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BDS 1 > Systems Physiology > Flashcards

Systems Physiology Flashcards

1
Q

What are the main functions of the skin?

A

Protection, sensation, thermoregulation, metabolic, physical and sexual identity

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2
Q

What are some of the protective functions of the skin?

A

Physical barrier to bacteria
Excessive dehydration, UV radiation
Physical, chemical, thermal insults
Penetration of drugs & chemicals

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3
Q

What are the metabolic functions of the skin?

A

Adipose tissue is a major energy store

Vitamin D synthesised in epidermis

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4
Q

What are the three layers of the skin?

A

Epidermis
Dermis - dense irregular CT, highly vascular, many sensory receptors
Hypodermis - loose CT contains adipose tissue

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5
Q

What type of epithelial cells make up the epidermis?

A

Stratified squamous

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6
Q

What are the four major layers of the epidermis?

A 
Stratum basale 
Stratum spinosum 
Stratum granulosum
Stratum corneum
(Stratum lucidum in v thick skin between SG & SC)
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7
Q

What is keratinocyte?

A

Epithelial cell that produces keratin

Is abundant in the epidermis and has abundant intercellular junctions (desmosomes and adherens)

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8
Q

Describe keratin

A

Family of fibrous structural proteins
Intermediate filament made of 4 protofilaments which are pairs of coiled coils of 2 a-helices
Acidic (1) and basic (2) types
Is abundant in stratum corneum in soft form (undergone keratinisation) S-S bonds of cysteine define soft/hardness

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9
Q

Describe the germ layer

A

Stem cells and transit amplifying cells sitting on basement membrane
SC - unlimited self renewal, TA - limited division before terminal differentiation

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10
Q

What is keratinisation?

A

Migration of keratinocytes, which become tightly bound by desmosomes, from basal to corneal layer

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11
Q

Describe the stratum spinosum

A

Very thick layer; at least 3-4 cells thick
Has numerous desmosomes giving cells prickly appearance
Prominent nuclei and cytoplasmic basophilia-active protein synthesis, highly expressed keratin

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12
Q

Describe stratum granulosum

A

2-3 cells thick
Large, numerous basophilic keratohyalin granules - filaggrin, involucrin
Synthesise glycoprotein granules - intercellular cementing substance
Cell death occurs at the outermost layer

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13
Q

Describe the stratum corneum

A

Dead, terminally differentiated cells with unique morphology and staining
Fused flattened cells lacking organelles, filled with mature keratin providing protective barrier of skin
Thick, cornified cell envelope beneath PM

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14
Q

Describe the dermis

A

Complex mix of macromolecules supplied by many blood vessels which provides strength and elasticity to skin
Acts a support for epidermis
Split into Papillary and reticular

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15
Q

Describe papillary dermis

A

Is loose CT
Loosely packed T3 collagen with elastin fibres on superficial layer
Contains many blood capillaries (vascular papillae)

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16
Q

Describe reticular dermis

A

Dense CT
Closely packed T1 collagen and elastin
Provides mechanical strength of skin
Hydrophilic gel but flexibility decreases with age
GS - amorphous matrix that embeds collagenous and elastic fibres, skin appendages
GAGs - hyaluronic acid, dermatan sulphates, chondroitin sulphates

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17
Q

What is the role of fibroblasts in the dermis?

A

Repair of dermis

Synthesis of collagen, elastin, proteoglycans

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18
Q

What is the pilosebaceous unit?

A

Hair follicle and sebaceous gland

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19
Q

What are the two types of hair follicle?

A

Vellus - body hair

Terminal - scalp, secondary sexual hair

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20
Q

Describe the structure of hair follicles

A

Dermal papilla in hair bulb at root, contains fibroblasts which control hair growth by supplying growth factors
Matrix - surrounding papilla, keratinocytes produce hair
Bulge further up contains hair follicle stem cells, also repair skin
Shaft - dead, exposed head of hair
Root - 5 concentric layers of epithelial; inner 3 form hair shaft, outer 2 form epithelial sheath

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21
Q

What are the 3 stages of the hair cycle?

A

Anagen - active growth phase
Catagen - regressive, shaft cut off from blood supply and cells
Telogen - resting, hair sheds off

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22
Q

Describe the sebaceous gland

A

Exocrine gland which is androgen (male sex hormone) sensitive
Enlarges during puberty causing acne
Mature sebocytes contain sebum, cell ruptures and sebum released into sebaceous duct and onto skin (lubricates skin and hair)

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23
Q

Describe the eccrine sweat gland

A

Excretory duct - 2 layers of smaller cuboidal cells

Compact secretory coil - single layer of large cuboidal/columnar cells

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24
Q

What is the composition of sweat and its function?

A

99% water, aides thermoregulation as evaporating water cools skin

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25
Q

Describe the apocrine gland

A

Large sweat glands - widely dilated lumen in coiled secretory portion
Present in axilla (underarms) and pubic region
Releases volatile milky, viscous fluid that is odourless BO produced by breaking down of fluid by bacteria
Not functional until puberty

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26
Q

Describe a melanocyte

A

Dendritic (antigen-presenting immune cell) cell in epidermis on BM
Produce melanin in melanosome - eumelanin (brown/black), pheomelanin (red/brown) - which is injected into keratinocytes
Protects against UV

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27
Q

Describe langerhan cells

A

Dendritic present in basal and spinous layers

Antigen presenting cell that is 1st line of defence, presents antigen to T lymphocytes

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28
Q

Describe merkel and mast cells

A

Merkel - in stratum basale, sensory perception (differences in texture)
Mast - in dermis, immune response, produces histamine

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29
Q

What is endochondral ossification?

A

Formation of bone during fetal development from hyaline cartilage (T2 collagen) model
Model provides rough shape of mature bone
Is typical of long bone formation, allows stresses to be handled during growth

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30
Q

Describe endochondral ossification

A

Cartilage model forms in embryo
Blood capillaries invade perichondrium converting to periosteum around centre of model
Bone collar (periosteal bone around diaphysis) produced by osteoblasts in periosteum
Chondrocytes at middle of diaphysis mature, hyper trophy and die, cartilage matrix calcified leaving spicules of calcified cartilage
Nutrient artery from periosteum enters diaphysis through bony collar, carries osteoblasts that lay down trabecular bone in place of calcified cartilage
Appositional growth of epiphysis, chondrocytes in centre mature and die. Calcification of this cartilage occurs
Blood vessel enters degenerating cartilage, osteoblast activity replaces calcified cartilage with bone

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31
Q

In postnatal growth how is bone shaft diameter increased?

A

Appositional growth - formation of bone on periosteal surface
Thickness is maintained by resorption of inner surface allowing diameter to increase while maintaining strength and weight of bone

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32
Q

Where does growth in length occur in long bones?

A

Epiphyseal growth plate - area between diaphysis and epiphysis allowing growth in length by interstitial growth
Grows from epiphyseal to diaphysis
Proliferation of cartilage in epiphysis thickens layer
Degeneration of cartilage and replacement with bone at diaphysis

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33
Q

What are the 5 zones of the epiphyseal growth plate?

A
  1. Resting - resting/reserve chondrocytes
  2. Growth - proliferating chondrocytes
  3. Hypertrophic zone - hypertrophying chondrocytes (increase in size of cells)
  4. Calcification - dying chondrocytes, calcification of cartilage
  5. Ossification - osteoblastic activity, cartilage resorbed replaced with bone
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34
Q

What is intramembranous ossification?

A

Bone formation within fibrous membrane

Is typical of flat bones (mandible, skull)

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35
Q

Describe intramembranous ossification

A

Mesenchymal cells within fibrous CT membrane cluster at multiple sites where they spontaneously differentiate into osteoblasts, secrete osteoid at centres of ossification
Osteoid matrix is calcified
Further osteoblast activity on surface of sites, small trabeculae from and fuse together producing trabecular bone (woven bone remodelled into lamellar bone)
Layer of compact bone covers core of trabecular bone
Appositional growth permits increase in size

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36
Q

What supplies blood to the periosteum and outer compact bone of diaphysis?

A

Periosteal arteries through Volkmann’s and Haversian canals

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37
Q

What parts of bone does the nutrient artery supply?

A

Inner portions of diaphyseal compact bone, trabecular bone, bone marrow

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38
Q

What are the epiphyseal and metaphyseal trabecular bones supplied by?

A

Epiphyseal and metaphyseal arteries

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39
Q

Why does bone remodelling occur?

A

Constantly occurs to skeleton
Repair fractures and micro-damage caused by normal activity
Functional demands of mechanical stress detected by mechanosensors i.e. tennis player will have stronger arm

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40
Q

How does bone remodelling occur?

A

Usually bone resorbed by osteoclasts, osteoblasts line surface and produce new lamellar bone

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41
Q

What factors can affect remodelling?

A

Mechanical stress
Demands of Ca homeostasis; parathyroid hormone usually inhibits bone formation but given intermittently will encourage formation; calcitonin directly binds to osteoclasts and limits their activity
Fracture/micro-damage

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42
Q

What are the three types of muscle and what are their shared characteristics?

A

Skeletal, cardiac, smooth

All contract, contain actin and myosin plus accessory proteins

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43
Q

Describe the appearance of smooth muscle

A

No striations
Central nucleus
Spindle shaped
Bundles of contractile proteins criss-cross cell, insert into focal densities (anchorage points in CM)

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44
Q

How is smooth muscle cell held and why?

A

Held by meshwork of laminae composed of T4 collagen binding cells into functional mass

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45
Q

What is the function of calmodulin in smooth muscle?

A

Senses increase in Ca triggering off contraction: Ca enters cell, Ca released from sarcoplasmic reticulum, binds to calmodulin, activates myosin heads to bind to actin

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46
Q

How is contraction in smooth muscle regulated?

A

Autonomic nervous system, hormones, local physiological conditions (high BP causes friction on surface of blood vessels, induces release of NO which causes vasodilation)

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47
Q

Do smooth muscle cells retain mitotic capability?

A

Yes - able to make more smooth muscle
Uterus during pregnancy
Fibroids (leiomyoma) - benign tumour of SM

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48
Q

Describe the appearance of cardiac muscle

A

Striated - actin and myosin in regular arrangement
Central nucleus
Long branched cardiac fibres - formed from linking muscle cells end-to-end, allows contraction in 1+ direction (twist)
Intercalated disks (specialised junctional system) - wavy to increase SA allowing lots of gap junctions to rapidly transfer electrical energy, allows contraction in syncytium (1 functional unit)

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49
Q

Can cardiac muscle regenerate?

A

No - cardiac muscle lacks steam cells, there is no regeneration after damage

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50
Q

Describe contraction in cardiac muscle

A

Similar to skeletal muscle

Under autonomic nervous system control

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51
Q

Define hypertrophy and hyperplasia

A

Hypertrophy - increase in size

Hyperplasia - increase in number

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52
Q

Describe the appearance of skeletal muscle

A

Striated - regular arrangement of actin and myosin
Multinucleated fibres - fusion of multiple cells
Peripheral nucleus

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53
Q

What are the regeneration capabilities of skeletal muscle?

A

Contain stem cells - able to repair self only if sarcolemma is intact
If damaged - region replaced with fibrocollagenous tissue

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54
Q

Describe the sarcolemma

A

Muscle cell PM
Extends transversely into muscle
Surrounds each myofibril at junction of A and I bands (T-tubules)
Between T-tubules - 2nd membrane system derived from SR
Forms membranous network around each myofibril allowing coordinated contraction

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55
Q

Describe contraction in skeletal muscle

A

Lack Ca - tropomyosin covers myosin binding sites on actin
Depolarisation - carried into muscle fibres via T-tubules
Ca release - from SR, binds to troponin causing conformational change and exposure of myosin binding head
Hydrolysis - myosin hydrolyses ATP changing shape of head, producing ATP + Pi
Contraction - myosin head binds to actin, pulls
Relaxation - myosin releases actin

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56
Q

What is a sarcomere?

A

Basic unit of muscle tissue of parallel interdigitating myosin (thick) and actin (thin) myofibrils
Runs from z-disk to z-disk
Contains titin a buffer of contraction to prevent over stretching

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57
Q

What are the two muscle fibre types?

A

Fast twitch and slow twitch
Average person will have 50/50
Sprinter more fast than slow
Marathon runner more slow than fast

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58
Q

What do chondro, osteo, blast, cyte mean?

A

Chondro: cartilage
Osteo: bone
Blast: immature
Cyte: mature

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59
Q

What is the role of CT?

A
  1. Binding and structural support
  2. Protection
  3. Energy storage (adipose)
  4. Insulation (adipose)
  5. Transportation (blood)
  6. Immunity (blood)
  7. Mineral storage (bone)
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60
Q

What is CT?

A

A primary tissue type: epithelial, connective, muscle, nerve

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61
Q

What are the 5 CTs?

A
  1. Fibrocollagenous tissues
  2. Adipose tissue
  3. Cartilage
  4. Bone
  5. Blood
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62
Q

What are the characteristics of CT?

A

Few cells compared to epithelia
Large amounts of ECM, usually made by its intrinsic cells
Common origin: mesenchyme cells

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63
Q

What are all cells of CT derived from?

A

Embryonic mesoderm

Some stem cells remain in adult (mesenchymal cells)

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64
Q

What are the 3 components of the ECM?

A
  1. Ground substance
  2. Structural glycoproteins
  3. Fibres
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65
Q

Describe the GS

A

Water/gel-like
Specific composition gives CT distinctive properties
Composed of polysaccharides +/- protein with water, solutes:
glycosaminoglycans: long, unbranded polysaccharide chains
proteoglycans: many GAGs linked to protein core

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66
Q

Describe the characteristics of GAGs and proteoglycans

A

-ve charge, open conformation retains water, +ve ions

hydrated gel which allows selective passage of molecules (nutrient diffusion)

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67
Q

Describe structural glycoproteins

A

Functional molecules
Abundant in living organisms
Many roles: linking, organising, catalysing
e.g. laminin, fibronectin (adhesion), fibrillin (elastic fibre formation), osteocalcin (bone mineralisation)

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68
Q

Describe the fibres of CT

A

Collagen and elastic fibres
Important for mechanic properties of CTs
Fibre precursors secreted by CT cells - fibres polymerise outside cell

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69
Q

Describe collagen fibres

A

Tensile strength, precursor tropocollagen
Many types (>19)
T1: thick bundles, very strong; dermis bone
T2: thin, interwoven fibres; cartilage
T3: delicate branching; reticulin fibres
T4: meshwork; basement membrane

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70
Q

Describe elastic fibres

A

Stretch and resilience, precursor tropoelastin
Elastic forms fibrils with fibrillin
arteries, skin, lung, cartilage

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71
Q

Describe fibrocollagenous tissues

A

Cell: fibroblast Roles: structural, supportive

Classed according to: amount, organisation, type of collagen

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72
Q

What are the 3 types of fibrocollagenous tissues?

A

Loose (areolar)
Dense
Reticular (loose but with T3)

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73
Q

Describe loose fibrocollagenous CT

A

Relative to GS relatively few fibres
Abundant viscous GS - hyaluronic acid (non-S GAG)
Organisation: little
T1 collagen with elastic fibres

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74
Q

Describe the cells and role of loose fibrocollagenous CT

A

Cells: fibroblasts, stem cells, adipocytes, defence immune cells
Role: physical, metabolic, defensive support

e.g. lamina propria: constituent of mucosa

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75
Q

Describe dense fibrocollagenous CT

A

Many fibres, little GS
Organisation: random (dense irregular), structure (dense regular)
T1 collagen, some elastic fibres

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76
Q

Describe the cells and role of dense fibrocollagenous CT

A

Cells: fibroblasts
Role: mechanical support, tensile strength

Irregular: dermis, capsules
Regular: tendon (M-B), ligament (B-B)

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77
Q

Describe reticular fibrocollagenous CT

A

Few fibres, little GS
Organisation: fine branching network
T3 collagen

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78
Q

Describe the cells and role of reticular fibrocollagenous CT

A

Cell: fibroblasts
Role: structural support in some highly cellular tissues

e.g. lymph nodes, spleen, liver, glands

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79
Q

Describe adipose tissue

A

Abundant adipocytes
Supporting loose CT (with fibroblasts)
Located beneath skin, around internal organs, bone marrow, breast issue

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80
Q

Compare the 2 types of adipose tissue

A

White vs brown
Unilocular (one space for lipid); multilocular
Adult; new born
Widespread; restricted
Energy store, shock absorber, insulator; heat source
-; rich in mitochondria

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81
Q

What is the function of cartilage?

