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respiratory 5-8 Flashcards

1
Q

What is blood?

A

liquid CT which supports, connects, separates different tissues

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2
Q

What is the ECM of blood?

A
  • plasma (clotting fibres)
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3
Q

State the 3 functions of blood.

A
  1. transports: dissolved gasses, hormones, nutrients
  2. regulation: pH- buffers, temperature
  3. protection: clot, WBC’s, antibodies
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4
Q

Name the 3 formed elements of blood.

A
  1. RBC’s
  2. platelets
  3. WBC’s (granular and agranular leukocytes)
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5
Q

Name the granular and agranular leukocytes.

Hint - BEN

A
  • granular - eosinophils, basophils and neutrophils

- agranular - small lymohocytes (T and B-cells) and monocytes

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6
Q

What is haematocrit?

A

volume taken up by RBC’s (clinically-relevant feature)

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7
Q

What is the haematocrit in males compared to females and why?

A
  • females 38-46%

- males 40-54%- (more testosterone causes erythropoietin to produce RBC’s)

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8
Q

How does haematocrit affect anaemia?

A
  • low haematocrit

- reduced ability of blood to carry O₂ as less RBC’s

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9
Q

What is polycytheamia?

A
  • haematocrit raised to 65%

- leading to increased viscosity of blood, resistance in vessels, BP and stroke risk (so heart must work harder)

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10
Q

What are the causes of polycytheamia?

A
  • improper RBC production
  • tissue hypoxia
  • dehydration
  • blood doping
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11
Q

What controls RBCs and platelet number?

A

-VE feedback controls in RBM

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12
Q

What is haemopoiesis?

A

formation of blood cells in red bone marrow

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13
Q

What is found in RBM and which two subtypes does it give rise to?

A
  • pluripotent stem cells
  • subtypes:
    1. myeloid cells
    2. lymphoid cells
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14
Q

Where do myeloid cells develop and give rise to?

A
  • in RBM

- platelets, RBC’s + all WBC’s but lymphocytes

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15
Q

Where do lymphoid cells develop and give rise to?

A
  • in RBM

- B + T lymphocytes

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16
Q

How can bone marrow be examined?

A

by bone marrow exam (pelvic girdle) producing histological images

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17
Q

What do some myeloid cells differentiate into?

A
  • progenitor cells

- which cannot reproduce, so form CFU (colon-forming unit of myeloid cells)

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18
Q

What do some lymphoid cells differentiate into?

A

precursor cells

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19
Q

What do precursor cells develop into?

A

actual formed elements

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20
Q

What is hormone erythropoietin regulated by and used for?

A
  • testosterone levels

- kidney

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21
Q

What is hormone thrombopoietin used for and where is it found?

A
  • platelet formation

- liver

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22
Q

What is carboamino haemoglobin?

A

CO₂ bound to the AAs of a globulin molecule

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23
Q

Why do RBC’s bind and carry NO?

A
  • vasodilation

- thrombotic control

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24
Q

What is the equation for buffer control and which enzyme is involved?

A
  • CO₂ + H₂O → H₂CO₃

- carbonic anhydrase

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25
Q

What happens to the oxygen-dissociation curve, when:

a) blood in the lungs becomes more alkaline due to a loss in carbonic acid?
b) carbon dioxide diffuses in from the tissue to blood in the capillaries?

A

a) shifts to LHS

b) shifts to RHS

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26
Q

What does it mean for temperature if the curve shifts:

a) left?
b) right?

A

a) decreased temperature, decreased [H+]

b) increased temperature, increased [H+]

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27
Q

Is oxygen water-soluble?

A

no

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28
Q

What shape is the oxygen dissociation curve?

A

sigmoidal

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29
Q

What does exercise create in oxygen dissociation and which effect does this lead to?

A
  • acidic conditions (lactic acid)

- the Bohr Effect

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30
Q

What does the oxygen dissociation curve shifting curve RHS/LHS require?

A

a higher/lower pO₂ to get same saturation of oxygen

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31
Q

Describe the activity of RBC’s.

A
  • rapidly damaged in transit
  • no nucleus/organelles so cannot synthesise repair proteins
  • as PMs become fragile, may burst
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32
Q

What are ruptured RBCs removed by and what happens to their contents?

A
  • macrophages

- contents recycled

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33
Q

Describe the process of recycling RBCs using the following diagram in 14 stages.

