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BME 265 > Test 3 Study Guide > Flashcards

Test 3 Study Guide Flashcards

1
Q

Functions of circulatory system?
Transportation
Regulation

A 
Transportation
o	Respiratory
	Erythrocytes transport oxygen
o	Nutritive
	Absorbed products of digestion transported to liver and other body parts
o	Excretory
	Metabolic waste, excess ions, and water excreted by the kidneys
Regulation
o	Hormonal
	Carry hormones to target tissues
o	Temperature
o	Protection 
	Blood clotting
o	Immune
	Leukocytes, complement, and cytokines act against pathogens
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2
Q
  1. Whats the normal rate per minute of the heart?
A

a. Normal HR 60-100 BPM

b. Bradycardia = 100 BPM

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3
Q

a. Step 1: Ventricular Isovolumetric Contraction

A

i. QRS just occurred = ventricular depolarization
ii. Both AV and semilunar closed
1. Ventricle contracts (Ventricle P > atrial P)  AV valves close S1 sound
2. (Ventricle P

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4
Q

b. Step 2: Ejection

A

i. Initial, rapid ejection of blood from the left ventricle into the aorta and the right ventricle into the pulmonary artery
ii. AV closed semilunar open
1. Ventricle P > aortic P  Semilunar valves open
2. No sound produced; sound = abnormal function
iii. SV = volume of blood ejected

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5
Q

c. Step 3: Reduced Ejection – T wave occurs

A

i. Ventricular P

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6
Q

d. Step 4: Isovolumetric Relaxation

A

i. All valves closed; semilunar close due to backflow (S2 heart sound), AV remain closed
1. Valves close as ventricles relax
ii. Pressure declines in ventricles
iii. ESV = blood in ventricle

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7
Q

e. Step 5: Rapid Filling of Ventricles

A

i. Ventricular P

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8
Q

f. Step 6: Reduced Filling - Atrial Systole

A

i. P wave occurs: depolarization of atria
ii. Atrial contraction squeezes 10-30% more blood into ventricles
1. 90% of blood is already passively filled
iii. AV open and semilunar closed

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9
Q

g. P wave

A

i. Depolarization of atria

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10
Q

h. PR interval

A

time between atrial and ventricular depolarization

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11
Q

i. QRS

A

i. Ventricular Depolarization

ii. Causes S1 sound

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12
Q

j. T wave

A

i. Ventricular repolarization (relaxation)
Pressure falls below aortic
ii. Causes S2 sound

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13
Q

k. ST Segment

A

i. End of S  beginning of T

ii. Period between ventricular depolarization and repolarization

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14
Q

When do aortic and pulmonary valves open as related to the EKG and heart sounds? AV valves?

A

S1 occurs immediately after the QRS
AV valves close when ventricles contract

S2 occurs during the T wave
Pulmonary and aortic close when ventricles relax and cause backflow

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15
Q

a. Preload

A

i. Heart loading up for next big squeeze of ventricles
ii. Amount of ventricular stretch after diastole
iii. Ventricular end diastolic pressure
iv. EDV directly proportional with SV and contractility

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16
Q

b. Afterload

A

i. Pressure the heart must overcome to push blood out of the aortic valve into systemic circulation
ii. Known as TPR – Total Peripheral Resistance
iii. SV inversely proportional to TPR

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17
Q

Components of blood?
lipid
formed elements
plasma

A

a. Lipid portion: Mainly fatty acids and cholesterol in vesicles
b. Formed elements = cellular components
i. RBC, WBC, platelets
c. Plasma = water, dissolved solutes, and proteins, Na = major ion

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18
Q

e. WBC – Leukocytes 5-9,000/mL

A

i. Leukocytosis = elevated WBC count
ii. Leukopenia = Low WBC count
iii. Have nuclei and mitochondria; move like ameoboids
iv. Granulocytes – show up with staining; digestion of endocytosis particles
1. Neutrophils (50-70%)
2. Basophils
3. Eosinophils
v. Agranulocytes
1. Lymphocytes
2. Monocytes

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19
Q

d. RBC – Erythrocytes 5 million/mL

A

i. Polycythemia = elevated RBC count
ii. Anemia = low RBC count
iii. No nuclei or mitochondria

Each contains 280 million hemoglobin, with 4 heme chains

Removed by phagocytic cells in liver, spleen, and bone marrow

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20
Q

Leukocytes, granulocytes?

