Slide 6 Flashcards

1
Q

What is atherosclerosis?

A

blocked artery due to plaque buildup causing abnormal blood flow or blocking it

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2
Q

What happens if the coronary artery is blocked?

A

heart attack

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3
Q

What are catheters for?

A

for coronary artery

they expand the stent to compress the plaque so that there is a widening artery

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4
Q

What is the blood composed of?

A

formed elements

  • erythrocytes
  • platelets
  • leukocytes

plasma 55%

  • plasma protein
  • water
  • other solutes

these percentages can change with disease

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5
Q

What is the role of albumin?

A

synthesized by the liver

contribute to colloid osmotic pressure of plasma
carry many substance

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6
Q

What are globulins for?

A

synthesized in the liver and lymphoid tissue

act as clotting factors
enzymes
antibodies
carrier for substances

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7
Q

What is fibrinogen for?

A

source is the liver

forms fibrin threads for blood clot

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8
Q

What is transferrin for?

A

from the liver and other tissues

iron transport

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9
Q

Why is liver disease associated with edema?

A

liver disease is dysfunctional

edema: fluid accumulation in the interstitial fluid due to leaky capillaries

less circulation protein synthesis = even less water retention by osmosis

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10
Q

What are the formed elements composed of?

A

RBCs

WBCs
granulocytes:
monocytes
lymphocytes

agranulocytes:
basophils
neutrophils
eosinophils

Platelets

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11
Q

Describe the structure and function of RBC. What is the spectrin molecule look like and its function?

A

structure: biconcave disk
flexibility

SPECTRIN cytoskeleton create this unique shape of RBCs by binding to the membrane and gives them elastic strength under deformation

it is two intertwined polypeptide chains

contains hemoglobin composed of four protein chains [globins], each heme has one iron = give the red colour

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12
Q

What happens during RBC differenciation?

A

takes 4 days to mature

hematopoietic stem cells [hemocytoblast] -> proerythroblasts - mitotic divisions -> basophilic erythroblasts - differentiation -> polychromatic erythroblasts [produce hemoglobin] - lose their nuclei-> reticulocytes

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13
Q

What is aplastic anemia?

A

serious form of anemia

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14
Q

What is leukopenia?

A

reduction of WBC leaving a person with many infections

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15
Q

What is thrombocytopenia?

A

reduce production of platelets leaving a person at high risk for hemorrhage

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16
Q

What does erythropoiesis do?

A
  1. when low oxygen levels detected by kidneys
  2. releases erythropoietin
  3. red bone marrow receives signal to make more RBCs = increased erythropoiesis so increased number of RBCs
  4. when levels are normalized, kidneys stop release of EPO
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17
Q

Why would athletes train at high altitudes?

A

at high altitudes, there is lower oxygen availability
therefore more production of erythropoietin and more erythropoiesis so they have more red blood cells for more oxygen carrying capacity [ get used to low oxygen supply, will perform better at a higher oxygen supply]

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18
Q

What is the process of RBC breakdown?

A

macrophage cells in the liver and spleen phagocytose the aged/abnormal/fragmented RBCs

they breakdown hemoglobin = amino acids used for energy or synthesis of new protein
iron is recycled by returning to bone marrow for synthesis of new hemoglobin
bilirubin brought to the liver where it is excreted into the intestine as bile

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19
Q

Describe iron homeostasis and metabolism.

A

iron comes from the diet binds to transferrin where it is transported to the bone marrow for the synthesis of new RBC. It is added to heme and heme combines with protoporphyrin to make a RBC. It then circulates for 120 days and becomes mature where a macrophage engulfs it in the liver or spleen. Once digested, it partitions the bilirubin for excretion by sending it back to the liver then to intestine into the bile out of the body. The iron is recycled by storing it in the ferritin stores of the liver or brought back to the bone marrows for synthesis of more RBCs.

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20
Q

What separate layers can be seen if the blood is allowed to stand or centrifuged?