A
  1. RBC death and phagocytosis in spleen
  2. heme and globin split
  3. globin converted to AAs to be for protein synthesis
  4. Fe3+ ion is removed from heme group
  5. enzyme transferrin converts Fe3+ into for liver storage
  6. bound transferrin and Fe3+ remain
  7. transferrin and Fe3+ used in endocytosis
  8. Fe3+ + globin + VitB12 + erythropoietin (hormone-driven) so erythropoiesis occurs in BM; to recycle heme, Fe3+ and transferrin transported to red bone marrow (where RBCs are made) and they return to circulation
  9. biliverdin from heme is converted to bilirubin (for bodily disposal)
  10. some bilirubin stored in liver
  11. other bilirubin transported to small intestine via bile duct (all else by bloodstream)
  12. bilirubin to urobilinogen converted by bacteria
  13. urobilinogen → urobilin → urine in kidney (yellow colour) - excreted
  14. in large intestine, urobilinogen → stercobilin → faeces (broken down bilirubin - brown) - excreted
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34
Q

What can iron overload cause?

A
  • toxic Fe build-up across the body
  • can cause serious damage to vital organs (i.e. heart/liver)
  • or can result in infection (iron-dependent microbes which flourish in excess Fe)
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35
Q

What is erythropoiesis?

A

RBC production

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36
Q

Describe the stages of erythropoiesis.

A

pro-erythroblast (RBM) → cells which make haemoglobin → reticulocytes → eject their nuclei

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37
Q

What is hypoxia?

A

lack of oxygen in tissues

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38
Q

What is blood doping?

A
  • injection of epoetin (epo) alfa (anemia treatment)

can be dangerous, hard to measure, done in Kenya

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39
Q

What do mast cells do and where are they found?

Hint - like a flag/mast as they do all of the main roles

A
  • vasodilation, inflammation, recruitment of phagocytes, allergic reactions
  • CT, mucous membranes
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40
Q

What do macrophages do and where are they found?

A
  • phagocytes which stimulate other WBC’s

- tissues

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41
Q

What do monocytes do and where are they found?

A
  • differentiate into macrophages + dendritic cells → respond to inflammation
  • infected tissues, stored in spleen
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42
Q

What do neutrophils do and where are they found?

A
  • first responders to infection, abundant phagocyte, release toxins, inhibit microbes and recruitement
  • tissues
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43
Q

What do basophils do and where are they found?

A
  • defence from parasites, release histamines for inflammation, allergic reactions
  • circulate in blood and tissues
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44
Q

What do eosinophils do and where are they found?

Hint - toxic, damaging and all around

A
  • release toxins and cause tissue damage

- circulate in blood and in tissues

45
Q

Describe neutrophil migration in 3 stages using the following diagram.

A
  1. antigen presentation, neutrophil begins to roll, adheres to PM so cell lines blood vessel
  2. diapedesis (= WBC leaves blood vessel)
  3. cell gets out by piercing cell membrane to escape the tissue
46
Q

State what each lymphocyte attacks:

a) B-cells (outside cells)
b) T-cells (inside cells)
c) NKC’s (Big Cs and germs)

A

a) (outside cells) - bacteria and toxins
b) (inside cells) - viruses, fungi, transplanted cells
c) variety of microbes and some cancers

47
Q

What does a complete blood count mean and what can its proportions indicate?

A
  • anaemia, haematocrit, WBC, haemoglobin

- events of IS

48
Q

What does a high or low blood counts for each WBC indicate?

a) neutrophils
b) lymphocytes
c) monocytes
d) eosinophils
e) basophils

A

a)
- high: bacterial infection, stress, burn, inflammation
- low: radiation exposure, SLE/lupus (= autoimmune disease)
b)
- high: viral infection, some leukemia’s
- low: prolonged illness, immunosuppression
c)
- high: viral or fungal infection, TB, some chronic illnesses
- low: bone marrow suppression
d)
- high: allergic reactions, parasitic infections
- low: drug toxcity, stress
e)
- high: allergic reactions, leukemia’s
- low: pregnancy, ovulations, stress

49
Q

How are platelets produced and what is the lifespan of a megakaryocyte?

A
  • (thrombopoietin) HSCs differentiate → megakaryoblasts → megakaryocytes (anucleate cells for haemostasis) → platelets
  • megakaryocytes = lifespan of 5-9 days
50
Q

Upon injury, which 3 steps occur in haemostasis?