A

Help detoxify foreign substances, release heparin

  1. Neutrophils (50-70%)
  2. Basophils
  3. Eosinophils
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21
Q

Leukocytes, agranulocytes?

A

Phagocytic; produce antibodies

  1. Lymphocytes
  2. Monocytes
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22
Q
  1. What’s the buffycoat?
A

a. Little middle section of centrifuge

b. Contains Leukocytes and platelets

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23
Q
  1. Serum vs plasma difference?
A

a. Serum is the part of blood after fibrinogen has been removed. Fluid from clotted blood.
i. Liquid part of plasma after blood has been allowed to clot

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24
Q
  1. What is the conducting system of the heart?
A

a. SA Node
i. Pacemaker; stimulates atrial contraction
ii. P wave
b. AV Node
i. Provides delay between atrial and ventricular contraction
c. Bundle of his  bundle branches  purkinje fibers
i. Stimulate individual groups of myocardial cells to contract
ii. QRS complex generated

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25
Q
  1. Whats the chronotropic effect vs ionotropic effect?
A

a. Chronotropic = Regulation of Heart Rate
i. Cardiac Control Center = Medulla oblongata
1. Autonomic innervation of SA
a. Easier to depolarize SA node
3. ACh stimulates opening of potassium channels
a. Easier to hyperpolarize SA node
b. Ionotropic = Change force of heart contraction
i. Sympathetic
NE and Epi stimulate opening of calcium and sodium channels
1. More calcium available to sarcomeres
ii. Parasympathetic
1. No change in contraction strength

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26
Q

What is the frank starling law of the heart? What “tropic” effect does it have?

A
  1. Increased stretching of myocardium due to greater EDV = more forceful contraction

Ionotropic

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27
Q
  1. What percent of blood is in the veins, capillaries, heart?
A

a. Veins = 60-70%
b. Arteries = 10-12%
c. Lungs = 10-12%
d. Capillaries = 4-5%

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28
Q
  1. Distributions of blood in the body organs?
A

a. Liver, kidneys, GI = 2500 ml/min
b. Skeletal muscles = 1200 mL/min
c. Brain = 750 mL/min
d. Others = 500-1100 mL/min
e. Coronary arteries = 250 mL/min

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29
Q
  1. What causes edema?
A

a. Increased bp or a venous obstruction
b. Increased tissue protein concentration
c. Decreased plasma protein concentration
d. Obstruction of lymphatic vessels

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30
Q
  1. What happens in right side (goes to lungs) heart failure vs left?
A

a. Right side failure causes blood returning from the body to back up
b. Left side failure stops pumping of blood to the body
i. Can’t bring in fresh blood from the lungs
ii. Blood pools in the left lung

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31
Q
  1. Hypertension; normal bp? Systolic over diastolic; What is mild, sever elevation?
A

a. Normal = less than 120/80
b. Hypertension = Excess of 140/90 mmHg
c. Prehypertension (mild) = 120-140/80-90 mmHg

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32
Q
  1. Pulse pressure, mean arterial pressure?
A

a. Pulse pressure = systolic – diastolic

b. Mean arterial Pressure = diastolic P + (1/3)*pulse pressure

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33
Q

Chemotaxis

A

i. Movement towards chemical attractants i.e. attracting phagocytic cells

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34
Q

b. Opsonization

A

i. Binding to a pathogen to mark is for phagocytosis i.e antibodies
ii. Formation of antigen-antibody complex

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35
Q

c. Diapedesis

A

i. Process by which leukocytes squeeze through intact capillary walls into tissue

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36
Q

d. Cytokines

A

i. Released by cells to affect behavior of other cells i.e. released chemical attractants in chemotaxis

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37
Q

General info about B lymphocytes?

A

i. Produced in bone marrow
ii. Humoral response – secretes antibodies into blood and lymph; can act from a distance
iii. Combat bacterial and viral infections
iv. Memory cells and Plasma cells
v. Have surface antibodies for antigen receptors

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38
Q

General info about t lymphocytes?

A

i. Produced in bone marrow, seed in the thymus
1. These then seed blood lymph nodes and spleen
ii. Attack infected host cells – do NOT produce antibodies
iii. Cell-mediated immunity – requires contact with cell
iv. Cannot bind directly to antigen through T cell receptor proteins, require the use of antigen presenting cells such as macrophages or dendritic cells
1. Dendritic cells engulf pathogen, digest, and display protein fragments and secrete cytokines

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39
Q

B vs T (chart)

Site where processed?

