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Liv vet med yr1 > Urinary/respiratory > Flashcards

Urinary/respiratory Flashcards

1
Q

Respiration vs ventilation

A

Respiration = the exchange of gases at the alveoli

Ventilation = the movement of air through the airways

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2
Q

Pleura

A

Double layer of simple squamous epithelium lying on connective tissue - lining the thoracic cavity

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3
Q

Layers of the pleura

A

Visceral pleura - invests the tissue of the lung

Parietal pleura - lines the remaining structures of the thorax

The two layers are continuous with each other, forming a sealed pleural sac

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4
Q

pneumothorax

A

When a hole is made in the pleura so air rushes in, causing the lung to collapse on that side

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5
Q

Larynx

A

A structure supported by multiple cartilages, lined by a mucous membrane.

It connects the pharynx and trachea and is involved in:
- Protection of the lower airways
- Phonation
- Swallowing
- Coughing and eructation/vomiting

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6
Q

Lobes of the lungs

A

Right:
- Cranial
- Middle
- Caudal
- Accessory

Left:
- Cranial
- Caudal

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7
Q

What epithelium are the airways of the ventilation system lined with?

A

Pseudostratified ciliated columnar epithelium

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8
Q

Type 1 alveolocytes

A

Flattened simple squamous epithelial cells of the alveolus

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9
Q

Nerve supply of the lungs

A

The lung receives sympathetic and parasympathetic supply via the pulmonary plexus.

The vagus nerve provides the parasympathetic portion.

The sympathetic nerve supply to the lung only innervateds the blood vessels, the smooth muscle of the airways has β₂ adrenoreceptors which respond to circulating adrenaline and noradrenaline.

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10
Q

Eupnoea

A

Normal, resting breathing - at a normal rate, depth and effort

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11
Q

Tachypnoea

A

An increased respiratory rate

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12
Q

Hyperpnoea

A

Increased respiratory depth

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13
Q

Dyspnoea

A

Laboured breathing

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14
Q

Compliance

A

The degree to which a change in transpulmonary pressure causes a change in the volume of the lung

C=𝞓V/𝞓P

It depends on the elasticity in the lung tissue and the surface tension of the alveoli

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15
Q

Surfactant

A

To counteract resistance, type II alveolar cells produce surfactant.

It is a mixture of phospholipids, proteins and Ca²⁺ which reduce the formation of H bonds between water molecules

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16
Q

Carbon dioxide transport

A

CO₂ is transported in the blood in 3 ways:
- Dissolved in plasma (5%)
- As carbamino compounds (30%)
- As bicarbonate ions (65%)

it is ~20x more soluble than oxygen

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17
Q

Carbamino compounds

A

CO₂ combined with Hb (or other proteins)

CO₂ binds more strongly to deoxyHb meaning that the offloading of O₂ in the tissues facilitates loading of CO₂

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18
Q

Carbonic anhydrase

A

The majority of CO₂ combines with water to form carbonic acid under the influence of carbonic anhydrase.

Carbonic acid quickly dissociates into bicarbonate and hydrogen ions.

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19
Q

The chloride shift

A

When the HCO₃₋⁻ produced in the carbonic anhydrase reaction is transported out into the plasma in exchange for chloride ions to maintain the electrochemical neutrality of the erythrocyte

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20
Q

Pulmonary vascular responses

A

The net effect of sympathetic stimulation is usually vasoconstriction.

Parasympathetic stimulation has a net effect of vasodilation.

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21
Q

Nitric oxide

A

It is an important vasodilator.

Its release from vascular endothelial cells is stimulated by the parasympathetic nervous system and by the action of mediators such as Bradykinin. it is also released from the endothelium in direct response to an increased speed of flow.

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22
Q

Alveolar hypoxia

A

Potent vasoconstrictor.

A low PAO₂ occurs where ventilation of alveoli is reduced - this alveolar hypoxia causes vasoconstriction of the small arteries supplying that portion of the lung.