Hint - Apples with Peanut Butter

A
  1. arterial vasospasm - constriction to reduce blood flow
  2. platelet plug formation - stops blood from leaking
  3. blood clotting
51
Q

Describe platelet plug formation.

A
  • activation
  • adhesion (outside-in signalling- integrin activation and secretion)
  • aggregation (thrombin production, requires exposure of ECM proteins vWF, fibrinogen, collagen)
52
Q

Which two adhesion receptors are found and used for platelet plug formation?

A
  • GP Ib/V/IX - main adhesion receptor for vWF

- integrin αIbβ3 (inactive) - second adhesion receptor which binds fibrinogen

53
Q

Name two platelet disorders and what is deficient in them both.

A
  • Bernard-Soulier – abnormality in the genes for glycoprotein Ib/CD42 which binds vWF
  • Glanzmann thrombasthenia – abnormality in genes for glycoproteins IIb/IIIa (2B/2A) for aggregation stage

(lead to lots of easy bleeding)

54
Q

Name two storage pool platelet deficiencies and what they caused by.

A
  • delta storage pool deficiency – lack of dense granules
  • grey platelet syndrome – lack of alpha granules, so platelets cannot stick to blood vessel walls, clump together or repair injured vessels (very rare)
55
Q

Which 3 pathways are involved in the coagulation cascade and how are they activated?

A 
• intrinsic pathway
- more complex + slower
- outside tissue damage not required
• extrinsic pathway
- less complex and rapid
- initiated by TF leaking into bloodstream 
• common pathway
- both pathways lead into this one in order to activate FX and complete the blood clot
56
Q

Summarise the 3 pathways of the coagulation cascade into a single diagram.

A

INTRINSIC:
(surface contact) FXII(a) → FXI→ bradykinin (vasodilator) release → FXIa (+ Ca2⁺) → FIX (serine protease) → FIXa → FX (+ Ca2⁺ + phopshatidylserine + FVIIIa - tenase complex) → FXa
——————————————————————————–
↕
——————————————————————————–
COMMON:
FXa
↓
prothrombinase complex (Ca2⁺, phospholipids, prothrombin and FVa)
↓
prothrombin (FII) → thrombin → fibrinogen (I) → fibrin clot (FXIIIa) → cross-links formed
——————————————————————————–
↕
——————————————————————————–
EXTRINSIC:
FVII (thrombin and FXa from IP)→ FX→ FVIIa (+ FIII/Tissue Factor) → FXa
——————————————————————————–

57
Q

Describe the role of fibrinolysis in clot localisation and which deficiencies lead to haemophilia A and B.

(Hint - first one octo not hepto)

A
  • fibrinolysis dissolves small inappropriate clots and ensures they don’t end up in your circulation
  • inactive plasminogen incorporated into clots → (thrombin and t-PA) plasmin (a)
    → digests fibrin threads + inactivates fibrinogen, prothrombin, FV and FXII
    (this stops the cascade from re-occurring)

• haemophilia A = FVIII (8) deficiency
• haemophilia B = FIX (9) deficiency
(both x-linked and both only affect aPPT time and not PT)

58
Q

What are thrombosis and atherosclerosis?

A
  • build-up of fats and cholesterol on artery walls obstructing blood flow
  • build-up of clots on artery walls obstructing blood flow
59
Q

Name and describe the action two anticoagulants, aspirin and thrombolytic agents.

A
  • warfarin – vit K antagonist to prevent clotting factor activation (blood-thinner)
  • EDTA – chelates calcium in donated blood
  • aspirin – inhibits TxA2 synthesis which decreases platelet aggregation
  • streptokinase – activates t-PA
60
Q

What are blood groups?

A

range of glycoproteins/glycolipids as antigens on surface of RBCs

61
Q

State the antigen/s, antibodies and blood transfusions each blood type can receive:

a) Type A blood
b) Type B blood
c) Type AB blood
d) Type O

A

a) - A antigen, anti-B antibodies, A or O blood
b) - B antigen, anti-A antibodies, B or O blood
c) - A + B antigens, no antibodies, A, B, AB and O blood
d) - no antigens, anti-A and anti-B antibodies, only O blood

62
Q

When do people develop Rhesus antibodies and when do they result in?

A
  • can develop them after blood transfusion/inherited

- means 8 blood groups (+VE and-VE of A,B AB and O)

63
Q

What are the stages of HDN?