A

Structural - solid but flexible, resists compression

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82
Q

What are the 3 types of cartilage?

A

Hyaline: most prevalent, many joint surfaces; T2
Elastic: outer ear, larynx; T2 and elastic
Fibrocartilage: T1 and T2, pubic symphysis

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83
Q

Describe the GS and cells of cartilage

A

GS: unique, proteoglycans containing chondroitin sulphate, keratan sulphate linked to fibres

Cells: chondroblasts form cartilage
Chondrocytes maintain cartilage

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84
Q

Describe the function of bone

A

Structural, shape, locomotion, supportive, protective, metabolic, synthetic
Highly organised and metabolically active

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85
Q

What is responsible for the hardness of bone?

A

Inorganic salts

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86
Q

Describe the ECM of bone

A

GS: osteoid (hard)
T1 - lamellae in mature bone
Mineralised (apatite crystals)

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87
Q

What cells are involved in bone CT?

A

Osteocytes: maintain bone
Osteoblasts: secrete osteoid form bone
Osteoclasts: resorb bone

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88
Q

What is the role of blood?

A

Metabolic support
Transport of molecules and cells to/from tissues
Defensive

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89
Q

Describe the ECM of blood

A

GS: fluid, plasma
Proteins: albumins, globulins, fibrinogen, regulatory proteins

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90
Q

Describe the cells in blood

A

Circulating blood cells formed in bone marrow: erythrocyte, neutrophil, eosinophil, basophil, lymphocyte, monocyte, platelets

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91
Q

What are the common features of epithelial?

A

Closely apposed cells with little/no intercellular materials
Membranes and glands
Membranes: sheets of cells covering external surface or line internal - protective function
Glands: specialised for secretion; down growth into underlying CT connection to surface (exocrine) or to vascular (endocrine)
Supported by CT
No blood vessels within
Line wet cavities (except skin)

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92
Q

Describe the functions of epithelial

A

Protection, sensation, absorption, digestion, secretion, excretion, cleaning

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93
Q

What is the basal lamina?

A

Layer of epithelium that separates epithelial from underlying CT

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94
Q

What is the function and structure of the basal lamina?

A

Supportive functions
Proteoglycans and collagen T3,4
Epithelium and CT both contribute to formation
anchor down epithelium to its loose CT (in dermis)

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95
Q

How are epithelia classified?

A

Number/arrangement of cells: simple (single layer), stratified (multi)
Shape of cells: squamous (flattened), columnar (H>W), square

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96
Q

Describe simple epithelia

A

Single layer of cells, all rest on BM
Cells vary in shape from flattened to columnar according to function
Thin, little mechanical stress protection
May have specialisations such as microvilli or cilia

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97
Q

Describe where simple epithelia are found

A

Absorptive/secretory surfaces

Minimum barrier to diffusion required

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98
Q

Describe simple squamous epithelia

A

Single layer flattened cells
Line surfaces involved in transport of gases (alveoli), fluids (blood vessels)
Series body cavities

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99
Q

Describe simple cuboidal epithelia

A

Single layer square shaped cells
Line small ducts, tubules that have secretory/excretory/absorptive function
e.g. bile duct, medulla, salivary

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100
Q

Describe simple columnar epithelia

A

Similar to cuboidal expect taller, elongated nuclei at base of cell
Absorptive/secretory surfaces
e.g. SI, stomach

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101
Q

Describe stratified epithelia

A

2+ layers of cells
Protective function
Not suited to absorption/secretion due to thickness
Degree and nature of stratification depends on type of stress
Can be keratinised (skin resist friction, bacteria infection, waterproof)

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102
Q

What layer(s) of cell is used to define classification?

A

Only the surface layer

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103
Q

Describe stratified squamous cells

A

Several layers thick (skin)
Matures progressively from basal layer - has cuboidal cells until surface
Degenerates when reaches surface, sheds off
Withstand moderate abrasion but doesn’t cope with desiccation (cervix) unless keratinised (skin)

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104
Q

Describe stratified cuboidal epithelia

A

2/3 layers of cuboidal cells
Line larger excretory ducts - salivary, sweat, pancreas
No absorptive/secretory function but robust lining

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105
Q

Describe pseudo-stratified epithelia

A

All cells rest on BM but not all reach surface, nuclei at different levels giving appearance of stratified
Ciliated or non-ciliated

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106
Q

Describe transitional epithelium

A 
Special from of stratified epithelium found in urinary tract
Withstand toxicity of urine
Accommodate distension (stretching)
In relaxed state: 4/5 thick, cuboidal
Stretched: 2/3 thick, flattened
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107
Q

Describe the structure of the mucous membrane

A

Composed of: epithelium, BM, lamina propria (loose CT), SM

Specialised cells: mucus secreting goblet cells, absorptive enterocytes

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108
Q

Describe the function and name the 2 types of glands

A

Epithelial structures which discharge secretory products
Composed of secretory portion and non-secretory portion

Exocrine: discharge via duct onto epithelia surface
Endocrine: secrete hormones directly into bloodstream, highly specialised

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109
Q

Describe the structure of exocrine glands

A

Excretory duct, secretory portion
Simple glands, few branches or compound, multiple branches
Secretory portions tubular or alveolar

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110
Q

What are the three types of exocrine secretory mechanism and secretions?

A

Mechanism: eccrine/merocrine, apocrine, holocrine
Secretions: mucous, serous (proteins/enzymes), sebum(lipids)

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111
Q

Describe the mechanism of eccrine secretion

A

Exocytosis
Secretory granules fuse to PM, secreted
e.g. eccrine sweat gland

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112
Q

Describe the apocrine secretion mechanism

A

Unbroken, membrane bound vesicles accumulate in apical cytoplasm, pinched off, cell loses part of PM
e.g. apocrine sweat gland (body odour)

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113
Q

Describe the holocrine secretion mechanism

A

Whole cell lysis, entire contents secreted, cells lost in process
e.g. sebaceous

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114
Q

Describe endocrine secretion

A

No duct
Supporting tissue thin, sparse (reticular CT) associated with rich blood supply
Cord and clump - most common
Follicle - thyroid

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115
Q

Describe chondroblasts

A

Immature
Form cartilage
Found in perichondrium fibrocollagenous tissue surrounding cartilage
Nutrient supply from outside

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116
Q

Describe chondrocytes

A

Mature
Maintain cartilage
Found in lacunae surrounded by cartilage

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117
Q

Describe hyaline cartilage

A

Found in trachea, bronchi, sternal ends of ribs, nasal septum, joints
Forms model template for long bone formation

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118
Q

Describe elastic cartilage

A

Similar to hyaline with large amounts of elastic fibres

Found in outer ear, epiglottis, larynx

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119
Q

Describe fibrocartilage

A

Alternating layers of cartilage matrix and collagen fibres - confers strength
Found in intervertebral disks, knee joint meniscus, symphysis pubis

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120
Q

Describe woven bone

A

Formed 1st after break/fracture
Mechanically weak
Random organisation of collagen

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121
Q

Describe lamellar bone

A

Mature - remodelled bone
Lamellae due to regular organisation of collagen
Mechanically strong
Compact or trabecular

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122
Q

Describe compact lamellar bone

A 
Bony columns (osteons) with central Haversian canals, convey blood to surrounding osteocytes 
Forms cortical shell of most bones (shaft of long bone)
Periosteum surrounds most of outer surfaces
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123
Q

Describe trabecular lamellar bone

A

Beams/spicules along lines of stress - strong but lightweight
No osteons: blood supply obtained from outer surfaces (surrounded by bone marrow)
Found in central medullary portions of most bones

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124
Q

Describe long bone structure

A

Proximal epiphysis
Metaphysis (epiphysis growth plate)
Diaphysis
Distal epiphysis

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125
Q

Describe an osteon

A

Lengthwise bony column in compact bone
Circular structure, run longitudinally with bone
Haversian canal carries bloody supply and nerves to osteocytes
Volkmann’s canal connect Harversian and periosteum (outer surface)
Lined by delicate tissue continuous with periosteum (endosteum) - inactive osteoblasts
Canaliculi: tiny canals that connect osteocytes to blood supply, allow communication, control osteoblasts

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126
Q

Describe the musculoskeletal wall of the thorax

A

Flexible

Consists of segmentally arranged vertebrae, ribs, muscles and the thernum

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127
Q

What are the three major compartments of the thoracic cavity?

A

Left pleural cavity
Right pleural cavity
Mediastinum

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128
Q

What is the thoracic cavity enclosed by?

A

Thoracic wall and diaphragm

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129
Q

What are the superior/inferior thoracic apertures?

A

Openings at top/bottom of thoracic cavity

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130
Q

Describe the superior thoracic cavity

A

Completely surrounded by skeletal elements
Body of vertebra T1 posteriorly
Medial margin of rib 1 each side
Manubrium anteriorly

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131
Q

What is the importance of the thoracic apertures?

A

Airtight to prevent O2 leakage

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132
Q

Describe the inferior thoracic aperture

A

Large, expandable
Margins made from bone, cartilage, ligaments
Closed by diaphragm
Passing structures pierce/pass posteriorly to diaphragm

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133
Q

What is the mediastinum?

A

Thick midline partition

Extends from sternum anteriorly to thoracic vertebrae posteriorly, from superior to inferior thoracic aperture

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134
Q

The pericardium and heart lie in which section of the mediastinum?

A

The middle

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135
Q

How do the lungs remain attached to the mediastinum?

A

Root formed by airways, pulmonary blood vessels, lymphatic tissues, nerves

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136
Q

What are the parietal and visceral pleura?

A

Parietal: pleura lining walls of cavity (outer layer)
Visceral: pleura lining surface of lungs (inner layer)

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137
Q

What lie in the intercostal spaces?

A

Filled by intercostal muscles

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138
Q

What is the role of the costal grove?

A

Provides protection for intercostal nerves, associated major arteries and veins

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139
Q

Which intercostal muscle is responsible for inspiration and which for expiration?

A

External intercostal muscle: inspiration

Internal intercostal muscle: expiration

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140
Q

What are bronchi?

A

Branches of the trachea which air enter and leaves lungs via

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141
Q

Describe the flow of blood to and from the lungs

A

Pulmonary arteries deliver deoxygenated blood to lungs from right ventricle
Oxygenated blood returns to left atrium via pulmonary veins

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142
Q

What is the hilum?

A

Point of entry and exit to lung

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143
Q

What is located within root and hilum of lung?

A 
Pulmonary artery
2 pulmonary veins
Main bronchus
Bronchial vessels
Nerves
Lymphatics
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144
Q

Describe division of the trachea

A 
2 bronchi - left and right 
Right is wider, smaller angle with trachea thus more likely to receive inhaled foreign bodies
4 lobar bronchi
16 segmental bronchi
Small bronchi
Terminal bronchioles
Respiratory bronchioles 
Alveolar ducts
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145
Q

Describe the features of alveoli that make them efficient at gas exchange

A

Thin cell wall

RBCs in close contact

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146
Q

Define ventilation

A

Movement of air in/out of lungs (breathing)

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147
Q

What are the boundaries of the upper respiratory system?

A

Nasal cavity to start of oesophagus and trachea

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148
Q

Define inspiration and expiration

A

Inspiration: pressure around elastic alveoli made low by expanding chest
Expiration: pressure increased by decreasing size of chest, compressing gas in lungs

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149
Q

Describe the flow of air

A

Only flow from high pressure to low pressure

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150
Q

What do lung muscles control?

A

Diameter of airways

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151
Q

What muscles control respiration?

A

Respiratory muscles - generate pressure differences

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152
Q

In quiet breathing which process is the only active part?

A

Inspiration

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153
Q

Explain expiration in quiet breathing

A

Passive result of elastic recoil of lungs - pull lungs and diaphragm back to resting position

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154
Q

What is the diaphragm?

A

Major respiratory muscle (not essential however)

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155
Q

What nerves innervated the diaphragm?

A

Phrenic

Cause diaphragm to flatten, descend creating negative pressure, drawing air into chest

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156
Q

What is the role of the intercostal muscles?

A

2 movements: increase diameter of chest, draw air into lungs by reducing pressure
Stiffen chest during inspiration preventing it being sucked in

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157
Q

Describe the 2 movements of the external intercostals

A

Pump-handle: anterior end of each rib elevated

Bucket-handle: diameter of chest increases by rib on either side raised from horizontal position

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158
Q

What nerves innervated the inner and innermost intercostals?

A

Segmental

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159
Q

What happens when the inner intercostals contract?

A

Pull ribs down, reduce diameter of chest

Reinforce spaces between ribs to prevent chest from bulging out during expiration

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160
Q

When do abdominal muscles contribute to expiration?

A

Only during heavy exercise

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161
Q

How to the abdominal muscles contribute to expiration?

A

Squeeze contents of abdomen up against the diaphragm, force up chest thus expelling air

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162
Q

Define intrapleural pressure

A

Pressure in small amount of liquid between parietal and visceral pleurae
Usually negative with respect to atmosphere

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163
Q

How are the lungs expanded?

A

By creation of negative pressure outside inflating lungs

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164
Q

Describe the interaction between the lungs and chest wall

A

Chest wall elasticity causing to spring outwards, lungs causing to collapse thus are locked together and expand/contract as single unit

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165
Q

What happens to the lungs if the thorax is punctured?

A

Air enters pleural space, pressure will increase causing lungs to collapse

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166
Q

What are the elastic properties of lungs caused by?

A

Elastic fibres and collagen in tissues, surface tension caused by alveolar-liquid interface

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167
Q

What is lung compliance (CL)?

A

Measure of easily lungs can be stretched

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168
Q

What is the compliance equation?

A

Change in V/change in pressure

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169
Q

How can diseases effect compliance?

A

Kyohoscoliosis: progressive spine deformity
Emphysema: destruction of elastic fibres, collagen causing increased compliance but lungs don’t deflate as easily

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170
Q

Define airway resistance (Raw)

A

Resistance to the flow of gas within the airways of the lung

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171
Q

What are the 3 types of obstructive pulmonary disease?

A

Reversible: reduction of airway diameter due to contraction of SM or swelling due to inflammation - asthma (hyperplasia)
‘Chronic’: blocking of airways by secretions - bronchitis
Chronic: collapse due to disruption of supporting parenchyma - emphysema

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172
Q

What are the types of airway flow?

A

Laminar: parallel, orderly, streamlined
Turbulent: chaotic

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173
Q

What are the main sites of airway resistance?

A

Vocal cords of larynx, open during inspiration, close during expiration
Nose (inflammation, cold)
Reduced resistance through mouth (exercise)

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174
Q

Using Poiseuille’s law explain resistance in lower respiratory tract

A

Law predicts major resistance would occur in smaller radius

Although each airway is small there is large number; total cross-sectional area increases down tracheobronchial tree

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175
Q

Explain resistance in bronchi and bronchioles

A

Almost no cartilage, innervated by SM
Increase in number of airways not yet exerted effects, cross-sectional area relatively small
Variable, under influence of neuronal and hormonal factors

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176
Q

What are the 2 circulatory systems?

A

Pulmonary

Circulatory

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177
Q

Describe the systemic circulatory system

A

High pressure developed in systemic arterial system provides driving force to perfuse all body tissues (except lungs)
Pressure: 120/80mmHg

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178
Q

Describe the pulmonary circulatory system

A

Output of right side of heart
Serves low pressure pulmonary circuit (lungs)
Pressure: 20/8mmHg

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179
Q

What is unusual about the pulmonary artery?

A

Only artery in body to carry deoxygenated blood

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180
Q

Why is the pulmonary circulatory system low pressure?

A

As the membrane separating capillaries and alveoli is very thin
High pressure would rupture membrane causing fluid to leak into alveoli

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181
Q

Describe the relationship between trachea division and diameter

A

Each time trachea splits into 2 diameter rapidly increases

Pulmonary vessels also double up to supply greater number of alveoli

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182
Q

Compare the flow of systemic and pulmonary circulation

A

Pulmonary flow is much greater than systemic

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183
Q

What are the 2 respiratory functions of pulmonary circuit?

A

Re-oxygenate blood

Remove CO2

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184
Q

What are the non-respiratory functions of pulmonary circuit?

A

Aid lung fluid balance
Angiotensin converting enzyme(ACE): convert angiostensin 1 to 2
Supply nutrients to lung tissue, alveolar ducts and alveoli
Blood reservoir: imbalance in perfusion can be absorbed by pulmonary

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185
Q

What is the blood flow at rest in alveolar capillary and explain the length

A

0.8s - 3x longer than gaseous transfer

During exercise when flow rate increased can still completely re-oxygenate blood

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186
Q

What is the function of distension in pulmonary blood vessels?