This response reduces blood flow to poorly oxygenated alveoli and increases flow t well oxygenated alveoli.

This response becomes problematic if the alveolar hypoxia is not localised but generalised, leading to a generalised vasoconstriction of the pulmonary circulation.

This increases the after load on the RHS of the heart and can lead to right congestive heart failure.

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23
Q

Respiratory receptors

A
  • Pulmonary stretch receptors
  • Irritant recepotors
  • Muscle spindle stretch receptors
  • Peripheral chemorecptors
  • Central chemoreceptors
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24
Q

Pulmonary stretch receptors

A
  • Associated with the smooth muscle of the airways
  • Participate in the Hering Breuer reflex
  • They send impulses in increasing frequency throughout inspiration via myelinated axons to the pons to signal degree of lung inflation
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25
Q

Irritant receptors

A

Fast acting receptors in the epithelial lining of the airways.

They initiate mechanisms designed to protect the airways from further invasion:
- Cough
- Increased secretion of mucus
- Bronchoconstriiction
- Shallow breathing

26
Q

Muscle spindle stretch receptors/golgi tendon organs

A

Monitor the movements of the respiratory muscles to enable their strength of contraction to be modulated

27
Q

Peripheral chemoreceptors

A

In the carotid and aortic bodies monitor PaO₂, PaCO₂ and arterial [H⁺].

They receive a high blood supply and obtain their O₂ from dissolved O₂ in the plasma which enables them to to accurately sense the PO₂ of the blood.

Gloms cells in the carotid bodies depolarise when PO₂ drops, sending Ads via the carotid sinus of CN IX to the brain to increase ventilation

28
Q

Central chemoreceptors in the brain

A

Only monitor PaCO₂ - the most important factor affecting respiration.

The major effect on ventilation from increases in PaCO₂ is due to the action of central chemoreceptors

29
Q

Normal blood pH in domestic animals

A

7.4

30
Q

Respiratory vs metabolic acidosis/alkalosis

A

Respiratory = ⬆/⬇in blood [H⁺] due to increased PaCO₂

Metabolic = ⬆/⬇in blood [H⁺] for other reasons

31
Q

Mechanisms to reduce [H⁺] in ECF

A

Buffering - 1st line of defence, fast acting

Lungs - 2nd line of defence, fast acting

Kidneys - take longer to act in a pH abnormality but have the highest capacity to effect change and form the 3rd line of defence

32
Q

Development of pulmonary circulation

A

The cardiac tube develops prior to development of the lungs.
Folding and chamber development of the cardiac tube brings the venous end of the tube ventral to the foregut so the mesoderm of the cardiac tube is in contact with the ectoderm of the developing foregut - this enables the connection between heart and lungs to develop

The pulmonary circulation develops along the airways

33
Q

Stages of lung development

A

1) Embryonic
From the formation of the larynges-tracheal groove to the formation of segmental bronchi

2) Pseudoglandular
Lungs extend into the surrounding mesenchyme. all the major conducting branches of the bronchial tree form and vascularisation begins

3) Canalicular
Tracheal and bronchial lumens enlarge, respiratory bronchioles form and vascularisation progresses so capillaries are in direct contact with epithelium in the respiratory bronchioles

4) Terminal sac
Terminal sacs lined with cuboidal epithelium arise from the respiratory bronchioles. The epithelium organises into type I + type II alveolar cells, so the terminal sacs become alveoli. Type II alveolocytes start to produce surfactant

5) Alveolar
Capillaries become closely associated with the alveolar lining cells, forming the blood-air barrier. Type II alveolocytes proliferate and surfactant production increases. The alveolar stage of development continues post nasally for some time

34
Q

Gas exchange in the foetus

A

The early embryo achieves gas exchange by diffusion via uterine fluids. As the embryo grows, placentation occurs, to facilitate exchange of gas and nutrients from the dam to the foetus.