A

B: bone marrow
T: thymus

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40
Q

B vs T (chart)

Type of immunity

A

B: Humoral (secretes antibodies)
T: Cell-mediated

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41
Q

B vs T (chart)

Subpopulations

A

B: Memory and plasma
T: cytotoxic killer cells, helper, and suppressor cells

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42
Q

B vs T (chart)

Presence of Surface antibodies?

A

B: Yes, IgM or IgD
T: Not detectable

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43
Q

B vs T (chart)

Receptors for antigens?

A

B: present, are surface antibodies
T: Present, are related to immunoglobulins

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44
Q

B vs T (chart)

Life span?

A

B: short
T: long

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45
Q

B vs T (chart)

Tissue distribution?

A

B: high in spleen, low in blood
T: high in blood and lymph

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46
Q

B vs T (chart)

Percentage of blood lymphocytes?

A

B: 10-15%
T: 75-80%

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47
Q

B vs T (chart)

Transformed by antigens into?

A

B: plasma cells
T: activated lymphocytes

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48
Q

B vs T (chart)

Secretory product?

A

B: antibodies
T: lymphokines

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49
Q

B vs T (chart)

Immunity to viral infections?

A

B: enteroviruses, poliomyelitis
T: Most others

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50
Q

B vs T (chart)

Immunity to bacterial infections?

A

B: streptococcus, staphylococcus, and many others
T: tuberculosis, leprosy

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51
Q

B vs T (chart)

Immunity to fungal infections?

A

B: none known
T: many

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52
Q

B vs T (chart)

Immunity to parasitic infections?

A

B: trypanosomiasis, maybe to malaria
T: Most others

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53
Q
  1. How does an antibody work? How does it cause destruction of an organism?
A

a. They coat the pathogen to prevent it from entering more cells.
b. Stimulate complement proteins to destroy the pathogen
c. Label pathogens for opsonization  phagocytosis, lysis, and inflammation

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54
Q
  1. What is complement system?
A

a. Classical Pathway: Proteins in plasma that activate when an antigen binds an antibody
b. Alternative pathway: polysaccharides binding on bacterial membranes
c. Results in chemotaxis, opsonization and stimulation of mast cells to secrete histamine.
d. Part of Non-specific immunity; Integrates the innate and adaptive immune responses
e. Complement activation = complement fixation

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55
Q

a. Exposure to antigen activates B lymphocyte, then…

A

i. Enters secondary lymphoid organ (primary = bone marrow,thymus)
1. Lymph nodes, spleen, tonsils, and peyers patches (in mucosa of intestine)
2. Function to capture and present pathogens to macrophages
3. Lymphocytes migrate between lymphoid organs to sample blood and lymph
4. Filter lymph for pathogens
ii. Cloning occurs to produce memory cells and plasma cells which produces antibodies

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56
Q

b. Killer (cytotoxic)T cells do…

A

i. Have CD8 surface molecules
ii. Destroy body cells that harbor foreign antigens
iii. Perforins create pores and granzymes trigger apoptosis

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57
Q

c. Helper T cells do…

A

i. CD4 surface molecule
ii. Enhances ability of B lymphocytes to become plasma cells and produce antibodies
iii. Enhances ability of cytotoxic T cells to kill by secreting lymphokines

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58
Q
  1. Parts of the conducting system?
A

a. Conducts air to the respiratory system
b. Nasal cavitypharynxlarynxtracheaprimary bronchi, secondary, tertiary(more branching), terminal bronchioles
c. Respiratory Zone
i. Respiratory bronchioles, alveolar sac, alveolus

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59
Q
  1. 3 types of cells in the lung?
A

a. Type 1 Alveolar
i. Thin, squamous; cover alveolar surface
ii. Involved in gas exchange
b. Type 2 Alveolar
i. Produce surfactant to decrease surface tension
c. Macrophage
i. Destroy foreign material

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60
Q
  1. Difference between the parietal and visceral pleura? What do they do?
A

a. Parietal pleura is the outer layer below the rib cage
b. Visceral pleura covers the lungs
i. Produce the intrapleural space
c. Provides a fluid filled space that protects the lungs and provides lubrication, as well as allowing movement of the lungs

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61
Q

Myoglobin

A

Stores oxy during diastole to release during systole in myocardial cells.
Greater oxygen affinity
Greater red pigment in muscle

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62
Q
  1. What controls the production of red blood cells?
A

a. Erythropoietin: a hormone produced in the kidneys controls RBC production
i. Binds to membrane receptors of cells that will become erythroblasts.
ii. Erythroblasts transform into normoblasts.
iii. Normoblasts lose their nuclei to become reticulocytes.
iv. Reticulocytes change into mature RBCs.
stimulate cell division

Need iron, vitamin B12, and folic acid to produce RBCs

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63
Q

Where does hematopoiesis occur? leukopoises?