A

Keeps pressure low when cardiac output increases without damaging tissue

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187
Q

What are the 2 mechanisms that can lower pulmonary blood pressure?

A
  1. Dilating (distending): small increase in diameter can dramatically reduce resistance
  2. Recruiting: opening of vessels that are normally closed

Both decrease pulmonary resistance when cardiac output increases

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188
Q

What can happen to pulmonary arteries if alveolar pressure increases too much?

A

Can increase resistance and reduce blood flow as alveoli inflated so much constrict capillaries

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189
Q

Explain the pressure change between pulmonary artery and capillary

A

Small change

As small change in venous pressure can make a considerable change to driving force

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190
Q

Explain the function of pulmonary circulation as a blood reservoir

A

As vessels highly compliant accommodate large blood volume serving as reservoir for left ventricle
Useful when left ventricular output exceeds venous return
Cardiac output can be increased rapidly by drawing upon reservoir without requiring instantaneous venous return

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191
Q

Describe the function of bronchial circulation

A

Part of systemic circulation that supplies structures of lung including upper respiratory tract
Doesn’t reach terminal or respiratory bronchioles/alveoli

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192
Q

What is a pulmonary embolism and how does it effect circulation?

A

Blockage of pulmonary circulation by embolus/clot
Whole cardiac output passes through lungs thus major obstruction to circulation
R ventricle not designed for high pressure, can’t sustain blood flow
Mismatch between ventilation and perfusion causes arterial hypoxia
Reduced filling of L, circulation fails

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193
Q

How is perfusion and ventilation matched?

A

Fraction of alveolar ventilation is matched to fraction of cardiac output per fusing that alveolus

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194
Q

What is the ideal ventilation/perfusion ratio of the lungs?

A

Between 0.8-1.0

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195
Q

How is distribution of blood flow affected in the lungs?

A

Gravity
Alveolar gas pressure
Hypoxia pulmonary vasoconstriction

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196
Q

In the systemic circulation what determines blood flow?

A

High resistance arterioles that regulate blood flow through capillary beds

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197
Q

Describe the effects of gravity on the upright lung

A

Ventilation: 2x greater in base than in apex
Perfusion: 4x greater in base than in apex

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198
Q

What is the effect of alveolar gas pressure on capillaries?

A

If BP less than alveolar gas pressure capillary will be compressed

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199
Q

Explain how hypoxic pulmonary vasoconstriction promotes optimum V/Q

A

Systemic arteries dilate in response to hypoxia - increasing O2 delivery
Arterioles in lung constrict - direct blood flow away from less ventilated areas, maintaining V/Q matching
Promotes optimum V/Q for whole lungs by increasing V/Q in areas where it is lower than normal

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200
Q

Describe the effect of Symp innervation on pulmonary vessels

A

Release NAdr acts on a1 and a2 receptors

a1: vasoconstriction
a2: vasodilation

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201
Q

Describe the effect of vestigial M3 receptors on pulmonary vessels

A

ACh acts on M3 causing release of NO via NO synthase resulting in vasodilation as NO activates guanylate cyclase producing more cGMP which phosphorylates myosin

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202
Q

What is minute ventilation? (VI)

A

Vol. of air passing through lungs each minute

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203
Q

On average how many breaths do we take a min and what is their vol.?

A

12 breaths/min, 0.5L

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204
Q

Define tidal volume (VT)

A

Vol. air displaced during normal (quiet) inhalation and exhalation

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205
Q

What is the net flow of tidal volume?

A

0

Vol. breathed out = vol. breathed in

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206
Q

What are inspiratory reserve volume and expiratory reserve volume?

A

IVR: max. vol. inspired above VT (2/3L>VT)
EVR: max. vol. expired after VT expiration (1-1.5L>VT)

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207
Q

Define vital capacity (VC)

A

Total vol. air can be moved in 1 breath from full inspiration to full expiration

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208
Q

How is VC calculated?

A

VC = VT + IRV + ERV

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209
Q

What is functional residual capacity (FRC)?

A

Vol. air remaining in lungs after quiet expiration

Usually 3L

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210
Q

What is residual volume (RV)?

A

Vol. air remaining in lungs after full expiration
Cannot be expired
1.5L

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211
Q

What 3 factors influence static volumes?

A

Anatomy (size)
Elasticity of lungs, chest wall - exercise increases
Strength of respiratory muscles - exercise increases strength

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212
Q

What do changes in lung volume indicate?

A

Lung disease - early indicator

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213
Q

What is spirometry and what 2 things does it measure?

A

Most common pulmonary function test (PFT) measures lung function
Vol. and/or flow of air than can be in/exhaled

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214
Q

What is pulmonary ventilation?

A

Normal breathing

Air flowing into lungs during inspiration and out during exhalation

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215
Q

What 3 pressures are involved in pulmonary ventilation?

A
  1. Atmospheric
  2. Intra-alveolar
  3. Intrapleural
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216
Q

What is alveolar ventilation?

A

Vol. of gas per unit time that reaches alveoli and takes part in gaseous exchange

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217
Q

What is the importance of alveolar ventilation?

A

Insufficient ventilation (hypoventilation) and excess ventilation (hyperventilation) occur in many lung diseases

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218
Q

Define anatomical dead space

A

Vol. air in upper respiratory tract (mouth, pharynx, trachea, bronchi up to terminal bronchioles) that cannot be exchanged
Expired unchanged

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219
Q

What is alveolar dead space?

A

Vol. of air in alveolar with insufficient blood supply to effectively respire
Increases with age and disease

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220
Q

What is the physiological dead space?

A

Anatomical + alveolar dead space

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221
Q

What factors influence physiological dead space?

A

VL - determined by age, sex, training

Breathing pattern - high-freq. artificial respiration still ventilates alveoli

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222
Q

How is alveolar ventilation calculated?

A

(VT - anatomical dead space) * respiratory rate = alveolar ventilation L/min

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223
Q

What is the respiratory exchange ratio (respiratory quotient) (R)?

A

CO2 output/O2 uptake

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224
Q

What is the importance of the respiratory exchange ratio?

A

Estimate respiratory quotient (RQ) indicating which fuel (carbs/fat) supply body
If more O2 already present in molecule being oxidised then less has to be brought in thus fat diet R=1 as more O2 required

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225
Q

What factors can affect RQ?

A

Exercise: lactic acid in blood, forms carbonic acid with bicarbonate, liberates large vols. CO2 (high RQ)

Diabetes: poor metabolism of carbs, increases metabolism of fats (low RQ)

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226
Q

What are the 2 key tasks for the control of breathing?

A
  1. Establish automatic rhythm for contraction of respiratory muscles
  2. Adjust rhythm to accommodate:
    metabolic (arterial blood gasses, pH), mechanical (postural changes),
    non-ventilatory behaviours (sniffing, speaking)
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227
Q

What are the 3 centres of the pons?

A
  1. Pons
  2. Apneustic
  3. Pneumotaxic
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228
Q

What is the function of the pons?

A

Influence, modify activity of medullary centres

Smooth out inspiration, expiration transitions

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229
Q

Describe the function of the apneustic centre

A

Inspiratory cut-off info. from pneumotaxic centre and vagus integrated before projected onto DRG

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230
Q

What is the function of the pneumotaxic centre?

A

Act as cut-off neurons for inspiration

Stimulation causes earlier termination of inspiration, higher respiratory freq. reduced VT

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231
Q

Describe the dorsal respiratory group (DRG)

A

Located near root of nerve IX
Pacesetting respiratory centre by repetitive excitation/quiescence
Dormant during expiration

Input from apneustic centre, almost all peripheral afferents

Drives diaphragm, external intercostals, VRG neurons

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232
Q

Explain the sensitivity of chemoreceptors

A

Modify rate, depth of breathing to maintain arterial PaCO2 @ 40 mmHg
Sensitivity to changes in PaCO2 as O2 decreases more slowly in blood due to large reservoir attached to haemoglobin

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233
Q

What are the 2 types of chemoreceptors?

A
  1. Central

2. Peripheral

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234
Q

Describe central chemoreceptors

A

On ventral surface of medulla bathed in CSF
Respond to pH of CSF: CSF CO2 dissolves releasing H+ (via carbonic acid) which stimulates receptors causing increased depth, rate of breathing
Slightly responsive to increased PaCO2

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235
Q

Where are peripheral chemoreceptors found?

A

Carotid sinus

Aorta arch

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236
Q

Describe type 1 (glomus) chemoreceptors

A

Responsive to local changes in PO22, PCO2, pH
Prominent cytoplasmic granules
Associated with un/myelinated afferent fibres

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237
Q

Describe type 2 (sustenfacular) chemoreceptors

A

Interstitial cell wrapped around T1 and nerve endings

Function unclear

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238
Q

Explain how O2 can influence respiration

A 
Substantial drop (<60mmHg)
If CO2 not removed, chemoreceptors will become unresponsive to PCO2
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239
Q

Describe how pH can affect respiratory rate

A

Decreased pH, increases ventilation

Mediated by peripheral chemoreceptors

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240
Q

What are the 3 types of mechanoreceptors in lungs and airway?

A

Slowly adapting
Rapidly adapting
C-fibre endings

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241
Q

Describe pulmonary stretch receptors

A

In/close to SM of bronchial wall
Max. inflating of lung triggers reflex inhibiting inspiration thus limiting VT - important when central drive is increasing VT (exercise)
Increases respiration freq.

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242
Q

What are the 2 types of rapidly adapting stretch receptors (irritant receptors)?

A

Pulmonary C-fibres

Bronchial C-fibres

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243
Q

Describe pulmonary C-fibres

A

Present in walls of pulmonary capillaries
Sensitive to inflammation products - causes rapid shallow breathing
Sensitive to pulmonary vascular congestion + edema - causes dyspnea associated with LVF or severe exercise

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244
Q

Describe bronchial C-fibres

A

Present in conducting airways
Sensitive to inflammation products - causes bronchoconstriction and inc. airway vascular permeability
Stimulation causes hyperponea and reflex laryngeal constriction

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245
Q

What are the 2 examples of upper airway irritant receptors?

A

Nasal receptors

Pharyngeal and laryngeal receptors

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246
Q

Describe nasal receptors

A

Afferent pathway in trigeminal and olfactory nerves
Sneezing reflex
Diving reflex: water in nose causing, apnoea, laryngeal closure, bronchocontriction, bradycardia, vasoconstriction in skeletal muscle, kidney, skin

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247
Q

Describe pharyngeal and laryngeal receptors

A

Afferent pathway in laryngeal and glossopharyngeal nerves
Aspiration/sniff/swallowing reflexes
-be pressure induced abduction - ensure UAW patency during inspiration

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248
Q

Describe joint proprioceptors

A

Costovertebral joints contain mechanoreceptors sensitive to rib displacement
Sensation of dyspnoea arising from absence of chest movement when holding breath

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249
Q

Describe muscle stretch receptors

A

On stretching, discharge increases at rate dependant on rate of muscle movements
Responsible for increasing depth of breathing when made more difficult by inc. external elastic forces OR
resistance by breathing through narrow tube

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250
Q

What is a polymer and how are the made and broken down?

A

Long molecule consisting of many similar monomers
Built up in condensation reaction
Broken down by hydrolysis

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251
Q

What is the difference between nucleotides and nucleosides?

A

Nucleotides made of phosphate, sugar, base whereas nucleosides have no phosphate

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252
Q

What name is given to nucleotides with ribose or deoxyribose sugars?

A

Ribonucleotides

Deoxyribonucleotides

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253
Q

What are the 7 nitrogenous bases that can generate nucleosides?

A

3 purines: adenine, guanine, hypoxanthine
3 pyrimdines: cytosine, thymine, uracil
Nicotinamide

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254
Q

Describe the structure of purines

A

2 rings: 1 5 membered ring fused to 6 member ring

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255
Q

Describe the structure of pyrimdines

A

1 6 membered pyrimidine ring

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256
Q

How are nucleosides made and how can they form nucleotides?

A

Made by attaching base to a deoxy/ribose ring

Form nucleotides by phosphorylation with specific kinase

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257
Q

What are the 2 main roles of nucleotides?

A
  1. Short-term carriers of chemical energy (ATP)

2. Storage and retrieval of biological info. (nucleic acids - DNA)

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258
Q

What is Lesch-Nyhan Syndrome (LNS) and what does it cause?

A

Inherited disease caused by deficiency of hypoxanthine-guanine phosphoribosyltransferase
Causes build up of uric acid in body fluids - sodium irate crystals form in joints, kidneys, CNS, tissues leading to gout-like swelling and severe kidney problems

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259
Q

What is the function of hypoxanthine-guanine phosphoribosyltransferase?

A

Salvages purines from degraded DNA for purine synthesis

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260
Q

What is gout?

A

Painful condition caused by deposition of uric acid as needle like crystals in joints and/or soft tissue

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261
Q

What is asthma?

A

Chronic disease of airways characterised by:
Wheezing, breathlessness, chest tightness, nighttime/morning coughing

Widespread, variable airflow obstruction that is reversible either spontaneously or with treatment

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262
Q

Describe lung morphology in asthma

A

Bronchial inflammation
Oedema(build up of fluid), mucus plugging
Bronchospasm (sudden constriction)
Obstruction
Over inflation/Atelectasis (collapse of lung)
COPD

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263
Q

What 2 divisions is asthma separated into?

A

Extrinsic - antigen dependent

Intrinsic - exercise etc. (unclear)

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264
Q

Asthma is the interaction between what 3 components?

A

Cells: mast, eosinophils, macrophages
Mediators: histamine, prostaglandins, cytokines
Neuronal pathways: autonomic, sensory

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265
Q

Describe ParaNS innervation of the lungs

A

Muscarinic receptors
Bronchoconstriction
Inc. mucous secretions
Inc. ion transport

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266
Q

Describe SympNS innervation of the lungs

A

B2 receptors
Innervates blood vessels and glands NOT bronchial SM
Cause by circulating Adr (hormone), NAdr (NT)

Bronchodilation
Red. glandular secretions
Vasoconstriction

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267
Q

Describe non-adrenergic non-cholinergic innervation of the lungs

A

Mediator NO - bronchodilation

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268
Q

Describe sensory nerve innervation of the lungs

A

Non-myelinated C-fibres

Neurokinin A: bronchoconstriction
Substance P: inc. microvascular leakage/mucous secretion
Calcitonin gene-related peptide: vasodilation

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269
Q

Describe the activation of mast cells

A
  1. Directly activated by allergen cross link between 2 IgE receptors
  2. Rapid release of preformed and de novo mediators (histamine, prostaglandins, leukotrienes, oxidants, cytokines)
  3. Brochoconstriction, vasodilation, oedema

Can also be triggered by cold air, osmolality changes, exercise

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270
Q

What 3 processes does mast cell activation lead to?

A

Degranulation
Phospholipid metabolism
Gene transcription

271
Q

Describe macrophages

A

Infiltrate interstitial sites, lumen of bronchi
Ag/Ab interactions release cytokines (which are chemotactic)
Cause release of mediators from eosinophils
Role in antibody production

272
Q

Describe the activation of T-lymphocytes (Th2 cells)

A

Recruited, activated by dendritic cells (DC)
DC process allergen, present T-cell peptide to naive T-cell to activate Th2 cell - release cytokines
IL-4 activates B-lymphocytes to produce antibodies

Recruitment of eosinophils

273
Q

Describe basophils

A

Protein receptors on surface that bind IgE

Degranulate to release histamine, heparin, secrete lipid mediators (leukotrienes, cytokines)

274
Q

Describe eosinophils

A

Release granule derived basic proteins like major basic protein (MBP), eosinophilic cationic protein (ECP)
Cause endothelial damage and results in hyper-responsiveness of airways
Damage all cells - self and foreign

275
Q

What are the 5 ways in which the airways are remodelled?

A
  1. Thickening of sub-basement membrane
  2. Sub-epithelial fibrosis
  3. Airway SM hypertrophy, hyperplasia
  4. Blood vessel proliferation, dilation
  5. Mucous gland hyperplasia, hyper-secretion
276
Q

What are the 3 treatment areas of asthma?