Hint - acquired during first birth and then IS causes problems for next

A
  1. Rh-VE woman and Rh+VE man conceive child
  2. Rh-VE woman with Rh+VE fetus
  3. cells from Rh+VE fetus enter woman’s bloodstream at childbirth
  4. woman becomes sensitised - antibodies form to fight Rh+VE blood cells
  5. in the next Rh+VE pregnancy, maternal antibodies attack fetal RBC’s

(can be fatal)

64
Q

What is anaemia?

A
  • reduced oxygen-carrying capacity
  • can result from: iron- deficiency, megaloblastic (large RBC’s), pernicious (lack of haemopoiesis), haemorrhagic (excessive bleeding when loss of RBC’s exceeds production), haemolytic (low RBC count), thalassemias (Hb problems)
65
Q

How are carriers for sickle cell disease at a protective advantage?

A

inherited low K kills malaria

66
Q

What is leukaemia and what are the different forms?

A
  • production of malignant WBCs which suppress the synthesis of all normal cells in RBM
    (oncogenes on and tumour suppressors off)
  • acute lymphoblastic → lymphoid cells affected (children)
  • acute myelogenous → myeloid cells affected (all ages)
  • chronic lymphoblastic → lymphoid cell over-production (55+)
  • chronic myelogenous → myeloid stem cells affected (adults)
67
Q

What is haemophilia?

A

inherited, recessive, X-linked disorder which impairs the body’s ability tomake blood clots (stop bleeding)

68
Q

Why can leukaemia cause problems?

A
  • low RBC’s → low oxygen, development ofanaemia

- low platelets → low clotting, lose blood faster

69
Q

What is a bone marrow transplant and what can it lead to?

A
  • replacement of cancerous/abnormal RBM with chemotherapy/radiation
  • healthy RBM extracted + harvested
  • migrates to RBM cavities and multiplies
  • can create graft vs. host disease due to RBM being rejected (immunosuppressants needed)
70
Q

What is atmospheric pressure?

A

760mm Hg (to find pX x fraction out of 100)

71
Q

What is the percentage composition of gases in the atmosphere?

A
  • 79% N₂, 21% O₂, 0.03% C
72
Q

How long do gases dissolve into liquids and what does this depend on?

A
  • until they reach equilibrium

- gas’s pX and solubility in liquid (a gas concentration)

73
Q

Compare the solubility coefficient of CO₂ and O₂ in water.

A

solubility coefficient of CO₂ is 24x bigger than O₂ in water

74
Q

What is nitrogen narcosis?

Hint - “rapture of the deep”

A
  • N₂ has low solubility coefficient and its diffusion can be induced in high-pressure environments
  • i.e. as you dive deeper PN₂ increases and greater quantities diffuse across respiratory membrane
75
Q

What is decompression sickness and its symptoms?

A
  • rapid changes in pressure causing dissolved gases, (N₂) to come out of solution
  • bubbles forming in tissues (number of bubbles indicates severity)
  • symptoms: joint pain, dizziness, shortness of breath, fatigue, paralysis and unconsciousness
76
Q

What is hyperbaric oxygenation?

A
  • if PO₂ is increased, then diffusion of O₂ into blood will increase
  • used to treat decompression sickness
    (also treat gangrene, tetanus, CO poisoning, gas embolisms, bone infections, smoke inhalation, circulatory problems)
77
Q

What is a respiratory membrane made up of?

Hint - fluid, epithelium, basement, inters., BM, endothelium

A
  • thin fluid layer lining alveoli
  • thin squamous epithelium layer of alveoli
  • epithelial basement
  • interstitial space
  • BM of capillary endothelium
  • capillary endothelium
78
Q

Which 4 factors affect diffusion of gases across the respiratory membrane?

A
  • thickness of the membrane (0.5 mm normally)
  • diffusion coefficient: O₂ = 1, CO₂ = 20
  • SA (70m2 normally)
  • pX difference across membrane (higher in alveoli than capillaries - 104 vs 40mmHg)
79
Q

Which 2 factors can change the relationship between blood flow and respiratory rate?

A
  • when ventilation exceeds ability of blood to take up O₂ (result of HF)
  • (vice versa) when blood supply to lungs exceeds ventilation rate → lungs don’t contain enough O₂ to saturate blood → shunted blood (=partially oxygenated)
80
Q

What is regional blood flow? Provide an example.