A

i. Stem cells differentiate into blood cells
ii. Occurs in myeloid (bone marrow of long bones) tissue and lymphoid tissue

leukopoiesis: lymphoid
erthyropoeisis: myeloid

G-CSF = neutrophils
GM_CSF = monocytes and eosinophils
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64
Q
  1. How does the body determine the changes in arterial oxygen and carbon dioxide?
    Medulla
    corotid & aortic
    carotid
A

a. Medulla – Rhythmicity center
i. Chemoreceptors for pH in cerebrospinal fluid respond to increased CO2 levels
ii. Control long term response
b. Peripheral chemoreceptors in the aortic (vagus) and carotid (glossopharyngeal) bodies respond to pH levels
c. Carotid body
i. Low blood O2 augments the response to high CO2 levels, and if O2 is low enough, can stimulate ventilation directly

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65
Q

How does the pons function with the medulla? What occurs in the cerebral cortex?

A

d. Pons
i. Apneustic Area – Stimulate I neurons
ii. Pneumotaxic – antagonizes apneustic
e. Voluntary breathing = cerebral cortex
f. Involuntary breathing = respiratory control centers of medulla and pons

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66
Q
  1. How does the circulatory system provide protection to the body?
A

a. Blood clotting

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67
Q
  1. What are the Plasma proteins? What do they do?
A

a. Represents 7-9% of plasma
b. Albumin
i. 60-80% of protein
ii. Provides colloid osmotic pressure which pulls water into the blood and maintains blood pressure
c. Globulins
i. Alpha and beta = transport libids and fat soluble vitamins
ii. Gamma = antibodies
d. Fibrinogen
i. 4% of protein
ii. clot converts fibrinogen to fibrin

Plasmin digests fibrin

(separate topic)
Anticoagulants: heparin, coumadin

68
Q
  1. Main component of a RBC? What’s inside a hemoglobin moiety?
A

a. Hemoglobin
b. Heme = moiety
i. Iron in a flat poryphrin support

69
Q
  1. What happens to EKG if you damage the SA node, AV node, bundle of his, right bundle of …?
A

a. Flutter = rapid contraction/relaxation of atria or ventricle; degrades to fibrillation which is random coordination of contraction
b. SA = no p wave
c. AV = bad delay timing between p and QRS
d. Bundle of…. = no QRS complex generated

70
Q

What is sinus bradycardia?

A

sinus = SA node

slower rate of p waves

71
Q

Sinus tachycardia?

A

sinus = SA node

Faster rate of p waves

72
Q

Ventricular tachycardia?

A

Faster rate of ventricular contractions

Shorter QT interval

73
Q

Ventricular fibrillation?

A

Random coordination of ventricular contractions

74
Q
  1. What is the 1st 2nd and 3rd degree AV block?
A

a. 1st: rate of impulse conduction through AV node exceeds .2 seconds (too long)
i. increased PR interval

b. 2nd: AV node damaged so that only 1 of every 2-4 APs pass to the ventricles
i. P wave without QRS

c. 3rd: None of the atrial waves can pass through the AV node (on egg = negative spike)

75
Q
  1. What is the PR interval?
A

a. Normal, .12-.20s
b. 1st degree: greater than 0.2s
c. 2nd : longer and longer PR interval

76
Q
  1. Whats ischemic heart disease? What are all the risk factors?
A

Coronary heart disease

a. Inadequate oxygen supply to tissue
b. Common cause is atherosclerosis
c. Angina pectoris = substernal chest pain
d. High bp, high cholesterol, obese, smoking

77
Q
  1. What are the changes on the EKG during acute myocardial infarction?
A

Longer (indefinite?) ST interval, ventricle never repolarizes

78
Q
  1. What are the different layers of the blood vessels?

What differences are there between arteries, veins and capillaries?