Foetal arterial blood leaves the foetus and runs to the placenta via the umbilical artery which originates from the internal iliac artery.
Gas exchange occurs in the placenta. A high SA for exchange is provided by isterdigitatiting microvilli in the placenta.

Circulating blood in the foetus is relatively hypoxic cf animal after birth.

35
Q

Changes to respiratory system at birth

A

Foetal lungs contain fluid from secretion of alveolar cells and mucosal glands + some aspirated amniotic fluid. This helps to stimulate expansion of the alveoli as the lungs develop

The respiratory muscles begin contracting in the foetus at ~1/3 of gestation to prime them for respiration after brith

During birth, some of the fluid in the lungs is squeezed out. The remainder is absorbed into the lymphatic and vascular systems after birth.

36
Q

Stimuli for first breath after birth

A
  • Hypoxia
  • Hypercapnia
  • Lowering body temperature
  • ⬆ sensory stimulation from mother
37
Q

What happens in first few breaths

A
  • Fully inflate lungs and evenly distribute surfactant through the alveoli.
  • Pull open pulmonary vessels, causing a significant drop in vascular resistance.
  • The blood which was being diverted to the systemic circulation now follows the hydrostatic pressure gradient into the pulmonary vasculature and pulmonary gas exchange can begin.
38
Q

How does the body deal with increased O₂ consumption by skeletal muscle?

A
  • Increased cardiac output
  • Increased red blood cell count
  • Lower affinity Hb for O₂
  • Increased respiratory rate + depth
  • Myoglobin stores
  • Increased diffusion gradient for O₂ at tissues
39
Q

Urinary tract

A

Kidney - positioned either side of the spine, behind caudal rib

Ureters - conveys urine from kidneys to bladder

Bladder - storage of urine prior to evacuation

Urethra - convey urine from bladder to outside world

40
Q

Functions of the kidney

A

Regulation of fluid volume + electrolyte balance
- ECF + blood pressure
- Osmolarity
- Ion balance
- pH
Excretion of waste
- Metabolic waste
- Foreign substances
Production of hormones
- Activation of vitamin D3
- Synthesis of erythropoietin
- Synthesis and release of the enzyme renin

41
Q

Renal anatomy

A

Cortex - filtration to form filtrate
Medulla - collect + excrete urine

42
Q

Nephron

A

Renal corpuscle
- Production of filtrate

PCT
- Bulk reabsorption of water, ions and organic nutrients

Loop of Henle
- Further reabsorption of ions, water and set up of osmotic gradient in the renal medulla

DCT
- Variable secretion and reopsorption of water and ions

Collecting duct
- Variable secretion and reabsorption of water and ions

Papillary duct
- Delivery of modified filtrate to the renal pelvis

43
Q

Microstructures of the kidney

A

Cortex - contains mainly tubules but also renal corpuscles

Medulla - composed of exclusively renal tubules

44
Q

Blood supply to the kidney

A

The renal arteries directly branch from the aorta

20-25% cardiac output

45
Q

Renal corpuscle

A

Very high volume of blood flow

Large surface area across which filtration can occur

High level of glomerular capillary blood pressure

Low resistance to the movement of fluid - filtered substances move through 3 barriers:
- Capillary endothelium
- Basement membrane
- Bowman’s Capsule epithelium

46
Q

Glomerular filtration rate in dogs

A

~3ml/kg/min

47
Q

Nephron function - sequence of events

A

Filtration
- Pressure forces filtration of waste-laden blood in the glomerulus.

Reabsorption
- The process of returning important substances from the filtrate back to the body

Secretion
- The movement of waste materials from the body to the filtrate

48
Q

Bulk reabsorption in the PCT

A
  • ~70% of the filtrate is reabsorbed in the PCT
  • Selective but mostly unregulated
  • Active + passive

Most reabsorption in the PCT is through protein channels ∴ selective but not regulated by hormones

49
Q

Tubular cells of the PCT

A
  • Have microvilli border on apical membrane to increase SA
  • Have large amounts of NaK ATPase on basolateral membrane
  • Contain large amounts of carbonic anhydrase enzyme
50
Q

Is there a limit to how much glucose can be filtered into the PCT?

