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Medicine 1 > Anatomy - COPD > Flashcards

Anatomy - COPD Flashcards

1
Q

What happens to PaO2 and PaCO2 during exercise?

A

They remain normal

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2
Q

What does graph look like for ventilation against exercise intensity?

A
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3
Q

What is the mechanism during the start of exercise?

A

Neural mechanism - proprioceptors detect movement causing anticipation of extra demand

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4
Q

What happens to ventilation during moderate exercise and what is the mechanism?

A

Ventilation rate = exercise when graph plateaus

Mechanism = CO2 released from active cells causes increase in ventilation

Central chemoreceptors maintain PaCO2 and PaO2

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5
Q

What happens to ventilation during strenuous exercise and what happens?

A

Ventilation increases due to high body temperature and metabolic acid production

VR can increase from 5-6 l/min to 120 l/min

Hyperventilation = decrease in PaCO2

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6
Q

What are the cardiovascular adaptations to exercise?

A
  • Skeletal muscle contraction
  • Activation of sympathetic nervous system
  • Myocardial contractile force
  • Cardiac acceleration
  • Peripheral vasoconstriction
  • Blood vessel compression
  • Translocation of blood from peripheral vessels into heart and lungs
  • Cardiac output increase and blood-flow to active muscles
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7
Q

What happens during acute exposure to high altitude?

A

Peripheral chemoreceptors detect acute hypoxia so try to increase breathing

+ ventilation = less PaCO2 and alkylation of cerebrospinal fluid

+ breathing = die from alkalosis

  • breathing = die from hypoxia
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8
Q

What happens during chronic exposure to high altitude?

A

Mild hypoxia = less PO2

+ ventilation from hypoxic drive

  • PCO2
  • PCO2 = + cerebrospinal fluid alkylation = + HCO3-

HCO3- exported by choroid plexus cells to correct pH

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9
Q

What happens hours and days after chronic high altitude exposure?

A

Breathing controlled around lower PCO2 (hours)

Correction of blood alkalinity by HCO3- excretion in urine (days)

+ oxygen carrying capacity of blood

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10
Q

What happens on return from chronic high altitude exposure?

A

Left upper quadrant (abdomen) pain from spleen enlargement

+ cardiac output

Correction of systemic acid-base imbalance

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11
Q

What are the two types of chemoreceptors and where are they found and what are they sensitive to?

A

Central chemoreceptors –> in medulla –> sensitive to change in H+ concentration and pCO2

Peripheral chemoreceptors –> within aortic arch and carotid arteries –> sensitive to changes in arterial pO2 and pH

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12
Q

What happens in peripheral chemoreceptors?

A

Decreased arterial O2 = hyperventilation

Stimulated when arterial pO2 = below 13.3 mmHg

+ PCO2 = less importance than CCR response

Fall in pH = carotid detects it, not aortic bodies

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13
Q

What happens during acidic pH imbalance?

A

Hypoventilation = respiratory acidosis

Fall in pH

+ H+ concentration

+ CO2 in lungs

Compensation = kidneys excrete + [H+] and + [HCO3-] reabsorption

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14
Q

What happens during alkaline pH imbalance?

A

Hyperventilation = respiratory alkalosis

Increase in pH

  • [H+]

Decrease in CO2

Compensation = kidneys reabsorb + [H+] and + [HCO3-] excretion

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15
Q

What happens in uncontrolled diabetes when there’s a pH imbalance?

A

Metabolic acidosis

  • ability for kidney H+ excretion and HCO3- reabsorption

Compensation = + ventilation = - PaCO2

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16
Q

Why do you vomit?

A

pH imbalance causing metabolic alkalosis

  • acid

+ base - + HCO3-

  • ventilation = + PaCO2
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17
Q

What are the order of priority of responses to PCO2, PO2 and pH?

A

PCO2

pH

PO2

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18
Q

What are the properties of response to PCO2?

A

CCRs = most sensitive to PCO2 change

Levels held within 0.3kPa

PCRs detect rapid PCO2 changes but less sensitive

Levels held within 1.3 kPa

PCO2 controlled to avoid acid-base problems

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19
Q

What are the properties of the response to pH?