A

a. Tunica intima
i. Internal most layer
ii. Simple squamous epithelium
b. Tunica media (thickest in arteries)
i. Smooth muscle, connective tissue; middle portion
ii. Can change degree of contraction
c. Tunica external (thickest in veins)
i. Collagen; protect and reinforce; outermost; has accessory tissues
d. Capillaries = intima layer and occasional connective tissue

79
Q 
What are the heart valves?
All
Patients
Take 
Medication
A

Aortic
Pulmonary
Tricuspid
Mitral

80
Q

LORD

A

Left oxygenated

Right deoxygenated

81
Q
  1. Einthoven Triangle? And egg leads? (12 total; know 6 individual)
A

+ –> -
Left leg = + ground

3 Bipolar limb leads:
Lead 1: left arm –> right arm
Lead 2: left foot –> right arm
Lead 3: left foot –> left arm

3 Unipolar, augmented Limb Leads
IV/AVR: right arm –> LL & LA (rightward)
V/AVL: + on left arm –> RA & LL (leftward)
VI/AVF: left foot –> RA & LA (inferior)

finally…
6 Unipolar Chest leads

82
Q 
Different types of Shock?
Hypovolemic
Septic
Anaphylactic
Neurogenic
Cardiogenic
A

a. Hypovolemic Shock
i. Low blood volume
ii. Bleeding, dehydration, burns
b. Septic Shock
i. Low bp due to sepsis
ii. Endotoxins produce NO which causes vasodilation
iii. Treat with drugs to inhibit production of NO
c. Anaphylactic Shock
i. Vasodilation
d. Neurogenic Shock
i. Rapid fall in bp
e. Cardiogenic Shock
i. Cardiac failure

83
Q

What compensations occur at the onset of shock?

A

i. Baroreceptor reflex
1. Tachycardia
2. Vasoconstriction
ii. Renin-angiotensin-aldosterone system
iii. Increase in ADH

84
Q
  1. Difference between primary and secondary hypertension?
A

a. Primary/Essential = don’t know the cause
i. Increase in TPR is universal
ii. Sustained high stress and high sodium intake act in development
iii. Adaptive response results in atherosclerosis
iv. Kidneys can’t properly excrete Na+ and water is a universal characteristic
b. Secondary = result of known disease process

85
Q
  1. What happens on the receptors when you have high blood pressure? Baroreceptors, where are they located? How do they work and give feedback?
A

a. Stretch receptors (stretch = increased frequency of APs)

b. Located on aortic arch and the carotid sinus

86
Q
  1. Different types of immune defense mechanisms. Specific vs non specific immunity
A

a. Innate – non specific
i. Epithelial membranes
ii. High acidity in stomach
iii. Cells that can engulf/kill pathogens
iv. Fever
v. Skin, mucous membranes, secretions, digestive track, GI tract, phagocytic cells, antimicrobial proteins, inflammatory response, natural killer cells
b. Acquired – specific
i. Humoral response (antibodies)
ii. Cell mediated response (cytotoxic)

87
Q 
Types of phagocytic cells?
Neutrophils
Mononuclear
Kupffer cells
Alveolar macrophages
Microglia
A

a. Neutrophils
i. First to arrive
ii. In blood and all tissues
iii. Release NETS to trap pathogens
iv. Apoptosis, release digesting enzymes = pus
v. Release granule proteins to attract monocytes
b. Mononuclear
i. Monocytes in blood
ii. Macrophages and dendritic cells in all tissues
iii. Arrive later
c. Organ specific
i. Kupffer cells = liver
ii. Alveolar macrophages = lungs
iii. Microglia = CNS

88
Q
  1. What happens during local inflammatory response?
A
  1. Damage that causes necrosis
  2. Immune system exposed to DAMPs (danger associated mol. patterns)
  3. Non specific mechanism initiated by toll like receptors
    i. Macrophages and mast cells release cytokines and chemokines to attract phagocytic neutrophils.
    ii. Complement proteins are activated, which also attract phagocytic cells.
    iii. More phagocytic cells arrive via extravasation from nearby venules. T lymphocytes are the last to arrive.
  4. Mast cells degranulate and secrete heparin, histamine, prostaglandins, leukotrienes, cytokines, and TNF-α.
    i. These produce warmth, swelling, and pain (classic symptoms).
    ii. They also recruit more leukocytes.
  5. Neutrophils
    i. Kill microorganisms through phagocytosis
    ii. Release NETS (neutrophil extracellular traps) to trap pathogens
    iii. Undergo programmed cell death and spill protein-digesting enzymes into the surrounding tissues, causing pus
    iv. Release granule proteins that draw monocytes to the area
  6. Monocytes enlarge into macrophages and clean up dead neutrophils and release GF for repair.
  7. As inflammation progresses B lymphocytes produce antibodies which form complexes and amplify phagocytosis by neutrophils etc through opsonization
89
Q

What proportions of Leukocytes invade the site of local inflammation, in what order?