A
  1. Prevent mediator release
  2. Relax contracted bronchial SM
  3. Reduce inflammatory response
277
Q

Name a drug that can inhibit mediator release and explain its action

A

Sodium Cromoglycate
Membrane stabiliser(?): reduces release from mast, eosinophils, eosinophils by blocking Ca2+ channels, interferes with Cl- channels
Reduces effects of PAF: red. bronchial hyper-responsiveness, vascular permeability

Given prophylactically (before event) - no serious side effects

278
Q

Describe drugs that relax SM

A

B-agonists: salbutamol(short)/salmeterol(long)
Administered as aerosol: rapidly absorbed, lower conc., fewer systemic side effects

Effects: bronchodilation, inhib. mediator release from mast, inc. mucociliary clearance, red. microvascular leakage

Mechanism: Qs, adenyl cyclase inc. cAMP, activate PKA

Side effects: muscle tremor/tachycardia, B receptor desensitisation

279
Q

Where are B2 receptors found?

A

SM, epithelial, mucous glands, vascular endothelium, mast, cells of inflammation

280
Q

Describe theophylline

A

Mechanism: PDE inhibitor, inc. cAMP, cGMP levels, Adenosine receptor antagonist

Pharmacokinetics: narrow therapeutic index, overdose manifests as dysrhythmias + convulsions, alcohol/smoking inc. clearance, age/liver disease/obesity red. clearance

Administered orally or rectally

281
Q

Describe the anticholinergic drug ipratropium bromide

A

Action: non-selective muscarinic receptor antagonist, blocks vagal effects on bronchial SM, mucous secretions, poor action against antigen and exercise induced asthma, some protection against cold air induced asthma

Pharmacokinetics: quaternary ammonium, poorly absorbed (stays in lungs), few anticholinergic side effects, by aerosol

282
Q

Describe the anti-inflammatory beclomethasone dipropionate

A

Mechanism: binds intracellular receptors which bind to target genes in nucleus, modulate transcription, inc. production of lipocortin (inhibit PLA), red. 5-lipoxygenase synthesis, dec. cytokine/receptor production, red. no/activity of inflammatory cells and microvascular leakage

Side effects: adrenal, hypothalamic suppression (slowly reduce intake before coming off drug), oropharyngeal candidiasis, stunted growth (closure of epiphysis growth plate)

283
Q

What are leukotrienes?

A

Mediator released by mast, eosinophils, basophils
Associated with bronchoconstriction, inc. vascular permeability, inc. mucous secretion, attract and activate inflammatory cells

284
Q

Describe montelukast and zileuton and their effects

A

Montelukast: leukotriene D4 receptor comp. antagonist, maintenance treatment of asthma
Zileuton: 5-lipoxygenase inhib., inhib. leukotriene synthesis

Effects: inhib. bronchoconstriction, anti-inflammatory effects

285
Q

Name and describe an immunomodulator

A

Omalizumab - monoclonal antibody that binds IgE

Maintenance/prophylaxis against allergic asthma
By binding free IgE on mast cells, blocks release of histamine/leukotrienes
By reducing free IgE, leads to IgE-receptor down regulation further reducing allergic reactions

286
Q

What is a possible side effect of omalizumab?

A

Anaphylaxis - systemic vasodilation, inc. microvascular leakage, bronchoconstriction, drop in BP

287
Q

How is vascular permeability inc.?

A

Inc. size of fenestrations

288
Q

At which generation of division does respiration begin?

A

17 - respiratory bronchioles

289
Q

BOB Obstructed the Overseeing COPs

A

Lung morphology of asthma

Bronchial inflation 
Oedema, mucus plugging
Bronchospasm
Obstruction
Over inflation/atelectasis (collapse)
COPD
290
Q

Treacle Syrup Always Beats Maple

A

Asthma remodelling of airways

Thickening of subbasement membrane
Subepithelial fibrosis
Airways SM hypertrophy, hyperplasia
Blood vessel proliferation, dilation
Mucous gland hyperplasia, hypersecretion
291
Q

ASTHMA

A

Treatment of asthma

Anticholinergics (ipratropium bromide) and adrenergics (B2 agonist - salbutamol)
Steroids - beclomethasone diproprionate
Theophylline
Hydration
Monoclonal antibodies - omalizumab
Antagonists of leukotrienes - Montelukast, Zileuton

292
Q

What are the 4 specialities of RBCs specific for its function?

A
  1. No nuclei or organelles
  2. Biconcave shape: high surface/vol ratio
  3. Forms stacks: smoothes flow into narrow blood vessels
  4. Spectrin (MP) allows bend and flex into small capillaries
293
Q

What is RBC count?

A

Number of red blood cells in 1 microlitre whole blood

294
Q

What is haematocrit?

A

Percentage of RBCs in centrifuged whole blood

295
Q

What is the diameter of RBCs?

A

7.8 micrometres

296
Q

Explain cooperativity in haemoglobin

A

O2 binding to 1 subunit causes conformation change that increases subunit 2 affinity for O2, increases 3 and so on…

297
Q

Define allosterism

A

Change in activity and conformation of an enzyme resulting from binding of compound to allosteric binding site (not active site)

298
Q

What are the 2 haemoglobin states?

A

Tense (T) and relaxed (R)

299
Q

Compare the T and R states of haemoglobin

A

R higher affinity for O2

In absence of O2 T more stable, in O2 R stable so make conformation change

300
Q

What is the name for haemoglobin when no O2 is bound?

A

Deoxyhaemoglobin

301
Q

What is the name for haemoglobin when O2 is bound?

A

Oxyhaemoglobin

302
Q

What is the name for haemoglobin when Fe is oxidised and no O2 is able to bind?

A

Methaemoglobin

303
Q

Compare the affinities of CO, NO and O2 for Fe2+

A

CO, NO higher affinity so can displace O2

Accounts for toxicity

304
Q

What is the RBC count in M and Fs?

A

M: 4.5-6.3 million
F: 4.0-5.5 million

305
Q

What is the haemoglobin content for M and F?

A

M: 14-18 g/dL
F: 12-16 g/dL

306
Q

What is the haematocrit of M and F?

A

M: 40-54%
F: 37-47%

307
Q

What is the most important factor in determining saturation of Hb?

A

O2 partial pressure

308
Q

What is important about the saturation level at resting tissue O2 partial pressure?

A

75% saturation means there is reserve capacity

309
Q

Define homotropic and heterotropic effectors

A

Effectors: small molecules that influence O2 binding to Hb
Homotropic: +ve effector
Heterotropic: -ve effector

310
Q

Give an example of a heterotropic effector and explain how it works

A

2,3-bisphosphoglycerate
Stabilises T state (low O2 affinity) by binding to central pocket of deoxyhaemoglobin
Causes dissociate shift to right i.e. favour supplying O2 to tissue

311
Q

When is 2,3-BPG conc. inc.?

A

Hypoxia: inc. amount of O2 dissociated to tissue

312
Q

Explain the physiological importance of HbF having a greater affinity for O2 than HbA

A

If had same affinity O2 would not diffuse

HbF having higher affinity allows extraction of O2 from maternal circulation and offloading of CO2 from HbF

313
Q

Describe the effects of pH, PCO2 and temp. on O2 binding

A

pH: dec. pH/inc. H+ inc. O2 dissociation by altering Hb structure. O2 usually offloads H+ so inc. H+ offloads O2

PCO2: CO2 offloads O2 from Hb, high H+ conc. due to high CO2

Temp: inc. temp. offloads O2 from Hb, exercise inc. temp to inc. O2 availability

314
Q

What 3 ways is CO2 transported in the blood and by what %?

A

Dissolved - 7%
Carbamino compounds - 23%
Bicarbonate - 70%

315
Q

Describe external respiration/pulmonary respiration

A

O2: diffuse from alveolar air to pulmonary capillaries
CO2: diffuse from pulmonary capillaries into alveolar air

316
Q

Define O2 carrying capacity, O2 content and O2/haemoglobin saturation

A

Carrying capacity: amount of O2 in 1L blood in equilibrium with room air

Content: amount O2 carried by 1L blood at any given PO2

Saturation: % of carrying capacity at any given PO2

317
Q

What 4 things is rate of gas diffusion dependent on?

A
  1. Partial pressure difference
  2. Distance
  3. Surface area
  4. Molecular weight and solubility
318
Q

Why is arterial PO2 slightly lower than alveolar PO2?

A

Physiological shunt

Blood from bronchial circulation enters pulmonary vein

319
Q

Explain the Haldane effect

A

Deoxygenated blood carries more CO2 than oxygenated blood

  1. Hb transports more CO2 than HbO
  2. Hb buffers H+, removing H+ from solution promoting conversion of CO2 to HCO3- via carbonic anhydrase
320
Q

Describe gas exchange in the pulmonary capillaries

A
  1. O2 diffuse into RBC, displace H+ from Hb-H
  2. HCO3- enter, react with H+ to form H2CO3 which dissociates to CO2 and H2O
  3. O2 displaces CO2 from Hb-CO2
  4. CO2 diffuses into alveolar space
  5. Cl- exit RBC to maintain electrical balance
321
Q

Describe gas exchange in systemic capillaries

A
  1. CO2 diffuse into RBC from tissue cell, react with H2O to form H2CO3 via carbonic anhydrase, dissociate to H+ and HCO3- which exits cell
  2. Some CO2 displace O2 from Hb-O2 forming Hb-CO2
  3. H+ displace O2 from Hb-O2 forming Hb-H (Bohr)
  4. O2 diffuse out of blood into tissue cell
  5. Cl- shift to restore electrical balance
322
Q

What is the mediastinum?

A

Space between pleural cavities, occupies centre of thoracic cavity

323
Q

What is the pericardium?

A

Fluid filled sac that surrounds the heart and great vessels
2 layers
Serous: thin, 2 parts
Fibrous: rough CT outlayer

324
Q

What are the 2 parts of the serous layer of pericardium?

A

Parietal: lines inner surface of fibrous pericardium
Visceral: adheres to heart, forms outer covering

325
Q

What are the 4 function of the pericardial fluid?

A

Acts as shock absorber by reducing friction between membranes
Keep heart contained in chest cavity
Prevent over expanding when blood vol. inc.
limit heart motion

326
Q

What is the difference between the L and R ventricle wall size? Why is it important?

A

L ventricle wall much thicker as requires much larger pressure to pump blood around whole body

327
Q

What are sulci?

A

Grooves on the surface of the heart due to the partitions that separate the heart into 4 chambers

328
Q

What are the 3 sulci of the heart?

A
  1. Coronary sulcus: circles the heart, separates atria from ventricles
  2. Ant. and post. interventricular sulci: separate ventricles
329
Q

Describe the structure of the heart

A

4 chambers: 2 atria and 2 ventricles
Atria collect blood and pump into ventricles
L ventricle pumps blood to body
R ventricle pumps blood to lungs

330
Q

What is the function of chordae tendinae?

A

Stabilise heart and prevent back flow of blood

When contracted, close valve preventing prolapse and back flow

331
Q

What are the 4 heart valves and what types do they fall under?

A

Semilunar: pulmonary, aortic
Atrioventricular: mitral, tricuspid

332
Q

What is the function of heart valves?

A

Ensure uni-directional flow by preventing back flow

Tricuspid: R ventricle to R atrium
Mitral: L ventricle to L atrium

Pulmonary: pulmonary artery to R ventricle
Aortic: aorta to L ventricle

333
Q

What are the heart sounds causes by?

A

Closure of valves

334
Q

What are the 2 heart sounds and how are they caused?

A

S1 (lub): turbulence from closure of mitral and tricuspid valves at start of systole

S2 (dub): closure of aortic and pulmonary valves, end of systole

335
Q

What are 3 common valve diseases and what are their characteristics?

A

Incomplete: blood flows back into chamber
Stenosis: restricted valve impedes flow from chamber
Calcified aortic valve: narrowed and densely calcified

336
Q

What is the cardiac skeleton and what is its function?

A

Dense CT rings surrounding and connecting valve bases

Separate and electrically insulate atria from ventricles
Provide site of attachment for cusps
maintain integrity of openings
Prevent movement of valves

337
Q

When and how do the coronary vessels fill w/ blood?

A

During diastole

Aorta distended during systole and contracts at end
This forces blood in both directions: towards body and back towards heart
Aortic valve prevents back flow into L ventricle
Forces blood down coronary arteries
Thus most coronary blood flow occurs during diastole

338
Q

How is blood flow regulated?

A

By need: inc. O2 consumption and cardiac activity inc. in coronary blood flow proportionate to inc. in O2 consumption

339
Q

What 2 molecules can regulate coronary blood flow?

A

Andosine: mediator of active hyperaemia and autoregulation - metabolic coupler of O2 consumption and coronary blood supply

NO: stimulates soluble adenylate cyclase to produce more cGMP causing vasodilation

340
Q

What is angiogenesis and what is its importance?

A

Inc. number of new parallel blood vessels

Red. vascular resistance within myocardium
New vessels and collateralisation of vessels inc. coronary blood flow

341
Q

What is Ischemic heart disease?

A

Condition where blood flow to heart is restricted caused by plaque narrowing blood vessels
Less blood and O2 reaches heart
If cut off: necrosis i.e. heart attack

342
Q

What is the clinical relevance of Ischemic artery disease?

A

Patients may present w/ jaw/toothache

Treatment may provoke symptoms or acute complications

343
Q

How is the heart muscle supplied with blood?

A

2 coronary arteries arise from aorta supply heart
Start at base and have branches reaching apex
Branch into smaller vessels that penetrate into muscle

344
Q

Describe the structure of cardiac muscle

A

Long, thin myofibrils connected via gap junctions
Myocytes (cardiac muscle fibres) organised in branched mesh work running in various directions
Intercalated discs: site of thickening of sarcolemma where cells join

345
Q

What is the role of cardiac muscle?

A

Contract in a coordinated and rhythmic manner, cannot enter tetany as will stop heart function
Myocytes form electrical/functional syncytium allowing cells to contract synchronous fashion

346
Q

What is the resting potential of cardiac muscle cell?

A

-85mV

347
Q

Describe the flow of K+ in a cardiac muscle cell

A

Flows out down conc. gradient

Flows in down electrical gradient

348
Q

Why is K+ the greatest influencer of RMP in cardiac muscle?

A

Substantial K+ gradient

Membrane relatively permeable

349
Q

Describe the 5 phases of an AP in a ventricular myocyte

A

Phase 0: rapid depolarisation; Na+ channels causing influx of Na
Phase 1: inc. K+ permeability, flows down electrochemical gradient at inc. rate
2: simultaneous opening of VGCaCs and inward flow of Ca2+ resulting in plateau of MP (prevent repolarisation)
3: K efflux > Ca influx causes inactivation of Ca channels, inc. opening of K channels allows MP to fall
4: return to RMP, AP start again from MP

350
Q

What is the absolute refractory period?

A

Period when new AP cannot be generated as Na channels remain inactivated after closing at end of phase 0

351
Q

What is the relative refractory period?

A

From about -50mV to RMP, AP can be triggered but requires greater stimulation

352
Q

Describe the 3 phases of sinoatrial node AP

A

Phase 0: depolarisation; after hyperpolarisation slow Na channels open causing slow influx of Na, AP generated opening Ca channels and Ca influx

3: repolarisation; K channels open causing K efflux
4: unstable RP; gradually depolarises due to Na influx and dec. K efflux

353
Q

What are the main differences between SAN and ventricular APs?

A

SAN generated by Ca rather than Na
No phase 1 or 2
No plateau, need AP to fire

354
Q

Describe the transmission of AP throughout the heart

A

Beings in SAN, high in R atrium
Spreads across R and L atrium via Bachmann’s bundle, causing contraction
Enters AVN, acts as conductor of impulses from atria to ventricles
Conducts slowly allowing ventricles to refill
Impulse travels from AVN to His bundles which subdivide into Purkinje conducting system resulting in almost simultaneous contraction of ventricles

355
Q

Explain the main waves of a electrocardiogram

A

P: AP through atria, depolarisation SAN
QRS complex: AP through ventricles, depolarisation
T: repolarisation of ventricles

356
Q

What is the function of the cardiovascular system?

A
  1. Rapid supply of O2 and nutrients
  2. Rapid waste removal
  3. Control: body temp, hormone distribution
357
Q

Define flow rate and velocity

A

Rate: volume per unit time
Velocity: distance per unit time

358
Q

Compare total flow and flow volume

A

Total: constant throughout CVS

Flow volume: constant between serial segments

359
Q

What 2 things is resistance in blood caused by?

A
  1. Between blood and internal surface of vessel

2. Between blood constituents (viscosity)

360
Q

What is the importance of Poiseulle’s law?

A

Resistance inversely proportional to 4th power radius

50% dec. in diameter will cause 16 fold inc. in resistance

361
Q

What is the important of the pressure differences between arteries and veins?

A

Causes blood to flow

362
Q

What maintains the pressure difference between arteries and veins?

A

Heart maintains high pressure in arteries

Vessels maintain low pressure in veins

363
Q

How is pressure regulated?