A

No - glucose is freely filtered and does not saturate ∴ filtration depends on plasma concentration

51
Q

Is there a limit to how much glucose can be reabsorbed from the PCT?

A

Yes - Reabsorption will depend on:
- Rate of flow of the filtrate
- ⬇ rate of flow ⬆ absorption
- Number of protein transporters
- More transporters ⬆reabsorption

The rate of reabsorption is limited by the number of protein transporters

52
Q

Phosphate reabsorption

A

Like glucose

Linked to Na co-transport in the PCT
BUT unlike most reabsorption, it is hormonally regulated
- Regulated by parathyroid hormone
- PTH reduces phosphate reabsorption in the PCT and ∴ increases phosphate excretion

53
Q

Summary of reabsorption in the PCT

A

Occurs mainly in the PCT

Water is reabsorbed by osmosis, following extraction of sodium and chloride from the tubular fluid

The main energy for this transport from the lumen of the PCT back to the plasma is the action of the sodium/potassium pump

This in turn fuels secondary active transport (glucose, amino acids, ions), diffusion (urea, other solutes) and osmosis

Certain solutes such as glucose are reabsorbed under normal conditions before leaving the PCT

54
Q

Functional adaptations of the PCT

A
  • Large SA
  • Single layer of epithelial cells
  • High [Na⁺K⁺ATPase]
  • High [carbonic anhydrase]
  • Peritubular capillaries continuous with efferent arteriole have very high oncotic pressure
55
Q

Why is reabsorption advantageous to animals

A

GFR is relatively high in normal animals BUT filtrate is immediately reabsorbed - the animal is able to swiftly remove substances from the blood that are freely filtered at the renal corpuscle

56
Q

Why are many environmental toxins are highly lipid soluble?

A

Lipid-soluble substances can readily cross cell membranes and as water is absorbed from the filtrate a diffusion gradient is set up promoting reabsorption
It is ∴ difficult to excrete highly lipid soluble substances via the urine.
The liver converts many but not all foreign substances into water-soluble substances.

57
Q

Secretion in the PCT

A

Secretion provides an additional opportunity to increase urinary excretion of specific substances.

  • Always active
  • Not regulated
  • Substances must be ionised
58
Q

Secretion of H⁺ in the PCT

A

Protons are secreted into the filtrate via secondary active transport - sodium hydrogen exchanger

Some protons bind to non bicarbonate buffers and are excreted in urine

Protons can also be secreted via NH₄ sodium anti-porter on apical membrane

59
Q

Reabsorption of bicarbonate is linked to secretion + reabsorption of H+

A

Bicarbonate is reabsorbed in the PCT
No protein carrier on apical membrane
- Bicarbonate reabsorption is therefore linked to proton secretion
- This is made possible by large quantities of carbonic anhydrase enzyme

60
Q

Key features of bicarbonate reabsorption in PCT

A

The apical/luminal membrane of tubular cells is impermeable to bicarbonate

The basolateral membrane is permeable bicarbonate

Sodium hydrogen antiporter secretes H⁺ which binds to bicarbonate

Carbonic acid dissociates and carbon dioxide moves into the tubular cell

Carbon dioxide then combines with water to form carbonic acid which dissociates to form bicarbonate and protons

In this instance H⁺ is recycled back into the tubular cell and bicarbonate is reabsorbed from the filtrate

If secreted, H⁺ binds to non-bicarbonate buffer at point 3 then H⁺ is excreted into the urine

61
Q

Osmotic gradient in renal medulla

A

The interstitial fluid in the renal medulla gets increasingly hyperosmotic.

The limits for the osmolarity of urine are species specific and determined by the osmolarity of the renal medulla.

In this animal, urine can concentrate up to 1200mOsm/l

62
Q
A

Liv vet med yr1 (14 decks)

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