A

First: neutrophils

Second: monocytes

Third: T lymphocytes

90
Q
  1. What do mast cells do?
A

a. Degranulate and secrete histamine, prostaglandins, leukotrienes, cytokines, and TNF-alpha
b. Produce warmth, swelling, pain and recruit more leukocytes

91
Q
  1. Different types of immunoglobulin. IgG, IgA, IgE, IgM, and IgD?
A

a. IgG
i. Main form of antibody in circulation
ii. Produciton increased after immunization
iii. Secreted during secondary response
b. IgA
i. Main antibody for external secretions (saliva, mothers milk)
c. IgE
i. Allergic symptoms in immediate hypersensitivity reactions
d. IgM
i. Antigen receptor on lymphocyte surface prior to immunization
ii. Secreted during primary response
e. IgD
i. Antigen receptor on lymphocyte surface prior to immunization
ii. Other functions unknown

92
Q
  1. Clonal selection of lymphocytes?
A

a. Explains Secondary immune response and development of active immunity
b. Inherit lymphocytes specific to almost every pathogen, but only a few of each type
c. Exposed to foreign antigens; immune cells make copies of themselves
d. Germinal centers in secondary lymphoid organs develop to produce clones
e. Produce a ton, ones that match proliferate; Respond more quickly a second time

93
Q
  1. Hyaline membrane disease?
A

a. Disease in newborns
b. Proteins/dead cells line alveoli preventing gas exchange
c. ARDS
i. Inflammation increases capillary and alveolar permeability, which leads to accumulation of protein rich fluid in the lungs
ii. Decreases lung compliance and surfactant

94
Q

What info about the surfactant?

A

d. Surfactant—in alveolar fluid, phospholipid known as dipalmitoyl lecithin
i. Surface active agent, lowers surface tension
ii. Molecules become interspersed between water molecules, reducing the attractive forces that produce the surface tension
iii. Prevent alveoli from collapsing during expiration
iv. Produced by type II alveolar cells

95
Q

Vital Capacity

A

max air exhaled after max inhale

96
Q

Total lung capacity

A

amount in lungs after max breath in

97
Q

Tidal volume

A

amount of air expired or inspired in quiet breathing

98
Q

d. Expiratory reserve volume

A

amount of air that can be forced out after tidal volume

99
Q

e. Inspiratory reserve volume:

A

amount of air that can be forced in after tidal volume

100
Q

f. Residual volume

A

amount of air left in lungs after maximum expiration

101
Q

g. Inspiratory capacity

A

amount of gas that can be inspired after a normal expiration

102
Q

h. Functional residual capacity

A

amount of gas left in lungs after a normal expiration

103
Q

VC =

A

i. VC = IRV + ERV + TV

104
Q

FRC =

A

j. FRC = RV + ERV

105
Q

Restrictive lung disease?

A

Restrictive:
Lung tissue is damaged.
Vital capacity is reduced, but forced expiration is normal.
Cannot fully fill their lungs with air
i. Examples: pulmonary fibrosis and emphysema

106
Q

Obstructive lung disease?

A

Obstructive:
Lung tissue is normal.
Vital capacity is normal, but forced expiration is reduced.
Can’t exhale all the air from their lungs.
Shortness of breath and difficulty breathing during exercise.
i. Example: asthma, COPD (bronchitis + emphysema)

Diagnosed with forced expiratory volume test

107
Q

Emphysema and bronchitis?

A

Emphysema and chronic bronchitis are both COPD

COPD: excessive mucus production and inflammation (obstructive)

d. Emphysema
i. Destruction of alveoli
1. Reduced surface area
2. Bronchioles collapse
ii. Smoking
iii. Shortness of breath
e. Bronchitis
i. Causes lung inflammation
ii. Cough with mucus

108
Q

Lymphatic vessels transport…?

What do lymph nodes do?

A

Interstitial fluid

Cleanse lymph prior to return to venous blood

109
Q

Total blood volume?

Hematocrit?