A

Proportional to resistance

If resistance inc. pressure will drop proportionally to maintain blood flow

364
Q

What is blood flow proportional to?

A

4th power radius

365
Q

What are the 2 types of blood flow?

A
  1. Laminar

2. Turbulent

366
Q

Describe laminar flow

A

All particles flowing parallel to vessel wall

Particles in centre flow fastest

367
Q

Describe turbulent blood flow

A

Irregular path, may develop whirlpools in vessels

Causes vibrations heard as murmurs

368
Q

What is the critical velocity?

A

Velocity at which blood flow transitions from laminar to turbulent

369
Q

What 4 factors inc. the likelihood of turbulent flow?

A
  1. Flow velocity inc.
  2. Vessel radius inc.
  3. Blood density inc.
  4. Blood viscosity dec.
370
Q

How is blood viscosity determined?

A

By the haematocrit: percent blood volume which is RBCs

371
Q

What are the 3 layers of blood vessels?

A
  1. Tunica intima
  2. Tunic media
  3. Tunica adventitia
372
Q

Describe the tunic intima

A

Inner layer
Endothelial cells
Acts as barrier between blood and vessel
Filtration controls passage of WBCs

373
Q

Describe the tunica media

A

2 layers of elastic tissue: internal and external sandwich layer of SM
Mechanical strength
SM allows altering of diameter

374
Q

Describe the tunica adventitia

A

Layer of CT containing fibrous tissue
Holds blood vessel in place, mechanical strength and prevent over-expansion
Small vessels that supply large vessels pass through this layer

375
Q

Compare large and small arteries

A

Large: composed of fibrous (collagen) and elastic tissue
Elastic so expand and contract during cardiac cycle

Small: less fibrous, more SM
More involved in circulatory control

376
Q

Describe arterioles

A

SM major component, contraction regulated

377
Q

Describe capillaries

A

Single layer of endothelial cells
No tunica media or adventitia
Site of exchange of nutrients and waste between blood and interstitial fluid

378
Q

Describe venules

A

Endothelial lining and small amount of fibrous tissue

379
Q

Describe veins

A

Elastic and fibrous tissue, small amount of SM
V distensible: if pressure inc. will distend easily
Special properties: valves prevent back flow of blood

380
Q

What 4 factors influence venous return?

A
  1. Gravity: detrimental when standing to venous return
  2. Inc. exercise, depth and rate of breathing
  3. Skeletal muscle pump
  4. Abdomino-thoracic pump
381
Q

Explain how the skeletal muscle pump inc. venous return

A

Veins in limbs located between muscle blocks and contain valves
When muscle contracts pinches vein pushing blood back to heart

382
Q

Explain how the abdomino-thoracic pump inc. venous return

A

Great veins and atria exposed to intrathoracic pressure

Is usually negative, becomes more so during inspiration allowing veins to expand easing flow of blood to heart

383
Q

Describe the control of cardiac output

A

Inc. in HR will produce proportionate inc. in CO as long as venous return is inc. to provide blood
If HR >180bpm, CO will dec. as too fast to fill ventricles thus stroke vol. red.

384
Q

How does regulation of CO change during exercise?

A

Mild exercise: small changes in CO achieved by changes in HR and stroke vol
Heavy exercise: further inc. CO achieved by inc. HR

385
Q

Describe how SNS innervation controls HR

A

SNS fibres on R of body innervate SAN
NA act on beta receptors in SAN
Inc. rate of phase 4 depolarisation, threshold reached quicker, inc. rate of firing

SNS fibres of L innervate ventricles, related to cardiac contractility

386
Q

Explain how PSNS fibres controls HR

A

R and L vagus nerve innervate AVN and SAN
Ganglion on cardiac surface or in heart
Postganglionic fibres release ACh, act on muscarinic receptors in SAN
Red. intracellular signals, red. rate of depolarisation and slow HR

387
Q

Define end-diastolic volume and end-systolic volume

A

EDV: blood in ventricle prior to contraction
ESV: blood remaining in ventricle post contraction

388
Q

What 3 factors influence EDV?

A
  1. Filling pressure: inc. pressure inc. EDV
  2. Filling time: inc. time inc. EDV; inc. HR dec. EDV
  3. Compliance: easier to distend inc. EDV
389
Q

What 4 factors influence ESV?

A
  1. Preload: stretching and vol. before contraction, inc. EDV inc. stoke vol
  2. Afterload: factors against ejection, inc. afterload inc. ESV
  3. HR: more Ca available, dec. ESV
  4. Contractility: +ve iontropes inc. Ca, dec. ESV
390
Q

Define inotrope

A

NT/hormone/drug that alters force of contraction of heart

+ve: inc. contractility

391
Q

Describe right sided heart failure

A

Characterised by inability to pump blood to pulmonary circuit
Lead to build up of blood in systemic system: Edema, swellings
Causes: L sided heart failure, chronic bronchitis, emphysema

392
Q

Describe L sided heart failure

A

Inability to pump blood in systemic system
May become tired quickly as tissues lack O2, pressure build up in lung veins lead to accumulation of fluid in lungs resulting in breathlessness and pulmonary edema
Causes: heart attack, blockage of arteries, high BP, leaky/narrow valves

393
Q

What 2 things does maintaining BP require?

A
  1. Cooperation of heart, blood vessels and kidneys

2. Supervision of brain

394
Q

What are the 3 main factors affecting BP?

A
  1. CO
  2. Peripheral resistance
  3. Blood vol
395
Q

Define intrinsic and extrinsic autoregulation

A

Intrinsic: immediate response to changes in venous return, alters stroke vol.

Extrinsic: reflex control mediated by nerves of ANS and hormones, alter stroke vol and HR

396
Q

What is the Frank-Starling law?

A

Within physiological limits, the heart pumps all blood that comes into it w/o allowing accumulation of blood in vessels

397
Q

Describe short and long term control of BP

A

Short
Mediated by NS and blood borne chemicals
Counteract fluctuations in BP by altering CO and PR

Long
Regulate blood vol.

398
Q

Describe short term neural controls of BP

A

Operate via reflex arcs involving: baroreceptors; vasomotor centres of medulla and vasomotor fibres; vascular SM

Controls of PR: alter blood distribution; maintain mean atrial pressure by altering vessel diameter

399
Q

Describe the short term vasomotor controls of BP

A

Vasomotor centres
Cluster of sympathetic neurons in medulla that oversee changes in vessel diameter
Maintain blood vessel tone by innervation vascular SM especially arterioles

Cardiovascular centre
vasomotor centre + cardiac centres
Cardio inhibitory and cardio excitatory integrate BP control by altering BP and vessel diameter

400
Q

Describe the baroreceptor-initiated reflexes in short term control of BP

A

Inc. BP stimulates cardio inhibitory centre to inc. parasympathetic and dec. sympathetic effects: inc. vessel diameter; dec. HR, CO, PR, BP

Dec. BP stimulates cardio acceleratory centres to: inc. CO, PR; also stimulates vasomotor centre to dec. vessel diameter

401
Q

Describe the chemical controls for short term BP control

A

BP regulated by chemoreceptors (carotid and aortic bodies) sensitive to changes in O2 and CO2
Reflexes that regulate BP integrated in medulla
Higher brain centres (hypothalamus, cortex) modify BP via relays to medullary centres

402
Q

Describe the long term controls of BP

A

Vol. receptors: alpha and beta type stretch receptors in L atrium
Alpha: detect atrial systole and HR
Beta: detect ventricular systole and atrial vol.

Atrial stretch activates beta fibres, will have direct neuronal effect: inc. HR; dec. sympathetic tone to kidneys: inc. filtration and urine formation; dec. vasopressin production; cause atria to produce atrial natriuretic peptide: vasodilator and dec. Na reabsorption

Dec. blood vol

403
Q

What are the 4 effects beta stretch receptors have?

A
  1. Inc. HR
  2. Dec. sympathetic tone to kidneys: inc. filtration and urine formation
  3. Dec. vasopressin (ADH) production
  4. Cause atria to make atrial natriuretic peptide: vasodilator and dec. Na reabsorption
404
Q

What are 4 chemicals that inc. BP?

A

Adrenal medulla hormones: NA, AD
ADH: vasoconstriction in extremely low BP
Angiotensin II: intense vasoconstriction
Endothelium derived factors: endothelin, vasoconstriction

405
Q

Describe the anatomy of the microcirculation

A

Small arteries
First order arterioles: muscular walls, sympathetic nerves
Terminal arterioles (precapillary sphincters): SM, few nerves
Capillaries: capillary bed
Venules: metarterioles may bypass capillaries when blood needs to be redistributed such as during exercise

406
Q

Describe the capillaries

A

Smallest blood vessels, connect arterial outflow to venous return

Microcirculation: flow from metarteriole through capillary bed into post-capillary venule
Exchange vessels: blood and interstitial fluid
Lack tunica media and adventitia

407
Q

Describe capillary beds

A

Arise from single metateriole
Vasomotion: intermittent contraction and relaxation
Throughfare channel: bypass capillary bed

408
Q

Describe the 4 active function of capillary endothelium

A
  1. Prostacyclin: relaxation of vascular SM
  2. NO: relaxation
  3. CO: relaxation
  4. Endothelin: contraction
409
Q

What is the passive function of capillaries?

A

Exchange of CO2, O2, H2O, nutrients between blood and interstitial fluid by osmosis, diffusion and filtration

410
Q

What are the 3 types of capillary?

A
  1. Continuous
  2. Fenestrated
  3. Sinusoidal
411
Q

In which 6 locations are continuous capillaries found?

A
  1. Skin
  2. lung
  3. fat
  4. muscle
  5. heart
  6. brain
412
Q

Describe continuous capillaries

A

Endothelial cell and basal lamina do not form openings

413
Q

In which 2 locations is fenestrated capillaries found?

A
  1. Kidney

2. Gut

414
Q

Describe fenestrated capillaries

A

Endothelial cell body forms small openings

Allows components of blood and interstitial fluid to bypass endothelium

415
Q

In which 3 locations are sinusoidal capillaries found?

A
  1. Liver
  2. Spleen: breakdown of red blood cells
  3. Red bone marrow
416
Q

Described sinusoidal capillaries

A

Formed by fenestrated endothelial cells and incomplete basal lamina
From large, irregular vessels
Found where free exchange of substances/cells is advantageous

417
Q

What are the 3 methods of transport across the capillary bed?

A
  1. Diffusion: most important
  2. Transcytosis
  3. Bulk flow
418
Q

Describe diffusion across capillary bed

A

Down conc. gradient: O2/nutrients into interstitial fluid, CO2/waste into blood

Can cross capillary wall through fenestrations, intracellular clefts, endothelial cells:
Most plasma proteins can’t cross except in sinusoidal when proteins and blood leave
In BBB tight junctions limit diffusion

419
Q

Describe transcytosis in capillary bed

A

Transport of small quantities of substance

Substance in blood plasma enclosed within pinocytotic vesicles and enter endothelial cells by endocytosis, leave through exocytosis
Important for large, lipid-insoluble substances that can’t cross capillary in any other way

420
Q

Describe bulk flow in capillary bed

A

Passive process in which large numbers of ions, molecules, particles in fluid move together in same direction
Based on pressure gradient

Important for regulation of relative volumes of blood and interstitial fluid

421
Q

Describe the flow of molecules in filtration and reabsorption

A

Filtration: from capillaries into interstitial fluid
Reabsorption: from interstitial fluid into capillaries

422
Q

Compare fluid flow at the arterial and venous end of capillaries

A

Arterial: hydrostatic pressure greater than oncotic pressure resulting in net filtration pressure of 10mmHg, net filtration

Venous: OP greater than HP resulting in NFP of -8mmHg thus net reabsorption

423
Q

What can happen if ECF levels are not regulated?

A

Oedema: excessive accumulation of ECF as result of high BP; venous obstruction; leakage of plasma proteins into ECF

Myxoedema: excessive glycoprotein production in ECM due to hyperthyroidism can lead to: low plasma protein levels due to liver disease; obstruction of lymphatic drainage (infection)

424
Q

How is blood flow controlled?

A

All flow to particular vascular bed controlled by size of arterioles which is controlled by SM contraction

425
Q

What are the 2 areas circulation can effect and how?

A
  1. Local: regulates blood flow to tissue

2. Central: affects BP by acting on total peripheral resistance; affects central blood vol

426
Q

What are the 2 types of vascular smooth muscle control?

A
  1. Intrinsic: located in tissue

2. Extrinsic: hormones and nerves from outside tissue

427
Q

What are the 3 intrinsic control factors of VSM?

A
  1. Local temp
  2. Transmural pressure
  3. Local metabolites, autacoids, endothelium derived factors
428
Q

Explain how local temp can control VSM

A

Inc.: vasodilation of cutaneous arterioles and veins

Dec
Skin cooling 10-15C; vasoconstriction by slowing of Na/K pump causing repolarisation
Skin cooling <12C; cold vasodilation by paralysis of SM giving passive vasodilation

429
Q

Explain how transmural pressure can control VSM

A

External: compresses vessels, impairs blood flow

Internal: stretch causes contraction; myogenic control

  • stretch sensitive membrane areas i.e. stretch of muscle membrane opens ion channels, cells depolarise causing Ca2+ signal which triggers muscle contraction
  • local vasodilators from endothelium; inc. pressure, inc. shear force, vasodilators released
430
Q

What are 5 local metabolites that act as vasodilators?

A
  1. K ions
  2. Adenosine
  3. Acidosis
  4. Hypoxia
  5. Inc. interstitial osmolality
431
Q

Explain local metabolite control of VSM

A

Released by tissue in proportion to tissue metabolism
Act on VSM of arterioles
Functional hyperaemia: congestion of blood in organ/tissue
Removal rate proportional to blood flow

432
Q

What is inflammation?

A

Inc. permeability of the microcirculation

433
Q

What 4 autocoids can control VSM?

A
  1. Bradykinin
  2. Histamine
  3. Serotonin (5-HT)
  4. Arachidonic acid derivatives
434
Q

When are autocoids released and what are their 5 effects?

A

From cells and tissues in response to inflammation

  1. Redness
  2. Pain
  3. Loss of function
  4. Heat
  5. Swelling
435
Q

Explain how endothelium factors can cause vasodilation

A

EDRF: endothelium derived relaxing factor (NO)
Diffuses to underlying SM, activates soluble guanylate cyclase to inc. cGMP and cause relaxation
Basal production stimulated by shear stress and autocoids
Stimulated too much in infection

436
Q

What are endothelins?

A

Endothelium derived contraction factors

Proteins that effect vasoconstriction of blood vessels and BP

437
Q

Describe endothelin A receptors

A

Found in SM of blood vessels

Cause vasoconstriction, retention of Na resulting in inc. BP

438
Q

What is the function of Endothelin B receptors and how do they work?

A

Dec. BP

Found in endothelial cells lining interior of blood vessels

Release NO causing vasodilation 
Cause natriuresis (excretion of Na in urine) and diuresis
439
Q

Where is the shared location of endothelin receptors and what is their function there?

A

Nervous system

May mediate neurotransmission and vascular function

440
Q

Describe the effect of sympathetic vasoconstrictor nerves on peripheral circulation

A

NA released from varicosities on sympathetic nerves
Act on alpha-adrenoceptors
NA release modulated by local vasodilators
Vasodilation caused by fall in sympathetic vasoconstriction (part of baroreceptor reflex)

441
Q

What are the 3 effects of inc. sympathetic vasoconstriction on peripheral circulation?

A
  1. Red. local blood flow
  2. Venoconstriction: dec. vol. blood in organ
  3. Dec. capillary venous pressure: inc. interstitial fluid reabsorption and inc. venous pressure causes oedema
442
Q

Describe the effects sympatho-adrenal activation in regulation of peripheral circulation

A

Inc. CO and resistance in periphery and viscera

Blood flow to skeletal muscle inc. due to arterioles dilating in response to AD via beta-2 adrenoceptor stimulation
Blood shunted from viscera and skin to muscles

443
Q

Describe the effects of angiotensin II and ADH on peripheral circulation

A

General vasoconstriction of VSM causes inc. resistance and BP

444
Q

What are 3 paracrine regulators produced by endothelium that promote relaxation?

A
  1. NO
  2. Bradykinin
  3. Prostacyclin
445
Q

What is the importance of NO and how can levels be inc.?

A

Involved in setting resting tone of vessels
Inc. by PSNS activity

Vasodilators drugs (nitroglycerin) act through NO

446
Q

What is endothelin 1?