A

hematocrit, buffy coat and RBC [ measured by PCV~ 42-45%]

anemia: reduced PCV
polycythemia: increase PCV

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21
Q

Which WBC is the most abundant?

A

neutrophils: highly mobile and phagocytic
can diapedesis: migrate out of blood vessel to enter tissues
have granules that contain lysozyme for destruction of bacterial cells

eosinophils: line the respoatory and digestive tract, weak phagocytes but provide protection against infections against parasitic warms and allergic reactions, release anti inflammatory
basophils: motile and diapedesis, contain histamine [inflammatory chemical] and heparin [anticoagulant]

22
Q

Differenciate agrnulocytes.

A

lymphocytes: smallest have B and T –> produced in the thymus

T cells direct attack infect/cancerous cells, B cells produce antibodies to specific antigens

monocytes: largest type of leukocyte, mobile and highly phagocytic to ingest bacteria and cancerous cells

23
Q

What is the function of platelets?

A

circulate in the blood, small, pale bodies, irregular spindled shapes

properties: agglutinations, adhesiveness and aggregation

  • during hemostasis (stoppage of blood flow)but
  • if injury is too much=blood clotting mechanism is activated for blood coagulation

they form from megakaryocyte fragments on the edge

24
Q

What are megakaryocytes?

A

giant cells with many DNA copies in the nucleus

25
Q

Describe the platelet plug formation.

A
  1. collagen exposed, binds and activates platelets
  2. release platelet factors
  3. factors attract more platelets
  4. platelets aggregate into the platelet plug
26
Q

What is the blood clotting mechanism?

A

release clotting fators from injured tissues and sticky platelets
series of chemical reactions that form thrombin
formation of fibrin and traps clood cells to form aclot

27
Q

What happens if there is damage to the blood vessel wall?

A
  1. vasoconstriction
  2. platelet and coagulation cascade aggregate into a loose platelet plug = hemostasis
  3. clot is reinforced by platelet plug
28
Q

How do we know when to breath?

A

sensory input: pons receive signals form chemo receptors to medullary rhythmicity area relay information to respiratory muscles to drive breathing

cerebral cortex = can override automatic control of breathing

29
Q

What do the respiratory function include?

A
  1. external respiration
  2. transport of gases by blood
  3. internal respiration
  4. regulation of respiration
30
Q

How is the respiratory system divided?

A

upper respiratory tract: from larynx to nasal cavity

lower respiratory tract: from trachea to diaphragm,/bronchus

accessory structures

31
Q

What are the muscles of inspiration?

A

intercostals (external or internal)

32
Q

What muscles are for expiration?

A

abdominal muscles

33
Q

List the structures from out to in.

A

trachea - primary bronchi - bronchials- alveolar sacs - alveoli - pulmonary arterioles and veins

34
Q

Describe key features of the nose=upper respiratory division

A

lined with hair: filters air
turbinates: provides large mucus covered surface over which air travels to moisten it

mucus acts to trap particles before air enters respiratory system

35
Q

What is the cause of cleft palate?

A

cleft palate = palatine bones fails to unitecan be genetic or non genetic = mutant gene trisomy 13, teratogenic, corticosteroids, etc.

48% reduction by folic acid

36
Q

What are the 3 divisions of pharynx (throat)

A

nasopharynx

oropharynx

laryngopharynx

37
Q

What are some lower respiratory tract or accessory structures?

A

lower respiratory tract: organs in the thorax, trachea, bronchial tree and lungs

accessory structure: oral cavity, rub cage, diaphragm

38
Q

Describe the trachea and the bronchi.