A

5 liters; 8% of body weight

Hematocrit- formed elements - 45%

110
Q

Platelets - thrombocytes

A
  • smallest formed element
  • lack nuclei; ameboid movement
  • Clot by releasing serotonin, a vasoconstrictor
  • secrete growth factors
  • 5-9 days
  • 130,000-140,000/mL

Prostaglandins normally repel them from cell wall

Fibrin creates mesh net that platelets form to

Thromboplastin: released by damaged tissue to “short cut” formation of fibrin

111
Q

Type A blood

A

Has A antigens; lacks A antibodies

112
Q

Universal donor

A

type O

113
Q

Universal Recipient

A

Type AB

114
Q

Erythroblasts Fetalis

A

Rh- mother produces antibodies, which cross placenta.

Hemolysis of Rh+ RBCs in the fetus.

115
Q

What is the pathway of blood through the heart?

A

Superior and inferior vena cava carry deoxy blood to right atria –> right ventricle –> pulmonary artery to the lungs.

Once in the lungs, the pulmonary vein returns to the left atria, then to the left ventricle, and out the aorta. which completes the cycle back to the vena cava

116
Q 
What do the 4 valves separate?
All
Patients
Take 
Medication
A

Aortic: left ventricle –> aorta
Pulmonary: right ventricle –> pulmonary artery
Tricuspid: right atria –> right ventricle
Mitral(bicuspid): left atria –> left ventricle

117
Q

End diastolic volume?

A

Total volume of blood in the ventricle after diastole (relaxation)

Normally 120 mL

118
Q

End systolic volume

A

Total volume of blood left in the ventricle after systole

Normally 50 ml

119
Q

When do the AV valves close? S1 sound LUB

A

Isovolumetric Contraction
- Contraction of the ventricle
Immediately after the QRS
- when ventricular pressure spikes on graph and volume starts to fall

120
Q

When do the semilunar valves close? S2 sound DUB

A

After T wave begins
Ventricles Relax

When Ventricular pressure rapidly falls and volume starts to increase on graph

121
Q

When do the AV valves open?

A

During “rapid filling” of ventricles, just after ventricular pressure falls enough to close the semilunar valves

122
Q

When do the semilunar valves open?

A

Ejection;

contraction of ventricle, but not isovolumetric contraction

123
Q

What happens during a myocardial cell action potential?

A

Na influx causes dramatic spike
Ca influx maintains a slow fall
K efflux is total depolarization

100 times longer than other APs

Long APs = long refractory period

124
Q

Differences in artery and veins vessel layers?

A

Arteries have a larger tunica media

Veins have valves

125
Q

Differences between venues and arterioles?

A

Venue: tunica externa, endothelium, valve

Arteriole: endothelium , lumen, pre capillary sphincter

126
Q

Differences between fenestrated capillary (veinous) and continuous capillary (arterial)?

A

Fenestrated capillary: have capillary pores

in addition to common endothelial cells and a basement membrane

127
Q

Mechanism of atherosclerosis?

A

Monocytes become macrophages, engulf lipids, and become foam cells.

128
Q

What happens on an egg during myocardial infarction?

A

Changes in t segment (lengthen?)

Increased CPK and LDH

129
Q

Flutter vs fibrillation

A

Flutter = rapid contractions and relaxations, degenerates to fibrillation

Fibrillation: contraction of different myocardial cells at different times. Can’t coordinate pumping

130
Q

Each ventricle pumps the equivalent of _____ per minute during resting

A

Total blood volume

131
Q

ACh _____ the SA node

A

Hyperpolarizes

132
Q

What are the sympathetic effects on the SA, AV, atrial muscle, and ventricular muscle?

Parasympathetic?

A

Sa: increased rate of diastolic depolarization; increased cardiac rate
AV: increased conduction rate
Muscles: increased strength of contraction

Parasympathetic are opposite, except on ventricular muscle there is no effect instead of increased contraction strength

133
Q

Preload, after load?

A

preload: end diastolic volume; proportional to stroke volume and contractility

After load: total peripheral resistance
SV inversely proportional to TPR

134
Q

What is contractility?

A

Measure of strength of contraction

“volume of aorta, ejection fraction”

135
Q

Ejection fraction =

A

stroke volume/EDV

Normally 45-60%

136
Q

Sympa/parasympa….ionotropic or chronotropic?

A

Parasympathetic: - chronotropic effect. No inotropic effect

Sympathetic: + inotropic effect and + chronotropic

137
Q

___% of body water is within blood plasma

A

1/3rd total intracellular

20%

80% interstitial

2/3rd total intracellular

138
Q

Colloid osmotic pressure does what. Hydrostatic pressure?