A

Vasoconstrictor produced by endothelium

447
Q

Describe myogenic autoregulation of circulation

A

Intrinsic to VSM

VSM contracts when stretched and relaxes when not
Dec. arterial pressure causes cerebral vessels to dilate

448
Q

Describe metabolic autoregulation of circulation

A

Matches perfusion to local tissue needs

Low O2/pH or high CO2/adenosine/K+ from high metabolism cause vasodilation resulting in inc. blood flow (active hyperaemia)

449
Q

Describe the skeletal muscle pump

A

During contraction veins pinched pushing blood towards heart, lower valve prevent back flux of blood
During relaxation valves prevent back flux, vein refilled by capillaries

450
Q

Explain the role of the thoracic cavity in venous return

A

Inspiration creates -ve pressure allowing veins to dilate making route to heart easier, inc. venous return

451
Q

Why is standing up a problem for BP?

A

Gravity causes blood pooling in lower body preventing blood from reaching brain
Orthostatic/postural hypotension

452
Q

How does the baroreceptor reflex return BP to normal?

A

Detects drop in BP triggering response that inc. HR and force of contraction
This causes vasoconstriction which inc. peripheral resistance and CO returning BP to normal

453
Q

What are the changes in CO, HR and SV during exercise and how are these accomplished?

A

CO: 6.0-20 l/min
HR: 80-190 bpm
SV: 75-105 ml

Large inc. sympathetic nerve activation
Redistribution of CO

454
Q

How do sympathetic vasoconstrictor nerves cause circulatory changes during exercise?

A

Varicosities secrete NA @ nerve endings can red. blood flow through resting muscles to 1/3 normal

455
Q

How does inc. blood flow through muscle capillaries affect circulation during exercise?

A

Inc. SA for exchange allowing greater O2 and nutrient supply

456
Q

How is blood flow through skeletal muscle changed during exercise?

A

Dec. O2 in muscle enhances flow and causes release of local vasodilators

457
Q

What is the most important vasodilator? What are 4 others?

A

Adenosine

  1. K+
  2. CO2
  3. ATP
  4. Lactic acid
458
Q

What is shock?

A

Generalised severe red. in blood supply to body tissues

Inadequate perfusion leads to cellular hypoxia and tissue damage

459
Q

What is hypovolemic shock?

A

Condition in which rapid fluid loss results in multiple organ failure due to inadequate perfusion

460
Q

What are the 4 causes of hypovolemic shock?

A
  1. Trauma
  2. Vomiting/diarrhoea
  3. Burns
  4. Haemorrhage
461
Q

What are the 4 systems the body activates in response to hypovolemic shock?

A
  1. CVS
  2. Neuroendocrine
  3. Haematological
  4. Renal
462
Q

How does the CVS respond to hypovolaemic shock?

A

Primary: inc. NA release, dec. vagal tone

Secondary: inc. HR, myocardial contractility, constrict peripheral blood vessels

Redistribute blood to brain, heart, kidneys away from GIT, skin, muscle

463
Q

How does the renal system respond to hypovolaemic shock?

A

Kidneys stim. secretion of renin from juxtaglomerular apparatus
Angiotensinogen -> angiotensin II
Vasoconstriction of arteriolar SM, stim. aldosterone release by adrenal cortex

464
Q

How does the neuroendocrine system respond to hypovolaemic shock?

A

Causes inc. circulating ADH
Released from post. pituitary gland in response to dec. BP and Na conc.
Indirectly causes inc. reabsorption water and NaCl from distal tubule and collecting ducts

465
Q

How does the haematological system respond to hypovolaemic shock?

A

Activate coagulation cascade and contract bleeding vessels (via local thromboxane A2 release)
Platelets activated: form premature clot on bleeding source
Damaged vessel exposes collagen subsequently causing fibrin deposition and stabilisation of clot

466
Q

After a 20% haemorrhage what are the immediate responses?

A

Activation of CV reflexes: baroreceptor reflex

Maintenance of blood flow to heart and brain

467
Q

After 20% haemorrhage, what are the 3 intermediate responses? (Mins-hrs)

A
  1. Central activation of thirst
  2. Retention of salt and water to maintain central blood vol
  3. Autotransfusion of fluid from interstitial fluid by reabsorption

Inc. AD, ADH, angiotensin II

468
Q

After 20% haemorrhage, what are the 3 long-term responses? (Days-weeks)

A
  1. Restoration of fluid vol. by red. urine output, inc. fluid intake
  2. Synthesis of plasma proteins: oncotic pressure draws water in
  3. Replacement of RBCs
469
Q

What are the 4 effects of 20-40% haemorrhage?

A
  1. Red. BP
  2. Red. blood flow to brain and heart
  3. Almost no blood flow to kidney, liver
  4. Vascular stasis: inc. permeability and loss of fluid and protein to interstitial space
470
Q

What are the 6 effects of >40 haemorrhage?

A
  1. Inability to perfuse vital organs
  2. Obtunded: not full mental capacity
  3. Severe hypotension
  4. Severe tachycardia: red. venous return as beating too quickly
  5. Cold, clammy
  6. Death
471
Q

What are the 6 functions of the kidneys?

A
  1. Regulate composition and vol. of body fluids within narrow range by excretion of water and solutes
  2. Regulate osmolality and vol. of body fluid
  3. Electrolyte balance
  4. Acid-base balance
  5. Excretion of metabolic products and foreign substances
  6. Production, secretion of hormones: renin, erythropoietin, calcitriol
472
Q

Why is control of body fluid vol. important?

A

Required for CVS

Many metabolic functions sensitive to pH: maintained by buffers in fluid, activity of kidneys and lungs

473
Q

What 4 products are excreted by the kidneys?

A
  1. Urea: from AAs
  2. Uric acid: from nucleic acids
  3. Creatinine: from muscle creatine
  4. Haemoglobin and hormone metabolism end products
474
Q

What organs make up the upper and lower urinary system?

A

Upper: kidneys
Lower: bladder, urethra

475
Q

Describe the excretion of urine

A

Urine formed by kidneys passes into renal pelvis then ureter
Transported to bladder by peristaltic waves
Bladder elastic, acts as reservoir
Drains inf. by tubular urethra

476
Q

What does the renal vein drain into?

A

Inf. vena cava

477
Q

What is the minimum required daily urine production?

A

500-600ml

478
Q

Describe the structure of the kidneys

A

Cortex: outer reddish layer, outside pyramids
Medulla: inner paler layer
Papillae: points of the pyramids
Hilum: vertical slit through which renal and lymphatic vessels and nerves enter/leave

Nephrons concentrated in pyramids
Loops of Henle extend into medulla

479
Q

Described the blood supply of kidneys and pyramids

A

Renal artery breaks down to afferent arterioles for each pyramid
Efferent arteriole comes off afferent, descends and surrounds loop Henle
Ascent to same nephron, sit between afferent and efferent

480
Q

What are the 2 types of nephron?

A
  1. Cortical

2. Juxtamedullary

481
Q

Describe cortical nephrons

A

Originate in outer 2/3 cortex

482
Q

Describe juxtamedullary nephrons

A

Originate in inner 1/3 cortex

Have loops of Henle that pass deep into medulla

483
Q

Describe the structure of nephrons

A

Begin @ Bowman’s capsule which drains into proximal convoluted tubule then loop of Henle and DCT
These joint to form collecting ducts which drain into renal pelvis, the ureter which enters bladder

484
Q

What is the renal corpuscle?

A

Bowman’ capsule and glomerulus

485
Q

What is the function of the renal corpuscle?

A

Formation of ultra-filtrate

486
Q

What is the function of the PCT?

A

Bulk reabsorption of solutes and water, secretion of solutes (except K)

487
Q

What is the function of the loop of Henle?

A

Establish medullary osmotic gradient

Reabsorption of water (descending) and NaCl (ascending)

488
Q

What is the function of the DCT?

A

Fine-tuning of the reabsorption/secretion of small quantities of solute

489
Q

What is the function of the collecting duct?

A

Fine-tuning reabsorption of water, reabsorption of urea

490
Q

What are the 3 layers that glomerular filtrate has to pass through?

A
  1. Fenestrated endothelium of capillary: filtering membrane
  2. Continuous basal lamina of Bowman’s capsule
  3. Epithelial cells of capsule
491
Q

How are mesangial cells in the basal lamina believed to be able to reduce glomerular filtration rate?

A

By contraction to red. SA available for filtration

492
Q

What is glomerular filtration rate determined by?

A

Net filtration pressure

493
Q

Describe the forces involved in net filtration pressure

A

Outward hydrostatic pressure of ~60mmHg as afferent vessels are wider than efferent vessels

Opposed by oncotic pressure from plasma proteins: ~29mmHg
AND by fluid pressure in Bowman’s capsule: 15mmHg

NFP = 16 mmHg

494
Q

Define glomerular filtration rate

A

Vol. fluid filtered from glomeruli into Bowman’s capsule per unit time

495
Q

Despite low NFP how are large vol. filtrate produced?

A

Glomeruli capillaries extremely permeable and have large SA

496
Q

How is GFR regulated?

A

Via afferent arteries: constriction vs dilation

497
Q

Describe the 2 types of GFR regulation

A
  1. Extrinsic: sympathetic nerve

2. Intrinsic: renal auto-regulation

498
Q

Describe the 2 methods of auto-regulation of GFR

A
  1. Myogenic: afferent arterioles contract when arterial pressure inc.
  2. Tubular glomerular feedback: inc. flow rate in DCT causes cells in macula densa to contract afferent arterioles and dilate efferent arterioles, red. glomerular capillary hydrostatic pressure
499
Q

What 4 factors determine GFR?

A
  1. Glomerular capillary pressure
  2. Plasma oncotic pressure
  3. Tubular pressure
  4. Glomerular capillary SA
500
Q

Define renal plasma clearance

A

Vol. plasma from which a substance is completely removed in 1min by excretion in urine

501
Q

Define osmotic pressure

A

Hydrostatic pressure produced by difference in conc. between 2 fluids either side of a surface

502
Q

Define osmolarity and osmolality

A

Osmolarity: moles of solute/litre of solution
Osmolality: moles of solute/kg of solvent

503
Q

How is water transported? What is this dependent on?

A

Osmosis
Requires conc. gradient favouring return of water to vascular system
Reabsorption by osmosis only happen when osmolality of plasmas greater than that of filtrate

504
Q

What are the 4 main hormones involved in regulating kidney function?

A
  1. Angiotensin II
  2. Aldosterone
  3. ADH/vasopressin
  4. Atrial natriuretic peptide
505
Q

How does angiotensin II function?

A

Stimuli: low blood vol, BP stim renin induced angiotensin2 production
Mechanism: inc. Na/H antiporter in proximal tubule
Effect: inc. reabsorption, solutes, H2O; inc. blood vol, BP

506
Q

How does aldosterone function?

A

Stimuli: inc. angiotensin II, plasma K
Mechanism: enhance Na/K pump in basolateral membrane, Na channels in apical membranes of principal cells in collecting duct
Effect: inc. K secretion, Na, Cl reabsorption; inc. H2O reabsorption, inc blood vol, BP

507
Q

Describe how ADH functions

A

Stimuli: inc. osmolarity ECF, dec. blood vol
Mechanism: aquaporin-2 in apical membranes
Effect: inc. facultative reabsorption of water, dec. osmolarity body fluids

508
Q

How does atrial natriuretic peptide work?

A

Stimuli: atrial stretching
Mechanism: suppress Na, water reabsorption in proximal tubule and collecting duct; suppress aldosterone and ADH
Effect: inc. excretion Na in urine, inc. urine output; dec. blood vol, BP

509
Q

Describe the process by which Na is absorbed by the proximal tubule

A

Na/K ATPase on basolateral membrane: Na out, K in
Creates electrochemical gradient
Na/glucose co-transporter on apical membrane transport Na in from filtrate

510
Q

Described how Cl and water are absorbed by the proximal tubule

A

Na transport creates electrical gradient
Favours passive transport of Cl into interstitial fluid which inc. osmolality and osmotic pressure
Osmotic gradient between tubular fluid and interstitial fluid causes water to diffuse into epithelial, then interstitial and finally peritubular capillaries

511
Q

How are glucose and AAs absorbed by the proximal tubule?

A

Na/K ATPase on basolateral membrane: Na out, K in
Facilitated diffuse of glucose out on basolateral membrane
Na/glucose(/AA) co-transporter on apical membrane transport glucose/AAs in from tubular fluid

512
Q

What is the significance of reabsorption in the proximal tubule?

A

Highly permeable to water due to huge SA due to brush border
60-70% filtered load sodium, water, urea reabsorbed in proximal tubule
Almost complete reabsorption of bicarbonate , glucose, AAs, chloride, PO4, K, protein

513
Q

Why is hyper-osmotic urine more difficult to form compared to hypo-osmotic?

A

In hypo-osmotic solutes can be reabsorbed from tubule w/o water following
Hyper-osmotic require reabsorption water w/o solutes. Water can only move from low osmotic pressure to high osmotic pressure thus kidney requires of area of low osmotic pressure to remove water from tubular fluid

514
Q

Describe reabsorption of NaCl in the thick-walled ascending limb of Loop of Henle

A

Na/K ATPase on basolateral membrane pumps Na out, maintain low [Na] in cell
2Cl, Na, K pumped in via symporter from tubular fluid
Virtually impermeable to water, permeable to solutes (activity pumped out)
Fluid becomes isotonic then hypotonic

515
Q

How does the descending limb of Henle form hypertonic solution?

A

Hypertonic = high osmotic pressure = high solute conc. (low water conc)

Permeable to water, virtually impermeable to solutes
Water moves out via osmosis forming hypertonic solution

516
Q

What is the significance of NaCl reabsorption from the ascending loop on the osmolarity of the renal medulla?

A

Contributes to half the osmolarity (moles/L solute) of renal medulla
Diffusion of urea from inner medullary collecting ducts into interstitial fluid
Co-transport of K, Cl out of thick ascending limb

517
Q

What is the vasa recta?

A

Blood supply of the renal medulla

Surrounds collecting ducts, loop of Henle, convoluted tubules

518
Q

What is the role of the vasa recta?

A

Supply medullary tissues w/ nutrients, O2

Maintain hypertonicity of renal medulla: salt has to be retained; water, ions must be removed

519
Q

What are inputs and outputs of water balance?

A

Input: food, water, oxidation
Output: urine, stool, respiratory loss, sweat

520
Q

What factors contribute to water balance?

A

Hydrostatic and osmotic forces across biological membrane
Conc. gradients of electrolytes
Imbalances in Na, water lead to changes in osmolality and movement of water, cell expansion/contraction occurs

521
Q

Describe the distribution of water reabsorption in the kidneys

A

65% proximal tubule
20% loop Henle
15% fine tuned by hormones in distal tubule and collecting duct

522
Q

What does the reabsorption of water in distal tubule and collecting duct depend on?

A

Circulating ADH

Inc. permeability to water allowing to achieve equilibrium w/ interstitial fluid of medulla

523
Q

Describe the stimulation and mechanism of ADH

A

Inc. ECF osmolality detected by osmoreceptors in hypothalamus
Stimulate release of ADH from post. pituitary (and thirst)
Act on receptors in principal cells collecting duct
Activate synthesis of aquaporin-2, facilitate passage of water across membrane
Dec. urine vol.

524
Q

Describe how diabetes insipidus and and diabetes mellitus affect water balance

A

Insipidus: inadequate secretion/action ADH, collecting ducts impermeable to H2O, high vol. dilute urine; dehydration and intense thirst

Mellitus: inadequate secretion/action insulin, high vol. iso-osmotic urine as excreted glucose carries water and as result of osmotic pressure it generates in tubules

525
Q

What is the juxtaglomerular apparatus?

A

Specialised structure situated where distal tubule comes close to Bowman’s capsule between afferent and efferent arteriole
Regulate BP and GFR
Secrete renin in response to low BP in arteriole

Macula densa is collection of specialised epithelia cells in DCT, detect changes in Na conc.

526
Q

What 3 factors can trigger renin release from juxtaglomerular apparatus?

A
  1. Sympathetic stimulation
  2. Fall in renal perfusion pressure @ afferent arteriole
  3. Hyponatraemia (low Na)
527
Q

How does renin function?

A

Cleaves angiotensin I from angiotensinogen then converted to angiotensin II by ACE
Angiotensin II stim Na/H antiporters, inc. Na, water reabsorption

528
Q

What is the overall effect of angiotensin and the 4 individual?

