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Systems Physiology Flashcards

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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
Describe the apocrine gland
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
26
Describe a melanocyte
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
27
Describe langerhan cells
Dendritic present in basal and spinous layers | Antigen presenting cell that is 1st line of defence, presents antigen to T lymphocytes
28
Describe merkel and mast cells
Merkel - in stratum basale, sensory perception (differences in texture) Mast - in dermis, immune response, produces histamine
29
What is endochondral ossification?
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
30
Describe endochondral ossification
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
31
In postnatal growth how is bone shaft diameter increased?
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
32
Where does growth in length occur in long bones?
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
33
What are the 5 zones of the epiphyseal growth plate?
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
34
What is intramembranous ossification?
Bone formation within fibrous membrane | Is typical of flat bones (mandible, skull)
35
Describe intramembranous ossification
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
36
What supplies blood to the periosteum and outer compact bone of diaphysis?
Periosteal arteries through Volkmann's and Haversian canals
37
What parts of bone does the nutrient artery supply?
Inner portions of diaphyseal compact bone, trabecular bone, bone marrow
38
What are the epiphyseal and metaphyseal trabecular bones supplied by?
Epiphyseal and metaphyseal arteries
39
Why does bone remodelling occur?
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
40
How does bone remodelling occur?
Usually bone resorbed by osteoclasts, osteoblasts line surface and produce new lamellar bone
41
What factors can affect remodelling?
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
42
What are the three types of muscle and what are their shared characteristics?
Skeletal, cardiac, smooth | All contract, contain actin and myosin plus accessory proteins
43
Describe the appearance of smooth muscle
No striations Central nucleus Spindle shaped Bundles of contractile proteins criss-cross cell, insert into focal densities (anchorage points in CM)
44
How is smooth muscle cell held and why?
Held by meshwork of laminae composed of T4 collagen binding cells into functional mass
45
What is the function of calmodulin in smooth muscle?
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
46
How is contraction in smooth muscle regulated?
Autonomic nervous system, hormones, local physiological conditions (high BP causes friction on surface of blood vessels, induces release of NO which causes vasodilation)
47
Do smooth muscle cells retain mitotic capability?
Yes - able to make more smooth muscle Uterus during pregnancy Fibroids (leiomyoma) - benign tumour of SM
48
Describe the appearance of cardiac muscle
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)
49
Can cardiac muscle regenerate?
No - cardiac muscle lacks steam cells, there is no regeneration after damage
50
Describe contraction in cardiac muscle
Similar to skeletal muscle | Under autonomic nervous system control
51
Define hypertrophy and hyperplasia
Hypertrophy - increase in size | Hyperplasia - increase in number
52
Describe the appearance of skeletal muscle
Striated - regular arrangement of actin and myosin Multinucleated fibres - fusion of multiple cells Peripheral nucleus
53
What are the regeneration capabilities of skeletal muscle?
Contain stem cells - able to repair self only if sarcolemma is intact If damaged - region replaced with fibrocollagenous tissue
54
Describe the sarcolemma
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
55
Describe contraction in skeletal muscle
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
56
What is a sarcomere?
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
57
What are the two muscle fibre types?
Fast twitch and slow twitch Average person will have 50/50 Sprinter more fast than slow Marathon runner more slow than fast
58
What do chondro, osteo, blast, cyte mean?
Chondro: cartilage Osteo: bone Blast: immature Cyte: mature
59
What is the role of CT?
1. Binding and structural support 2. Protection 3. Energy storage (adipose) 4. Insulation (adipose) 5. Transportation (blood) 6. Immunity (blood) 7. Mineral storage (bone)
60
What is CT?
A primary tissue type: epithelial, connective, muscle, nerve
61
What are the 5 CTs?
1. Fibrocollagenous tissues 2. Adipose tissue 3. Cartilage 4. Bone 5. Blood
62
What are the characteristics of CT?
Few cells compared to epithelia Large amounts of ECM, usually made by its intrinsic cells Common origin: mesenchyme cells
63
What are all cells of CT derived from?
Embryonic mesoderm | Some stem cells remain in adult (mesenchymal cells)
64
What are the 3 components of the ECM?
1. Ground substance 2. Structural glycoproteins 3. Fibres
65
Describe the GS
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
66
Describe the characteristics of GAGs and proteoglycans
-ve charge, open conformation retains water, +ve ions | hydrated gel which allows selective passage of molecules (nutrient diffusion)
67
Describe structural glycoproteins
Functional molecules Abundant in living organisms Many roles: linking, organising, catalysing e.g. laminin, fibronectin (adhesion), fibrillin (elastic fibre formation), osteocalcin (bone mineralisation)
68
Describe the fibres of CT
Collagen and elastic fibres Important for mechanic properties of CTs Fibre precursors secreted by CT cells - fibres polymerise outside cell
69
Describe collagen fibres
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
70
Describe elastic fibres
Stretch and resilience, precursor tropoelastin Elastic forms fibrils with fibrillin arteries, skin, lung, cartilage
71
Describe fibrocollagenous tissues
Cell: fibroblast Roles: structural, supportive | Classed according to: amount, organisation, type of collagen
72
What are the 3 types of fibrocollagenous tissues?