A

Draws water back into the circulatory system. Net = oncotic pressure

Hydrostatic does the opposite, promotes formation of tissue fluid

139
Q

Para/Sympa regulation of blood flow? (extrinsic)

A

Sympathetic - increase CO and TPR
Norepi produce vasoconstriction in GI, skin, kidneys
Cholinergic (ACh) vasodilator to skeletal muscles

Parasympa: Cholinergic (ACh) vasodilator to all not skeletal

140
Q

Proportion of blood to organs in exercise, and rest

A

Organ: exercise,rest

GI: 3-5,20-25%
Heart:4-5,4-5
Kidneys: 2-4, 20
Bone: .5-1, 3-5
Brain: 3-4, 15
Skin: 0,4-5
Muscle: 85,15-20

Exercise CO- 25 L/min
Rest: 5 L/min

141
Q

how does ischemia affect an ECG?

A
  • inversion of T wave
142
Q

How does muscle injury affect the ECG

A

Elevates ST segment

143
Q

How does myocardial infarction influence an ECg

A

Negative Q, QS

St segment returns to normal first then the T wave due to disappearance of the muscle injury

144
Q

How do you treat hypertension?

A

Lifestyle modifications

diuretics, beta blockers (decrease HR), calcium antagonists (block Ca channels), ACE inhibitors (inhibit angiotensin conversion), angiotensin II antagonist (block receptor)

145
Q

How do cells distinguish self from non-self?

A

PAMPs: pathogen associated molecular patterns

146
Q

What are interferons?

A

Released by compromised cells to stop viral/bacterial progression

147
Q

What are immunoassays used for?

A

Tests that use antibodies to identify antigens through agglutination

148
Q

What are the secondary lymphoid organs? What do they do?

A
  • lymph nodes, spleen, tonsils, peers patch
  • capture and present pathogens to macrophages and house lymphocytes
  • lymphocytes migrate through blood and lymph to sample
149
Q

What does the spleen do? What about the other secondary lymphoid organs?

A

Spleen filters blood for pathogens

Rest filter the lymph

150
Q

What is the complement system?

A

innate response

Stimulates chemotaxis, opsonization, and mast cell release of histamine

151
Q

What do dendritic cells do?

A

Made in bone marrow and move to tissues. digest stuff and display fragments to other T lymphocytes.

152
Q

Difference in mechanism between cytotoxic t cells and helper t cells?

A

Helper t cells bind to dendritic/macrophages and proliferate.

Cytotoxic t cells bind to infected cell directly and proliferate and are activated by here t cells

153
Q

Delayed vs immediate hypersensitivity

A

Immediate releases histamines through B (mostly) and T cell IgE

Delayed is an abnormal t cell response to lymphokine secretion (poison oak,ivy)

154
Q

how does intrapleural pressure relate to intrapulmonary and atmospheric pressure i breathing?

A

Always less than both, in order to keep the lungs expanded

155
Q

What is lung compliance?

A

Change in lung volume per change in transpulmonary pressure.

Lungs can expand their volume. Reduced by infiltration of connective tissues

156
Q

What muscles are used in inspiration? Expiration?

A

Inspiration: external intercostals, diaphragm

Expiration: internal intercostals, abs

157
Q

Total minute volume =

A

tidal volume * breaths/min

158
Q

What is daltons law?

A

Partial pressures sum

Pressure of water is constant 47 mmHg

159
Q

Henrys law?

A

Amount of gas that can dissolve in a liquid depends on solubility, temperature, and partial pressure

160
Q

Low oxygen in alveoli causes…

A

Constriction of pulmonary arteries. low oxygen depolarizes by opening Ca channels

Opposite in systemic arteries

Follow diffusion of gasses

161
Q

The aortic body sends breathing feedback along the ____ nerve.

A

vagus

162
Q

The carotid body sends breathing feedback along the ____ nerve.

A

glossopharyngeal

163
Q

If CO2 levels rise, pH……

A

Falls

164
Q

Oxyhemoglobin vs methemoglobin vs. carboxyhemoglobin

A

Oxo = reduced Fe2+ and can bind oxygen

methemoglobin = oxidized Fe3+ can’t bind oxygen

Carboy = bound to CO

165
Q

Erythropoietin stimulates hemoglobin production when oxygen levels are….

A

Low

BME 265 (1 decks)

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