A

Act on VSM to cause vasoconstriction: inc. arterial BP, red. renal blood flow and GFR

  1. Stim Na reabsorption proximal tubule
  2. Stim aldosterone secretion by adrenal cortex
  3. Stim ADH secretion from post. pituitary
  4. Stim thirst by action on brain
529
Q

Why is acid/base balance important?

A

Many enzymes activity dependent on pH between narrow range

530
Q

Compare volatile and non-volatile acids

A

Volatile: metabolism of carbs, fats produces large quantities CO2, H2CO3; CO2 excreted via kings

Non-volatile: metabolism of proteins e.g. sulphur containing AAs produce sulphuric acid; can’t be excreted via lungs, kidneys regulate excretion

531
Q

What is the average plasma H conc. and pH?

A

Conc: 40nmol/L (0.00004mmol/L)
pH: 7.36-7.44

532
Q

What is a buffer?

A

Solution that resists/red. changes in pH

533
Q

What is buffer capacity determined by?

A
  1. Disassociate constant (pK): relationship between pK and pH determined by Henderson-Hasselbalch equation
  2. Quantity of buffer
534
Q

What is unique about the bicarbonate buffering system? Why is this important?

A

Remains at equilibrium w/ atmospheric air

[HCO3-] controlled by kidneys
PCO2 controlled by lungs

535
Q

In what 2 regions in bicarbonate reabsorbed by the body?

A

Proximal and distal tubules

Most (85%) in proximal

536
Q

Describe reabsorption of bicarbonate in PROXIMAL tubule

A
  1. Apical membrane impermeable to HCO3-, form H2CO3 w/ H+
  2. Carbonic anhydrase in brush border catalyse dehydration, produce CO2, H2O which enter cell
  3. CA in cell catalyse production of H+ and HCO3-
  4. H+ secreted into tubular fluid via apical membrane H+-ATPase, Na/H anti-porter
  5. HCO3- reabsorbed into blood via basolateral membrane Na/HCO3 symporter, Cl/HCO3 anti-porter
537
Q

Describe the reabsorption of HCO3- in the distal tubule

A
  1. CA in cell catalyse produce of H+ and HCO3-
  2. H+ secreted into tubular fluid via apical membrane H+-ATPase, K/H-ATPase
  3. HCO3- enters blood via basolateral membrane Cl/HCO anti-porter
538
Q

What is the main difference between distal and proximal tubule bicarbonate reabsorption?

A

Proximal tubule has CA intracellularly and extracellularly whereas distal only intracellularly

539
Q

Define acidosis and alkalosis

A

Acidosis: abnormal inc. in H+ blood conc., pH < 7.35
Alkalosis: abnormally high alkalinity of blood and fluids, pH > 7.45

540
Q

What 3 mechanisms minimise disturbances to acid/base balance?

A
  1. Buffering
  2. Adjusting renal excretion: H+/HCO3-
  3. Adjusting ventilation: blood PCO2
541
Q

Describe respiratory acidosis

A

Caused by red. in ventilation due to drugs or lung disease
Results in red. pH, raised PCO2

Renal response: inc. H+ excretion, inc. HCO3- reabsorption (buffer)
Can take several days

542
Q

Describe metabolic acidosis

A

Addition of nonvolatile acids to body (diabetic ketoacidosis) or in kidney failure
Low pH, low HCO3-

Respiratory: dec. pH stimulates respiratory centres, inc. ventilation; red. PCO2 minimises fall in plasma pH

Renal: inc. H+ excretion, inc. HCO3- reabsorption

543
Q

Describe metabolic alkalosis

A

Caused by addition of nonvolatile alkalis (antacid) or loss of nonvolatile acids (vomiting/gastric HCl) resulting in high pH, high HCO3-

Inc. pH inhibits respiratory centres, dec. ventilation rate; inc. PCO2
Inc. HCO3- excretion

544
Q

Describe respiratory alkalosis

A

Caused by inc. ventilation (drugs stimulating respiratory centres) or hyperventilation (anxiety)
High pH, red. PCO2

Red. acid excretion, red. HCO3- reabsorption

545
Q

What are the 6 functions of the GIT?

A
  1. Ingestion
  2. Secretion: 7L/d water, enzymes, acid, buffers into lumen
  3. Mixing and propulsion
  4. Digestion: mechanical; teeth-grinding, stomach/intestine-churning/mixing; chemical catabolic reactions
  5. Absorption: most small molecules, ions, water, through epithelial lining
  6. Defecation
546
Q

What 6 organs make up the GIT? What are the 6 accessory structures?

A
  1. Oral cavity
  2. Pharynx
  3. Oesophagus
  4. Stomach
  5. Small intestine
  6. Large intestine
  7. Teeth
  8. Tongue
  9. Salivary glands
  10. Liver
  11. Gall bladder
  12. Pancreas
547
Q

What are the 4 layers of the GIT from lower 1/3 oesophagus to anus?

A
  1. Mucosa
  2. Submucosa
  3. Muscularis
  4. Serosa
548
Q

Describe the mucosa of the GIT

A

Epithelial
Mouth, oesophagus, anal canal: lining
Stomach/intestines: secretion and absorption

Lamina propria: blood and lymphatic vessels

Muscularis mucosae: create folds, invaginations in epithelial, inc. SA

549
Q

Describe the submucosa

A

Highly vascular

Neuronal network: submucosal/Meissner’s plexus; primarily control secretions, also SM and blood vessel tone

550
Q

Describe the muscularis

A

Mouth, upper oesophagus, anal sphincter: skeletal muscle, voluntary control
Rest: smooth muscle; inner circular, outer longitudinal
Circular constrict behind food, longitudinal contract, shortening passage in front
Intrinsic nerve supply: myenteric/Auerbach’s plexus; GIT motility

551
Q

Describe the neuronal control of the GIT

A
  1. Autonomic
    Sympathetic: inhibitory
    Parasympathetic: excitatory
  2. Enteric
    Myenteric: between circular and longitudinal muscles; linear chain interconnecting neurons extending full length GIT, control motor activity

Submucosa: control secretions, local absorption function within inner wall each segment gut

552
Q

Define mastication

A

Breakdown of food mechanically and initial enzymatic digestion by ptyalin (alpha amylase)

553
Q

What are the 3 stages of swallowing?

A
  1. Oral: blows to back of OC; voluntary
  2. Pharyngeal: involuntary
  3. Oesophageal: involuntary
554
Q

Describe the structures that control oral stage of mastication and their nerve supply

A

Muscles of mastication: mandibular of trigeminal
Pterygoids, masseter, temporalis

Tongue: hypoglossal

Buccinator, orbicularis oris: facial

555
Q

What muscles are involved in the pharyngeal stage of swallowing?

A

Cricopharyngeus: CN10, sympathetic; relax, aid movement
Soft palate: CN5 7 9 12; close nasopharynx
Pharyngeal: CN9 10; propel

556
Q

What nerves control the oesophageal stage of swallowing?

A

CN10, sympathetic

557
Q

Describe the waves of peristalsis in the oesophagus

A

Initial -ve wave due to elevation of larynx drawing on cervical oesophagus

Primary: abrupt +ve wave coincides w/ bolus entering oesophagus

Stripping: smaller +ve wave, clears food from oesophagus

Secondary: generated in response to dilation of oesophagus

Tertiary: irregular, non-propulsive waves, during emotional stress

558
Q

What is the difference in peristalsis in oesophagus?

A

Upper part: peristaltic wave progresses rapidly

Lower 1/3: more sluggish

559
Q

What are the differences in peristaltic wave caused by?

A

Upper part musculature is striated, lower part smooth

560
Q

What are the 3 layers of the muscularis of the stomach?

A
  1. Outer longitudinal
  2. Middle circular
  3. Inner oblique (at 45 degree to other layers)
561
Q

What do the different layers of stomach muscularis allow for?

A

Movement in directions

Mix and churn food w/ acids/enzymes

562
Q

Describe gastric pits and glands

A

Epithelial cells form narrow channel: pits

And columns of secretory cells: glands

563
Q

What are the 3 exocrine glands of gastric glands? What do they secrete?

A
  1. Mucus neck cell: mucus, HCO3-
  2. Chief cells: pepsinogen
  3. Parietal cells: HCl, intrinsic factor for B12 absorption
564
Q

What are the 4 hormones secreted by enteroendocrine cells?

A
  1. Gastrin
  2. Secretin
  3. Choleocystokinin
  4. Gastric inhibitory peptide
565
Q

Describe gastrin

A

Stimulated by peptides and AAs in stomach

Stimulates G cells to release gastric juice

566
Q

Describe choleocystokinin

A

Stimulated by AAs, FAs in duodenum
Stimulates
Gall bladder: contract, release bile
Pancreas: release pancreatic digestive enzymes into pancreatic fluid

567
Q

Describe secretin

A

Stimulated by acidic chyme in duodenum

Stimulates pancreas to release HCO3- into pancreatic fluid

568
Q

Describe gastric inhibitory peptide

A

Stimulated by glucose and fat in duodenum

Inhibits release of gastric juice

569
Q

Describe cephalic regulation of the enteroendocrine

A

Sound, sight, smell
Initiates reflex via medulla, hypothalamus, vagal output to stim. submucosal plexus

Inc. gastrin, inc. peristalsis, inc. HCl

570
Q

Describe gastric regulation of enteroendocrine

A

Food distends stomach wall: stretch, chemoreceptors inc. submucosal plexus activity; inc. gastric juice, inc. myenteric plexus activity increasing peristalsis
Inc. parasympathetic -> release gastrin in pyloric Antrum

571
Q

Describe intestinal regulation of enteroendocrine

A

Receptors in duodenum/SI inhibit gastric motility and juice secretion
Secretin: inhibit gastric juice
CCK: inhibit gastric motility
GIP: both

Distension of duodenum and FAs cause reflex via medulla and local reflex to inhibit peristalsis and secretions

572
Q

Describe the vomit reflex

A

Reverse peristalsis in SI

Pyloric sphincter and stomach relax
Forced inspiration against closed glottis: red. intrathoracic, inc. intraabdominal pressures
Forceful contraction of abdominal muscles

Retching: against closed upper oesophageal sphincter
Vomiting: open upper oesophageal sphincter

573
Q

What are the 4 structures involved in the emesis?

A
  1. Area postrema CTZ
  2. Vestibular nuclei, N. tracts solitarius
  3. Vomiting centre
  4. Vagal nerve endings
574
Q

Describe receptor, agonist and antagonists for area postrema emesis

A

D2 receptor
Apomorphine, L-DOPA

Antidopaminergic

575
Q

Describe receptors, agonists, antagonists for vestibular nucleus and N. tractus solitarius

A

Vestibular: M, cholinomimetics (ACh, physostigimine), scopolamine

N. tractus solitarius: H1, histamine, Dramamine

576
Q

Describe receptor, antagonist, agonist for vomiting centre

A

M
Cholinomimetic: bethanechol, atenolol, pyridostigmine, clonidine, propranolol
Scopolamine

577
Q

Describe receptor, agonist and antagonist for vagal nerve ending involved in emesis

A

5-HT3
Serotonin
Ondansetron, granisetron, tropisetron

578
Q

What are the 4 functions of the SI?

A
  1. Segmentation mixes chyme w/ digestive juices and brings food into contact w/ mucosa for absorption
  2. Peristalsis propels chyme
  3. Completes digestion carbs, proteins, lipids; begins and completes digestion nucleic acids
  4. Absorption of 90% all nutrients
579
Q

What are the 3 regions of the SI?

A
  1. Duodenum
  2. Jejunum
  3. Ileum
580
Q

Describe the mucosa and submucosa lining of the SI

A

Simple, columnar epithelium containing absorptive, goblet, enteroendocrine, Paneth cells
Have microvilli that inc. SA, form brush border

Mucosa has deep crevasses between villi: intestinal glands
Goblet: secrete mucus, trap microorganisms
Enteroendocrine: secretin, CCK, GIP
Paneth (deepest part): lysozyme; bactericidal

Submucosa has duodenal glands secrete alkaline mucous that neutralises gastric acid

581
Q

Describe the control of SI motility

A

Neuronal

Extrinsic and intrinsic (myenteric plexus)
Hormonal factors

582
Q

What are the 2 movements of SI?

A

Mixing contractions: segmentation

Propulsive movements: peristalsis

583
Q

What is the migratory motility complex?

A

Internal housekeeper of SI
When most food absorbed, segmentation stops, MMC begins
Weak, repetitive, peristaltic waves, move short distance

Sweep food remnants, mucosal debris, bacteria; cleaning SI between meals
Regulated by motilin

584
Q

Describe the modulation of peristaltic activity

A

Gastroenteric reflex via myenteric plexus
Hormonal
inc.: gastrin, CCK, insulin, 5HT
dec.: secretin, glucagon

585
Q

What is the function of the ileocecal sphincter and valve?

A

Valve: prevent back flux of colon contents
Sphincter: prevent rapid emptying of ileum

Prevents contamination of SI by colonic bacteria

586
Q

How do the stomach and ileocecal sphincter interact?

A

Reflexly via intrinsic nerve plexus
Pressure build in cecum closes sphincter
Pressure build in ileum opens

587
Q

Describe the motility of the large intestine?

A

Proximal half concerned w/ absorption, distal 1/2 w/ storage

Mixing: Haustrations
Propulsive: mass movements

588
Q

What are the 6 regions of the LI?

A
  1. Cecum
  2. Ascending colon
  3. Transverse colon
  4. Descending colon
  5. Sigmoid colon
  6. Rectum
589
Q

Describe the ascending colon

A

Specialised for processing chyme

Short time compared to transverse colon

590
Q

Describe the transverse colon

A

Specialised for storage and dehydration
Chyme present for 24hrs
Primary site of water and electrolyte removal, storage

591
Q

Described the descending colon

A

Conduit between transverse colon and sigmoid

Accumulate for 24hrs an then instilled into caecum

592
Q

How is faecal continence maintained?

A

Musculature of rectosigmoid region, anal canal, pelvic floor

Puborectalis muscle and external anal sphincter functional unit to maintain continence

593
Q

Describe the muscularis of LI

A

Internal circular muscle
External longitudinal muscle thickened by 3 longitudinal bands called taeniae coli
Colon gathers into sacs called haustra

594
Q

What is the initiation of the propulsive movements of the LI?

A

Mass movements initiated by gastrocolic and duodenocolic reflexes initiated by distension of stomach and duodenum
Associated w/ parasympathetic

595
Q

Describe the Haustration movements

A

Ring-like circular contractions of circular muscle

Break up faeces, present portion to surface for water removal

596
Q

Describe the muscle secretion and the absorption function of the LI

A

Mucus: secreted by intestinal glands, under myenteric/PSNS control, bicarbonate also secreted; protect against friction and pH

Absorption: water, electrolytes in proximal 1/2 colon; water passively following active transport of Na, water-soluble vitamins

597
Q

What are the functions of colonic bacteria?

A

Ferment carbs to H2, CO2, CH4 gas

Convert proteins to AAs

598
Q

Describe the defecation reflex

A

Intrinsic: mediated by myenteric plexus. Stretching colon and inc. peristaltic activity in descending, sigmoid colon and rectum cause relaxation of internal anal sphincter by inhibitory signals

Parasympathetic: stretch nerve endings in rectum stim., signal descending, sigmoid and rectum to inc. force peristalsis and relax internal anal sphincter

599
Q

Describe the structure of the liver

A

Largest internal organ
In R hypochondrium
Divided into R and L by hepatic vein; subdivided into 8 segments by R, L, mid. hepatic vein
Dual blood supply: intestines and own hepatic arteries

600
Q

What are the 6 functions of the liver?

A
  1. Filtration, storage of blood
  2. Metabolism: carbs, proteins, lipids
  3. Production: bile, coagulation products
  4. Metabolism and excretion bilirubin
  5. Hormone and drug inactivation
  6. Storage vits and iron
601
Q

Describe the blood reservoir function of the liver

A

Normal blood vol. ~10% total
Heart failure: inc. up by 1L
Exercise/haemorrhage: dec. 30-40%

602
Q

Describe the blood supply of the liver

A

Hepatic artery: 25%
Branch of coeliac axis
Autoregulation of blood flow (by hepatic artery) ensure constant total liver blood flow

Portal vein: 75%
Drains most GIT and spleen
Branches pass between lobules and terminate in sinusoids

603
Q

What are hepatocytes?

A

Cells found in liver responsible for exocrine secretion, bile formation and endocrine products

604
Q

Describe liver lobules

A

Hexagonal structures consisting of hepatocytes
Hepatocytes radiate out from central vein
At each corner of lobule is portal triad

605
Q

What is in the portal triad?