A
  • pH = +ventilation

Influenced by PCO2 levels

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20
Q

What are the properties of response to PO2?

A

PCRs detect PO2 changes

Have wider control margin

PCRs stimulation when levels below 13.3 kPa

Controlled to avoid hypoxia

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21
Q

Health problem related to chemical ventilation?

A

Cheyne-Stokes –> CNS disease, head trauma, + intracranial pressure, heart failure

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22
Q

What is the function of neural regulation?

A

Sets ventilation rhythm and pattern

Controls respiratory muscles

Neural control = fast acting impulses

23
Q

What is the function of chemical regulation?

A

Detects central and peripheral arterial PCO2 and pH and peripheral PO2

24
Q

What is a health issue related to nervous ventilation?

A

Respiratory depression –> rate / depth of respiration = insufficient to maintain adequate gas exchange, a result of medullary and pons effects, some drug side effects, is reversed by analeptics

25
Q

What is the dorsal respiratory group and it’s function?

A

Medulla respiratory control system

  • DRG fibres innervate diaphragm and external intercostal muscles
  • Inspiration caused by diaphragm contraction and thoracic cavity expansion
  • DRG neurons = switch on (inspiration) for 2s and switch off (expiration) for 3s causing rhythmic pattern
26
Q

What is the ventral respiratory group and it’s function?

A

Medulla respiratory control system

  • VRG fibres innervate abdominal muscles and internal intercostal muscles
  • Activity = enhanced during forced expiration, small role in inspiration
27
Q

What are the 2 types of pons respiratory control systems and their function?

A

Pneumotaxic centre:
Signals transmitted to DRG

Role = limit inspiration

Fine-tunes breathing and sends inhibitory impulses to DRG

Limit inspiration period to 2s

Prevents lung over-inflation

Apneustic centre:

Responsible for prolonged inspiratory gasps (apneusis)

Prolong DRG stimulation

Apneusis observed in severe brain injury

28
Q

What is the role of the vague nerve in respiratory control?

A

Sends afferent information from lungs to DRG

Role = prevent over-inflation of lungs by switching off inspiration

29
Q

What is the function of the cerebral cortex in respiration?

A
  • Stimulates inspiratory muscle motor neurons
  • Bypasses medullary centres when consciously controlling breathing
  • Limited ability to breath-hold à respiratory centres automatically reinitiate breathing when O2 conc. in blood reach critical levels
  • Drowning victims = eventually reinstate breathing, water in lungs as result
30
Q

What is the function of the hypothalamus in ventilation?

A
  • Strong emotions, pain, changes in temperature = can alter respiratory rate and rhythm
  • Apnoea = can be induced by anger, pain or temperature decrease
  • Tachypnoea = can be induced by excitation or temperature increase
31
Q

What are stretch receptors and their function?

A

Respiratory reflexes

  • In smooth muscle of trachea and bronchi
  • Sensitive to lung expansion
  • Lung expansion – respiratory centre – inspiration is shorter and shallower – prevent lung over-inflation
32
Q

What are juxtapulmonary receptors and their function?

A

Respiratory reflexes

  • In alveolar wall between epithelium and endothelium close to pulmonary capillaries
  • Stimulation = congestion, oedema, histamine
  • Activation = apnoea or rapid shallow breathings, bronchoconstriction and mucus secretion
33
Q

What are irritant receptors and their function?

A

Respiratory reflexes

  • Between epithelial cells
  • Sensitive to irritant gases, smoke, dust
  • Activation = results in rapid, shallow breathing, cough, bronchoconstriction, mucus secretion, augmented breaths (gasps)
34
Q

What are the properties of respiratory reflexes?

A
  • Send signals via afferent fibres of vagus nerve, to respiratory centres
  • Stimulation of bronchiole receptors = airways constrict
  • Stimulation of tracheal receptors = coughing
  • Stimulation of nasal cavity receptors = sneezing
35
Q

What are the 6 steps of prescribing?