A
  • blood flow in different regions of lungs varies depending on exercise
  • i.e. standing person at rest will only ventilate using upper portion of lungs due to vasoconstriction/dilation
81
Q

Describe erythrocytes

A
  • erythrocytes: 7 µm wide, 700x more numerous than WBC’s

- 1/3 of weight - haemoglobin

82
Q

Describe a haemoglobin molecule.

A

made of:

  • 4 polypeptides called globulins; each binds 1 heme molecule (red) → binds 1 Fe molecule → binds 1 oxygen
  • adult haemoglobin consists of: 2x α-chains + 2x β-chains
83
Q

What is oxyhaemoglobin and deoxyhaemoglobin?

A
  • oxygen-rich Hb

- oxygen-deficient Hb

84
Q

What is the lifespan of erythrocytes in men and woman?

A
  • 120 days in men

- 110 days in women

85
Q

How is erythropoiesis stimulated and where does it occur?

A
  • low PO₂, by increasing formation of erythropoietin in kidneys
  • in BM (4 days)
86
Q

On which on 3 factors does transport of respiratory gases depend on?

(Hint - dissociation and d. gradients)

A
  1. O₂ diffusion gradients
  2. CO₂ diffusion gradients
  3. haemoglobin’s oxygen-dissociation relationship
87
Q

What is PO₂ of blood leaving alveolar capillaries compared to when it reaches end of pulmonary vein?

(Hint - minus 9)

A
  • PO₂ of 104mm Hg

- will end as 95mm Hg

88
Q

Describe the route of blood (→) including PCO₂ values in terms of carbon dioxide diffusion gradients.

A

How blood travels (PCO₂):

cells (46mm Hg) → interstitial fluid (45mm Hg) → capillaries supplying blood to tissues (40mm Hg) → pulmonary artery (45mm Hg) → bloodstream (45mm Hg)
→ alveoli of lungs (40mm Hg)

89
Q

Describe Haemoglobin’s oxygen-dissociation relationship.

A
  • Hb carries 97% of O₂ in blood
  • Hb in erythrocytes nearly 100% saturated with O₂ (PO₂ = 80 mm Hg)
  • blood in alveolar capillaries saturated
  • Hb in tissue capillaries (PO₂ = 40mmHg) is 75% saturated with oxygen, so 25% carried by erythrocytes to dissociate into interstitial fluid
  • during exercise, interstitial fluid in skeletal muscle drops (PO₂ = 15 mmHg) + Hb gives up 75% of O₂
90
Q

What is the role of pH in Haemoglobin’s oxygen- dissociation relationship?

A
  • ability of Hb to bind O₂ decreases when H⁺ and Hb interact (conformational change occurs)
  • PCO₂ increases means: CO₂ + H₂O → H₂CO₃
  • H₂CO₃ → (dissociates) H⁺ + HCO₃-
  • thus, a greater PO₂ required to saturate Hb-O₂
    (dissociation curve shifts to the right)
91
Q

What is the role of temp in haemoglobin’s oxygen-dissociation relationship?

A

increase in temp. shifts oxygen dissociation curve to right as does accumulation of acidic products

92
Q

What is the effect of heavy exercise on haemoglobin’s oxygen-dissociation relationship and what is this called?

A
  • CO₂, lactate accumulates and temp. increases
  • 85% of O₂ is released
  • increased respiration rate, so PCO₂ in lungs decreases
  • oxygen-dissociation curve shifts LHS allowing Hb to saturate readily
  • the Bohr effect
93
Q

What is the effect of BPG on haemoglobin’s oxygen-dissociation relationship and in which individuals would this have an effect?

A
  • BPG or 2,3-bisphosphoglyceride (produced by erythrocytes) modifies affinity of Hb for O₂
  • people in high altitudes have high concentrations and this increases O₂ delivery to tissues
94
Q

In which 3 ways can CO₂ be transported in blood?

A
  1. as CO₂ dissolved in plasma (8%)
  2. combined w/ blood proteins (20%)
  3. as bicarbonate ions (72%)
95
Q

What are carbamino compounds?

A

blood proteins that bind CO₂

96
Q

What is the Haldane effect?

Hint - about space

A

affinity of haemoglobin for CO₂ is greater if Hb molecule has just given up oxygen

97
Q

Describe how CO₂ can be transported in the blood as bicarbonate ions.

A
  • CO₂ diffuses into erythrocytes and reacts with water to form carbonic acid
  • carbonic acid dissociates into H⁺ and HCO₃- ions
98
Q

What is the chloride shift?