A

Artery
Vein
Bile duct

606
Q

Describe liver sinusoids

A

Wide blood vessels: single layered, have fenestrations, no basement membrane
Blood makes contact w/ hepatocytes and is filtered/detoxified

607
Q

Describe the metabolism of carbs in the liver

A

Glc homeostasis and maintenance major function
Immediate fasting
- blood glc maintained by glycogenolysis or gluconeogenesis
- gluconeogenesis sources: lactate, pyruvate, AAs (from muscle; alanine, glutamine)

Prolonged

  • ketone bodies and FAs used as alternative sources
  • body adapts to lower glc requirement
608
Q

Describe protein metabolism in the liver

A

Synthesis

  • AAs from intestine, muscle and regulates plasma levels
  • transport proteins: transferrin (iron transport) produced
  • coagulation factors and complement components

Degradation

  • AAs degraded by transamination and oxidative deamination to ammonia
  • ammonia converted to urea, excreted renally
609
Q

Describe fat metabolism in the liver

A

Carbs and proteins to fats
Beta oxidation of FAs
Synthesis of special lipids: lipoproteins, cholesterol, phospholipids

610
Q

Describe the metabolism of RBCs

A

Erythrocyte ruptures, haemoglobin phagocytosed by Kupffer’s cell
Globins-> AAs, released into blood
Haem groups-> iron (new RBCs in bone marrow) and bile pigments

611
Q

Describe the metabolism of bilirubin

A

Most from RBC metabolism and reticuloendothelial cells, some from breakdown of haem proteins
Biliverdin formed from haem, red. to bilirubin (unconjugated)

612
Q

Describe conjugated bilirubin

A

Water soluble
Secreted into biliary canaliculi reaching SI
In gut: bilirubin -> urobilinogen, oxidised in colon and excreted in stool
- some absorbed into portal blood, excreted in urine

613
Q

Describe the secretion of bile

A

Produced by hepatocytes
Secreted into narrow bile canaliculi
Carried by larger ducts to gallbladder; stored and water reabsorbed
Released into duodenum via bile ducts (leave liver through common hepatic duct)

614
Q

What are the contents of bile?

A

Hydrogen carbonate ions
Bile pigment and salts
Cholesterol

615
Q

What are the 2 methods by which bile acids are secreted?

A
  1. Bile salt dependent: uptake of acids across basolateral by transport proteins (driven by Na/K ATPase), Na, water follow passage of acids
  2. Bile salt independent: water flow due to osmotically active solutes (glutathione, bicarbonate)
616
Q

Describe the metabolism of bile acids

A

Synthesised in hepatocytes from cholesterol
Primary acids: cholic and chenodeoxycholic; conjugated w/ glycine/taurine to inc. solubility
Are amphipathic
Emulsify and transport lipids: essential for fat digestion and absorption

617
Q

What are the 2 important functions of bile?

A
  1. Fat digestion and absorption by emulsifying fat globules

2. Excrete waste products from blood: bilirubin, cholesterol

618
Q

What is the function of the gallbladder?

A

Concentrate bile

619
Q

Describe enterohepatic recirculation

A

94% bile salts excreted into duodenum reabsorbed by SI
Bile salts enter portal vein, taken to liver
- hepatocytes reabsorb ~100% from blood
- bile salts used 2x during single meal
Liver makes more to replace those lost in faeces

620
Q

Describe the control of gallbladder

A

Innervation from vagus, stim. by cholecystokinin
Release begins few mins after start of meal
During cephalic (sight, smell) and gastric (distend stomach) phase digestion, gallbladder contract and sphincter of oddi relax
- relaxation consequence of vagus and gastrin release

621
Q

Describe exocrine pancreas fluid

A

Colourless, odourless, isosmotic, alkaline fluid containing digestive enzymes

  • alkalinity result of bicarbonate: neutralise gastric acid and regulate pH intestines
  • enzymes digest carbs, proteins, fats
622
Q

Describe the control of bicarbonate secretion from the pancreas

A

Stim: secretin, CCK, gastrin, CCK
Inhib: atropine, somatostatin, pancreatic polypeptide, glucagon

623
Q

Describe the enzyme secretions of the pancreas and their control

A

Acinar cells secrete isoenzymes: amylases, lipases, proteases

Stim: CCK, ACh, secretin, vasoactive intestinal polypeptide

624
Q

Describe the role of amylase secreted by the pancreas

A

Only exocrine pancreas enzyme secreted in active form

Optimally active @ pH 7

Hydrolyse glycogen and starch to glucose, maltose

625
Q

Describe the role of lipase secreted by exocrine pancreas

A

Optimally active pH 7-9

Emulsify and hydrolyse fat in presence of FAs

626
Q

Describe the role of proteases secreted by exocrine pancreas

A

Essential for protein digestion

Secreted as proenzymes and required activation for proteolytic activity

627
Q

Describe the connection between the hypothalamus and pituitary gland

A

Hypothalamus controls release of ant. pituitary hormones through release of hypothalamic releasing and inhibitory hormones
Conducted to pituitary through minute blood vessels (hypothalamic-hypophysial portal vessels)

628
Q

What are the 4 trophic hormones of the ant. pituitary?

A
  1. Thyrotrophin (TSH)
  2. Corticotrophin (ACTH)
  3. Luteinising hormone (LH)
  4. Follicle stimulating hormone (LSH)
629
Q

What are the 6 hypothalamus factors that act on the ant. pituitary?

A
  1. Thyrotropin-releasing (TRH)
  2. Gonadotropin-releasing (GnRH)
  3. Corticotropin-releasing (CRH)
  4. Growth hormone-releasing (GHRH)
  5. Growth hormone-inhibiting (somatostatin)
  6. Prolactin-inhibiting (PIH)
630
Q

Describe the action and effect of TRH

A

A.P. action: stim. release thyrotrophin (TSH) by thyrotropes

Target organ: thyroid

T.O. action: inc. T3 and 4 release, inc. iodine uptake, synthesis and secretion thyroglobulin, hypertrophy, hyperplasia

631
Q

Describe the action and effect of gonadotropin-releasing hormone (GnRH)

A

A.P. action: stim. release luteinising hormone (LH) and follicle stimulating hormone (LSH) from gonadotropes

Target organ: sex organs

T.O. action

  • F: LH release pro-oestrogen, FSH oestrogen
  • M: testosterone
632
Q

Describe the action and effect of corticotropin-releasing hormone (CRH)

A

A.P. action: stim. release corticotrophin (ACTH) from corticotropes

Target organ: adrenal cortex

T.O. action: release gluco- and mineralocorticoids, inc. cholesterol availability, inc. blood flow through gland, hypertrophy and hyperplasia

633
Q

Describe the action and effect of grown hormone-releasing hormone (GHRH)

A

A.P. action: stim. release growth hormone by somatotropes

Target organ: body

T.O. action: inc. somatomedin, protein and cartilage synthesis, AAs uptake from skeletal muscle

634
Q

Describe the action to growth hormone inhibiting hormone (somatostatin)

A

Inhibit release of growth hormone from somatotropes

635
Q

Describe the action of prolactin inhibiting hormone (PIH)

A

Inhibit secretion of prolactin by lactotropes

636
Q

Describe the feedback inhibition of the hypothalamus and ant. pituitary

A

CNS stim. hypothalamus to release releasing factors
RFs act on ant. pituitary to release hormones
- hormones can have short -ve feedback on hypothalamus
Hormones stim. target organ that release products
- products can inhibit ant. pituitary and hypothalamus in long -ve feedback inhibition

637
Q

Describe the -ve feedback inhibitor of thyrotrophin

A

Products T3 and T4

T3: inhib. thyrotropin-releasing hormone from hypothalamus, stim. inhibitory somatostatin release from hypothalamus

T4: inhib. thyrotrophin secretion from ant. pituitary

638
Q

Describe the -ve feedback inhibitor of corticotrophin

A

Short: corticotrophin inhib. hypothalamus
Long: glucocorticoids inhib. CRH from hypothalamus and ACTH from ant. pituitary

639
Q

Describe the -ve feedback inhibition of gonadotrophins

A

F: pro- and oestrogen inhibit FSH and LH secretion from ant. pituitary, inhibit gonadotropin-releasing hormone release from hypothalamus

M: testosterone inhib. LH release from ant. pituitary and GnRH from hypothalamus

640
Q

Describe the -ve feedback inhibition of growth hormone and what stimulates and inhibits its release

A

Short: GH inhib. GHRH release from hypothalamus
Long: somatomedins inhib. GH secretion from ant. pituitary, stim. inhibitory somatostatin release from hypothalamus

Stim: dec. blood glucose, FAs
Inhib: ageing, obesity

641
Q

Describe the post. pituitary

A

Composed mainly of glial-like cells: pituicytes
Don’t secrete hormones; structural support of the large number of nerve fibres and endings
Controlled by supraoptic and paraventricular nuclei of hypothalamus

642
Q

What are the 2 post. pituitary hormones?

A
  1. ADH

2. Oxytocin

643
Q

Describe the release of ADH from post. pituitary

A

Formed primarily in supraoptic nucleus
Stim: high plasma osmolality (dehydration)
Disorder: diabetes insipidus

644
Q

Describe the release of oxytocin from post. pituitary gland

A

Primarily formed in paraventricular nucleus
Similar function to ADH due to similar AA structure
Stim: descent of foetus
Released by neuronal reflex: milk letdown

645
Q

What are the 5 causes of peptic ulcers?

A
  1. High acid and pepsin content
  2. Irritation
  3. Poor blood supply
  4. Poor mucus secretion
  5. Infection: H. pylori
646
Q

What are the 3 divisions of gastric secretion?

A
  1. Cephalic: sight, taste, smell, inc. vagal activity; inc. ACh inc. gastrin, HCl, histamine; mucous cells: inc. pepsinogen, epithelial cells inc. mucus
  2. Gastric: stomach distension inc. vagal and gastrin; peptide breakdown inc. gastrin
  3. Intestinal: initially gastrin, inc. inhibitory hormones: secretin, CCK, gastric inhibitory peptide
647
Q

What are the 3 major regions of the gastric glands?

A
  1. Pit: surface mucous cells
  2. Neck: neck mucous cells, mitotically active stem cells, parietal cells
  3. Body: major length of gland, upper and lower portion have different proportions of cells
648
Q

What are the 5 cell types found in the gastric gland?

A
  1. Mucous: including surface and neck
  2. Chief: peptic cells; secrete pepsinogen
  3. Parietal: oxyntic cells; secrete HCl
  4. Stem cells: required for repair
  5. Gastroenteroendocrine: enterochromaffin cells as stain from chronic acid salts
649
Q

What is cimetidine? How does it work?

A

Histamine (H2) receptor antagonist: inhibits histamine dependent axis secretion

ACh stim. gastrin (and pepsinogen) release
Histamine potentiates effects ACh and gastrin on parietal cell secretions
Histamine produced by enterochomaffrin-like cells in lamina propria surrounding gland

650
Q

Describe the secretion of HCl in the stomach

A

Secreted by parietal cells involving membrane fusion of tubulivesicular system w/ secretory granules

H/K ATPase exchanges H, K
Cl, Na actively transported into lumen of secretory canaliculus
- leads to HCl formation
K, Na recycled back into cell by pumps

651
Q

What is omeprazole?

A

H/K ATPase blocker

Inactivates acid secretion and is effective agent in treatment of peptic ulcer

652
Q

Explain the role of water in the inc. of blood plasma pH during digestion

A

Water enters cell by osmosis due to secretion of ions, dissociates to H+, OH-
CO2 enters from blood or formed during metabolism; combines w/ OH- to from H2CO3 (carbonic acid)
Dissociates to HCO3- (bicarbonate) and H+
Bicarbonate diffuse into blood accounting for inc. pH

653
Q

How do peptic ulcers arise?

A

Imbalance in rate of secretion of gastric juice and degree protection afforded by: gastroduodenal mucosal barrier, neutralisation of gastric acid by duodenal juices

654
Q

How is the duodenal protected from acidity?

A

By alkalinity of SI:

  • pancreatic secretions contain large quantities HCO3- neutralise HCl
  • inactivates pepsin and prevents digestion mucosa

HCO3- also provided in:

  • secretions from large a runner glands in duodenal wall
  • bile from liver
655
Q

What are the 2 feedback mechanisms that ensure neutralisation of gastric juice?

A
  1. Acid entering duodenum inhibits gastric secretion and peristalsis of stomach by nervous reflexes and hormonal feedback from duodenum. Dec. rate gastric emptying
  2. Acid in SI liberates secretin from intestinal mucosa. Secretin carried blood to pancreas and promotes release pancreatic juice (high HCO3- conc.)
656
Q

What are the 6 predisposing factors to peptic ulcers?

A
  1. Chronic inflammation due to Helicobacter pylori
  2. Non-steroidal anti-inflammatory drugs (NSAIDs)
  3. Tobacco
  4. Alcohol
  5. Stress
  6. Trauma
657
Q

What is a secretagogue?

A

Substance that causes release of another substance

658
Q

What are the 3 gastric secretagogues?

A
  1. Gastrin
  2. Histamine
  3. ACh
659
Q

Describe the role of gastrin as a secretagogue

A

Stim. H/K ATPase in parietal cells to release gastric acid (Ca dependent)
Stim. histaminocytes to release histamine

660
Q

Describe the role of histamine as a secretagogue

A

Stim. H/K ATPase in PCs to release gastric acid (cAMP dependent)

661
Q

Describe the role of ACh as a secretagogue

A

Stim. H/K ATPase in PC to release gastric acid (Ca dependent)
Stim. histaminocytes to release histamine
Stim. epithelial cells to inc. mucus and HCO3- secretion

662
Q

What are parietal cell secretions inhibited by?

A

Prostaglandin E (PGE) and prostacyclin I2 (PGI2) via cAMP

663
Q

Apart from ACh what 2 other secretagogue can stim. endothelial cells?

A
  1. PGE2

2. PGI2

664
Q

What is special about prostaglandins?

A

Cytoprotective

  • stim mucosal mucus and HCO3- secretion
  • inc. mucosal blood flow limits back diffusion of acid into epithelial of stomach
665
Q

What are the 3 phases of H Pylori pathogenesis?

A
  1. Active
  2. Stationary
  3. Colonisation
666
Q

Describe the active phase of H pylori

A

Produce ammonia (dec. pH) by action of urease (enzyme)
Makes conditions more favourable for self
Optimum pH 7

667
Q

Describe the stationary phase of H pylori

A

Enter mucus blanket, produce adhesion w/ affinity for fucose-containing receptors
Bind to apical membranes of epithelial cells w/ fucose-binding sites
Enables attainment of nutrients from epithelial which later die

668
Q

Describe the colonisation phase of H pylori

A

Well nourished bacteria detach from apical membranes, reproduce within mucus blanket
Attach to sialic acid containing mucous proteins, re-enter active phase

669
Q

What are the 8 characteristics of peptic ulcers?

A
  1. Appetite loss, weight loss
  2. Haematemesis (vomiting blood)
    - bleeding directly from ulcer
    - damage to oesophagus from severe/repeated vomiting
  3. Nausea, vomiting
  4. Waterbrash: rush saliva after sick to neutralise acid in oesophagus
  5. Abdominal pain: severe at mealtimes
  6. Bloating, abdominal fullness
  7. Gastric or duodenal perforations: peritonitis, pancreatitis
670
Q

What are the 4 types of drugs used to treat peptic ulcers?

A
  1. Acid release inhibitors
  2. Mucosal protection enhancers
  3. Antacids
  4. Antibiotics
671
Q

What are the 4 acid release inhibitors used for peptic ulcer treatment?

A
  1. Histamine antagonists: cimetidine/ranitidine; also promote duodenal ulcer healing
  2. Muscarinic antagonists: pirenzepine; inhib. gastric acid, antispasmodic
  3. Proton pump inhibitors: omeprazole
  4. Gastrin antagonists: proglumide
672
Q

What are the 4 mucosal protection enhancers used in peptic ulcer treatment?

A
  1. Colloidal bismuth: polymer-glycoprotein complex protect ulcer
  2. Sucralfate: thick gel adheres to base of ulcer
  3. Carbenoxolone: promote healing by inc. mucus
  4. Prostaglandins: inc. mucus, HCO3-, inhib. HCl
673
Q

What are the 4 antacids used in peptic ulcer treatment?

A
  1. Magnesium hydroxide
  2. Aluminium hydroxide
  3. Sodium bicarbonate
  4. Calcium salts
674
Q

What 2 antibiotics are used in treatment of peptic ulcers?

A
  1. Clarithromycin

2. Metronidazole

BDS 1 (11 decks)

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