A
  • Step 1: Define the patient’s problem
  • Step 2: Specify the therapeutic objective
    • What do you want to achieve with the treatment?
  • Step 3: Verify the suitability of your P-treatment
    • Check effectiveness and safety
  • Step 4: Start the treatment
  • Step 5: Give information, instructions and warnings
  • Step 6: Monitor (and stop?) treatment
36
Q

What 3 things must you remember when prescribing?

A

Allergies

Drug interactions

Monitoring

37
Q

What are the different unit types for dosages?

A
  • g, mg, or microgram
  • Microgram not mg or mcg
    • e.g. 125 micrograms digoxin
  • Nanogram not ng
  • mL for volumes e.g. 125 mg /mL
  • Write ‘Units’ in full (not u)
    • e.g. insulin, heparin
  • Check is appropriate for age, weight, renal function, hepatic function
38
Q

What information must you include for as required drugs?

A
  • Indication
  • Frequency
  • Minimum dosage interval
  • Maximum dose in 24 hours
39
Q

What to remember during patient counselling?

A
  • What the medicine is for
  • When to take the medicine
  • How to take the medicine
  • Dose
  • Frequency
  • Key side effects
  • What to do if miss a dose
  • How long for treatment
40
Q

What things stimulate acute inflammatory response?

A
  • Microorganisms
  • Trauma
  • Ischaemic necrosis
  • Radiation damage (sunburn)
  • Chemical damage
41
Q

What is the purpose of the acute inflammatory reaction?

A
  • Destroy and neutralise damaging agent
  • Liquefy and remove dead tissue
  • Prepare damaged area for healing
42
Q

What allows the acute inflammatory response to carry out it’s function?

A

Acute inflammatory exudate

Composed of:

  • Fluid
  • Fibrin
  • Neutrophils
43
Q

How does acute inflammatory exudate work?

A
  • Fluid dilates toxins
  • Fluid carries nutrients, mediators and antibodies
  • Neutrophils phagocytose living tissue (bacteria) and necrotic debris
44
Q

What happens during stage 1 of exudate formation?

A
  • Dilation of blood vessels near damaged tissue
  • Increase in blood flow initially, then slows
  • Axial flow pattern of blood is lost
45
Q

What happens during stage 2 of exudate formation?

A
  • Increased capillary permeability
  • Water, salts and protein leak into damaged area
  • Fibrinogen = important protein
46
Q

What happens during stage 3 of exudate formation?

A
  • Neutrophils adhere to endothelium
  • Neutrohpils migrate to damaged area
  • Fibring formed in tissues
47
Q

What are the 4 types of exudate?

A

Serous

Purulent

Fibrinous

Fibrino-purulent

48
Q

What happens during the resolution stage of inflammation?

A
  • Exudate eliminates damaging agent
  • Macrophages remove dead cells and exudate
  • Cells re-grow
  • Normal tissue function and structure returns
49
Q

What happens during the resolution stage with no tissue damage?

A
  • No damage to architecture
  • Exudate forms
  • Liquified exudate is reabsorbed
50
Q

What is an abscess and what causes them?

A

Large accumulation of liquid purple tissue exudate (puss) in area where tissue damage has led to extensive necrosis

Bacteria

51
Q

What are the steps of organisation of repair?

A
  • Remove debris
  • Grow new vessels
  • Lay down collagen
  • Mature collagen
  • Granulatin tissues matures to a scar
52
Q

What are the steps of organisation of exudate?

A
  • Capillaries grow into damaged area
  • Fibroblasts migrate and multiply
  • Fibroblasts synthesis collagen
  • New capillaries regress
  • Fibroblasts regress
53
Q

What are the mechanisms of chronic inflammation?

A
  • Macrophage is main effector
  • Acitvated by gamma interferon
  • Phagocytic role
  • Secretory role
54
Q

What is granulomatous inflammation?

A

Form of chronic inflammation where neutrophils are ineffective and macrophages are involved early

Granuloma formed from aggregates of macrophages around damaging agent

Medicine 1 (28 decks)

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