Loose (areolar) Dense Reticular (loose but with T3)
73
Describe loose fibrocollagenous CT
Relative to GS relatively few fibres Abundant viscous GS - hyaluronic acid (non-S GAG) Organisation: little T1 collagen with elastic fibres
74
Describe the cells and role of loose fibrocollagenous CT
Cells: fibroblasts, stem cells, adipocytes, defence immune cells Role: physical, metabolic, defensive support e.g. lamina propria: constituent of mucosa
75
Describe dense fibrocollagenous CT
Many fibres, little GS Organisation: random (dense irregular), structure (dense regular) T1 collagen, some elastic fibres
76
Describe the cells and role of dense fibrocollagenous CT
Cells: fibroblasts Role: mechanical support, tensile strength Irregular: dermis, capsules Regular: tendon (M-B), ligament (B-B)
77
Describe reticular fibrocollagenous CT
Few fibres, little GS Organisation: fine branching network T3 collagen
78
Describe the cells and role of reticular fibrocollagenous CT
Cell: fibroblasts Role: structural support in some highly cellular tissues e.g. lymph nodes, spleen, liver, glands
79
Describe adipose tissue
Abundant adipocytes Supporting loose CT (with fibroblasts) Located beneath skin, around internal organs, bone marrow, breast issue
80
Compare the 2 types of adipose tissue
White vs brown Unilocular (one space for lipid); multilocular Adult; new born Widespread; restricted Energy store, shock absorber, insulator; heat source -; rich in mitochondria
81
What is the function of cartilage?
Structural - solid but flexible, resists compression
82
What are the 3 types of cartilage?
Hyaline: most prevalent, many joint surfaces; T2 Elastic: outer ear, larynx; T2 and elastic Fibrocartilage: T1 and T2, pubic symphysis
83
Describe the GS and cells of cartilage
GS: unique, proteoglycans containing chondroitin sulphate, keratan sulphate linked to fibres Cells: chondroblasts form cartilage Chondrocytes maintain cartilage
84
Describe the function of bone
Structural, shape, locomotion, supportive, protective, metabolic, synthetic Highly organised and metabolically active
85
What is responsible for the hardness of bone?
Inorganic salts
86
Describe the ECM of bone
GS: osteoid (hard) T1 - lamellae in mature bone Mineralised (apatite crystals)
87
What cells are involved in bone CT?
Osteocytes: maintain bone Osteoblasts: secrete osteoid form bone Osteoclasts: resorb bone
88
What is the role of blood?
Metabolic support Transport of molecules and cells to/from tissues Defensive
89
Describe the ECM of blood
GS: fluid, plasma Proteins: albumins, globulins, fibrinogen, regulatory proteins
90
Describe the cells in blood
Circulating blood cells formed in bone marrow: erythrocyte, neutrophil, eosinophil, basophil, lymphocyte, monocyte, platelets
91
What are the common features of epithelial?
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)
92
Describe the functions of epithelial
Protection, sensation, absorption, digestion, secretion, excretion, cleaning
93
What is the basal lamina?
Layer of epithelium that separates epithelial from underlying CT
94
What is the function and structure of the basal lamina?
Supportive functions Proteoglycans and collagen T3,4 Epithelium and CT both contribute to formation anchor down epithelium to its loose CT (in dermis)
95
How are epithelia classified?
Number/arrangement of cells: simple (single layer), stratified (multi) Shape of cells: squamous (flattened), columnar (H>W), square
96
Describe simple epithelia
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
97
Describe where simple epithelia are found
Absorptive/secretory surfaces | Minimum barrier to diffusion required
98
Describe simple squamous epithelia
Single layer flattened cells Line surfaces involved in transport of gases (alveoli), fluids (blood vessels) Series body cavities
99
Describe simple cuboidal epithelia
Single layer square shaped cells Line small ducts, tubules that have secretory/excretory/absorptive function e.g. bile duct, medulla, salivary
100
Describe simple columnar epithelia
Similar to cuboidal expect taller, elongated nuclei at base of cell Absorptive/secretory surfaces e.g. SI, stomach
101
Describe stratified epithelia
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)
102
What layer(s) of cell is used to define classification?