Hint - chloride is Cl- ions

A
  • HCO₃- diffuse out of erythrocytes into plasma causing Cl- move into erythrocytes
  • maintains electrical balance
99
Q

How does carbonic acid control the pH of the blood?

A
  • H⁺ bound to Hb in erythrocytes
  • released to decrease plasma pH
  • when deoxy. blood reaches alveoli, CO₂ in blood diffuses into alveoli
  • if PCO₂ of blood decreases, HCO₃- moves into erythrocytes and Hb releases H⁺ ions
  • HCO₃- + H⁺ → H₂CO₃ (Cl- moves out of erythrocytes)
  • H₂CO₃ → H₂O and CO₂ (Cl- moves into erythrocytes)
100
Q

Give an overview of embryonic development.

A
  • fertilisation of a haploid egg by haploid sperm giving rise to a single diploid cell
  • (cell replication) 2-4 cells → 8 cells (totipotent) → 16 cells → (pluripotent, day 3)
  • blastocyst (trophoblast and ICM) day 5 →
  • implantation (ICM orientated to uterine endometrium/decidua becomes heavily vascularised) day 6 →
  • cell mass differentiates into 2 layers: hypoblast/primitive endoderm and epiblast/primitive ectoderm), day 8 →
  • exocoelomic/Heuser’s membrane forms around inner blastocyst and walls of egg sac, day 9

NB; trophoblast gives rise to foetal placenta, ICM to embryo

101
Q

What happens on days 15-21?

A
  • bilaminar disk develops into trilaminar structure

- gastrulation (gastrula → blastula) - 3 germ layers

102
Q

What happens during week 4?

A

cells in yolk sac develop into gonad (sex gland) and parts of GI tract

103
Q

What are pericardioperitineal canals?

A

narrow structures either side of foregut

104
Q

Summarise the embryological development of the respiratory system in 7 stages.

(Hint -

1) respiratory system
2) origins of the system parts
3) week 4, septum
4) week 5, 1°/2°
5) month 7 -
6) birth
7) postnatal life

A

1) respiratory system is outgrowth of ventral wall of foregut (betw/ 4th and 6th pharyngeal arches)
2) endodermal origin – epithelium of entire respiratory tract and mesodermal origin – cartilages and muscles of respiratory tracts
3) week 4 - lung bud separated from foregut by oesophagotracheal septum
4) week 5 - lung bud extends → 1° bronchi → 2° bronchi → bronchioles
5) month 7 -
- epithelial cells:
o flatten into type I alveolar epithelial cells
o become closely-associated w/ blood and lymph capillaries (gas exchange possible)
• type II cells secrete surfactant
• lungs filled with fluid
6) Birth - lung fluid reabsorbed and surfactant prevents lung collapse
7) 10th year of postnatal life - lungs grow until now

105
Q

What are oesophageal atresia and tracheoesophageal fistula?

A

(abnormal partitioning of oesophagus and trachea)

  • OA: oesophagus terminates in a blind-ending passage (blocked at end)
  • TEF: abnormal opening forms between oesophagus and trachea
  • babies can become cyanotic and stop breathing
106
Q

Which conditions can are oesophageal atresia and tracheoesophageal fistula be associated with?

A

Other developmental abnormalities of VACTERL association:

  • Vertebral
  • Anal atresia
  • Cardiac
  • Tracheoesophageal fistula
  • Eosophogeal atresia
  • Renal and Limb defects
107
Q

What can congenital cysts arise from and cause and how can they be treated?

(Hint - cysts and RAS treatment)

A
  • abnormal budding of diverticulum, resulting in dilated and poorly-vascularised terminal/larger bronchioles
  • cysts may be air/fluid-filled
  • treatment normally involves respiratory support, antibiotics and surgery
108
Q

Name some other congenital abnormalities of the bronchial tree.

A
  • formation of ectopic (abnormally-positioned) lung lobes from trachea/oesophagus
  • loss of a lung lobe/entire lung
  • formation of blind ending trachea with complete lung absence
109
Q

What is RDS caused by, what are its signs and how can it be treated?

A

• insufficient quantities of surfactant
• common cause of death in premature infants
• signs: rapid and shallow breathing, retractions of chest wall and flaring nostrils with each breath
• treatment:
- respiratory support
- glucocorticoids
- synthetic surfactants

CRR (11 decks)

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