A

trachea: windpipe - connects the larynx to the bronchi
open airway to the lungs so obstruction can cause death
smooth muscle is embedded cartilage C rings
ciliated epithelium [columnar] to move mucus to pharynx

bronchi: epithelial, smooth muscle and connective tissue
goblet cells and ciliated cells and hyaline cartilage as well

39
Q

Describe the alveoli

A

each alveolus is ventialed, bronchioles subdivided into alveolar ducts then to the alveolar sac and then alveoli in each sac connected by PORES OF KOHN

40
Q

What is the respiratory membrane made of? Differentiate type 1 and type 2 alveolar cells

A

alveolar epithelium, capillary endothelium and joined basement membranes

type 1 alveolar cells: form alveolar wall {single layer}

type 2 cells produce SURFACTANT that reduces surface tensions and coats the inside of alveolus

41
Q

How does the respiratory cycle work?

A

inspiration: taking air into the lungs - active phase of ventilation because muscles contract (diaphragm moves down and thoracic cavity increases in volume so the pressure in the alveoli decreases resulting in air flow into the lungs [flows from high atmospheric pressure to low aleovlar pressure]

Expiration is the process letting air out, it is relaxation of the diaphragm and elastric recoil of tissue decrease the thoracic volume which increase the alveolar pressure = expiration so air moves from low to high pressure outside

42
Q

What are the two pressure gradients to consider during breathing?

A
  1. pressure within the alveoli of lungs [lower than atmospheric pressure - produces inspiration]
    [pressure of the alveoli of lungs is ghier than atmospheric pressure - produces expiration]
  2. pressure gradients establish by change in the size of the thoracic cavity as a result of contraction or relaxation of muscles
43
Q

Describe the diaphragm in two different states.

A

at rest: relaxed, thoracic volume decreases

contracted: thoracic volume increases

44
Q

What are the three important ventilation pressures?

A

atmospheric pressure - outside

alveolar pressure - intrapulmonary pressure

intrapleural pressure - between the parietal pleura [outer membrane] and visceral pleura [membrane around the lungs]

45
Q

What is the concept of compliance?

A

ability of pulmonary tissues to stretch so inspiration is possible [filling of the lungs with air requires stretching]

46
Q

What is the main agent of expiration?

A

due to elastic recoil = when diaphragm relaxes

47
Q

What is surfactant?

A

lipoprotein formed from protein and phospholipid secretions of type 2 cells in the wall of the alveolus

it reduces surface tension and prevents alveolar collapse during exhalation = it acts to decrease the attraction between water molecules [causes a shrivelled alveolus due to strong water bonds that don’t break easily] and are interspersed between water molecules

48
Q

What are alveolar macrophages?

A
primary phagocytes of the innate immune system
clear the air space
secrete lysozyme
phagocytoses
eliminate small daily normal microbes
49
Q

What are the factors that determine the amount of oxygen diffusion into the blood

A
  • total functional surface area of the respiratory membrane
  • respiratory volume
  • alveolar ventilation

capillary bed = large surfaces and thin layer so each RBC is close to alveolar

50
Q

What is the negative feedback loop control of respiration?

A

in response to high plasma CO2:

  1. increased cell respiration during exercise = rise in CO2 in plasma detected by chemoreceptors in carotid sinus and aorta
  2. feedback information is relayed to which send correction signals to the effectors
  3. effector muscle increase alternate contraction and relaxation so respiratory rate increases and the rate of CO2 is lossed form the body so CO2 drops accordingly and the plasma CO2 is brought back to the set point value.
51
Q

Where are the sensors that influence breathing?

A

nervous system provides feedback to the rhythmicity area

  • chemoreceptors in medulla [PCO2 increased- faster breathing, decreased - slower breathing]
  • peripheral chemoreceptors in carotid and aortic bodies and central chemoreceptors [decrease in pH, less CO2 = slowed breathing]
  • arterial O2 blood has minimal influence

cerebral cortex influence breathing by increase or decreasing rate and strength of respirations

52
Q

What are some respiratory pathologies? (laboured breathing)

A

chronic bronchitits: air tubes narrows due to swollen or excessive mucous production = inflammation of alveoli and epithelium and glands

asthma: edema (swelling) of respiratory mucosa and excessive mucous production obstruct airways = inflated alveoli
emphysema: alveoli walls are torn and unrepairable so alveoli fuses into large space but cannot inflate properly