatic pressure?

A
  • Impaired venous return (e.g. blood goes out but isn’t returning to heart)
  • Arteriolar dilation (e.g. b/c exercise, injury)
  • Heart failure
228
Q

Edema is excess fluid in the ___ spaces and ___ between the cells. Effusion is excess fluid in the ___ of the body.

A

Edema is excess fluid in the INTERSTITIAL spaces and CT between the cells. Effusion is excess fluid in the POTENTIAL FLUID SPACES of the body.

229
Q

___ describes fluid in the perotineal (abdominal) cavity. This is most common in someone with ___.

A

Ascites. Common in someone with liver failure (portal hypertension in portal vein, volume that can’t get through portal vein)

230
Q

___ is massive, generalized edema

A

Anasarca

231
Q

In a pleural effusion, fluid is found in the pleural space, between the __ and __ pleura.

A

Pleural effusion: fluid in pleural space between PARIETAL and VISCERAL pleura

232
Q

In a pericardial effusion, fluid builds up in the __ around the heart. This puts pressure on the ___. During diastole, the passive filling of the [atria/ventricle] is effected by pressure and results in [more/less] volume in the [atria/ventricle] and a [increased/decreased] cardiac output.

A

In a pericardial effusion, fluid builds up in the PERICARDIAL SAC around the heart. This puts pressure on the MYOCARDIUM. During diastole, the passive filling of the VENTRICLE is effected by pressure and results in LESS volume in the VENTRICLE and a DECREASED cardiac output.

233
Q

In ___, there is active bleeding within the pericardial sac at a constant rate. This leads to the heart not being able to fill at all –> ____.

A

In CARDIAC TAMPANADE, active bleeding in pericardial sac at a constant rate. Heart can’t fill –> cardiac arrest

234
Q

What is treatment for a DVT?

A

ANTICOAGULANT! Stops clot from expanding but doesn’t break it up - your body does that. Activity is generally fine, but pt may not want to. It’s painful, red, swollen, and hot.

235
Q

Lymphedma is caused by increased lymphatic fluid in the ___. It is considered a [systematic/local] edema.

A

Lymphedma is caused by increased lymphatic fluid in the INTERSTITIAL SPACE. It is considered a SYSTEMATIC edema.

236
Q

Causes of lymphedma are (4!)

A
  • Low albumin
  • Lymphatic obstruction
  • Abnormal vessel distribution
  • Reduced activity (not moving around at all)
237
Q

Primary causes of lymphedema include… (3)

A

Hypoplasia or aplasia
Hyperplasia
Blockage

238
Q

Secondary causes of lymphedema include… (3)

A
  • Surgical removal of lymph nodes
  • Scar tissue (e.g. radiation therapy)
  • Infection
239
Q

Name the 4 stages of lymphedema

A

0: Latent
1: Spontaneously reversible
2: Spontaneously irreversible
3: Lymphostatic elephantiasis

240
Q

Name the stage! “Lymphatic vessels sustained damage which isn’t yet apparent. Transport capacity is still sufficient.”

A

0: LATENT

241
Q

Name the stage!

“Irreversible swelling, hard/fibrotic tissue, unresponsive”

A

3: Lymphostatic elephantiasis

242
Q

Name the stage!

“Spongy consistency & non-pitting. Beginning of hardening of the limbs with increasing size.”

A

2: Spontaneously Irreversible

243
Q

Name the stage!

“Pitting stage. Normal in the morning, but increases in size throughout the day.”

A

1: Spontaneously reversible

244
Q

Treatment of lymphedema includes __, __ and __.

A

Lymphatic massage
Skin care (anti-wounds!)
Compressive garments/wrapping
Exercise (muscle pump acts to move the fluid)

Pathophysiology (3 decks)

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