Only the surface layer
103
Describe stratified squamous cells
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)
104
Describe stratified cuboidal epithelia
2/3 layers of cuboidal cells Line larger excretory ducts - salivary, sweat, pancreas No absorptive/secretory function but robust lining
105
Describe pseudo-stratified epithelia
All cells rest on BM but not all reach surface, nuclei at different levels giving appearance of stratified Ciliated or non-ciliated
106
Describe transitional epithelium
``` 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 ```
107
Describe the structure of the mucous membrane
Composed of: epithelium, BM, lamina propria (loose CT), SM | Specialised cells: mucus secreting goblet cells, absorptive enterocytes
108
Describe the function and name the 2 types of glands
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
109
Describe the structure of exocrine glands
Excretory duct, secretory portion Simple glands, few branches or compound, multiple branches Secretory portions tubular or alveolar
110
What are the three types of exocrine secretory mechanism and secretions?
Mechanism: eccrine/merocrine, apocrine, holocrine Secretions: mucous, serous (proteins/enzymes), sebum(lipids)
111
Describe the mechanism of eccrine secretion
Exocytosis Secretory granules fuse to PM, secreted e.g. eccrine sweat gland
112
Describe the apocrine secretion mechanism
Unbroken, membrane bound vesicles accumulate in apical cytoplasm, pinched off, cell loses part of PM e.g. apocrine sweat gland (body odour)
113
Describe the holocrine secretion mechanism
Whole cell lysis, entire contents secreted, cells lost in process e.g. sebaceous
114
Describe endocrine secretion
No duct Supporting tissue thin, sparse (reticular CT) associated with rich blood supply Cord and clump - most common Follicle - thyroid
115
Describe chondroblasts
Immature Form cartilage Found in perichondrium fibrocollagenous tissue surrounding cartilage Nutrient supply from outside
116
Describe chondrocytes
Mature Maintain cartilage Found in lacunae surrounded by cartilage
117
Describe hyaline cartilage
Found in trachea, bronchi, sternal ends of ribs, nasal septum, joints Forms model template for long bone formation
118
Describe elastic cartilage
Similar to hyaline with large amounts of elastic fibres | Found in outer ear, epiglottis, larynx
119
Describe fibrocartilage
Alternating layers of cartilage matrix and collagen fibres - confers strength Found in intervertebral disks, knee joint meniscus, symphysis pubis
120
Describe woven bone
Formed 1st after break/fracture Mechanically weak Random organisation of collagen
121
Describe lamellar bone
Mature - remodelled bone Lamellae due to regular organisation of collagen Mechanically strong Compact or trabecular
122
Describe compact lamellar bone
``` 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 ```
123
Describe trabecular lamellar bone
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
124
Describe long bone structure
Proximal epiphysis Metaphysis (epiphysis growth plate) Diaphysis Distal epiphysis
125
Describe an osteon
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
126
Describe the musculoskeletal wall of the thorax
Flexible | Consists of segmentally arranged vertebrae, ribs, muscles and the thernum
127
What are the three major compartments of the thoracic cavity?
Left pleural cavity Right pleural cavity Mediastinum
128
What is the thoracic cavity enclosed by?
Thoracic wall and diaphragm
129
What are the superior/inferior thoracic apertures?
Openings at top/bottom of thoracic cavity
130
Describe the superior thoracic cavity
Completely surrounded by skeletal elements Body of vertebra T1 posteriorly Medial margin of rib 1 each side Manubrium anteriorly
131
What is the importance of the thoracic apertures?
Airtight to prevent O2 leakage
132
Describe the inferior thoracic aperture
Large, expandable Margins made from bone, cartilage, ligaments Closed by diaphragm Passing structures pierce/pass posteriorly to diaphragm
133
What is the mediastinum?
Thick midline partition | Extends from sternum anteriorly to thoracic vertebrae posteriorly, from superior to inferior thoracic aperture
134
The pericardium and heart lie in which section of the mediastinum?
The middle
135
How do the lungs remain attached to the mediastinum?
Root formed by airways, pulmonary blood vessels, lymphatic tissues, nerves
136
What are the parietal and visceral pleura?
Parietal: pleura lining walls of cavity (outer layer) Visceral: pleura lining surface of lungs (inner layer)
137
What lie in the intercostal spaces?
Filled by intercostal muscles
138
What is the role of the costal grove?
Provides protection for intercostal nerves, associated major arteries and veins
139
Which intercostal muscle is responsible for inspiration and which for expiration?
External intercostal muscle: inspiration | Internal intercostal muscle: expiration
140
What are bronchi?
Branches of the trachea which air enter and leaves lungs via
141
Describe the flow of blood to and from the lungs
Pulmonary arteries deliver deoxygenated blood to lungs from right ventricle Oxygenated blood returns to left atrium via pulmonary veins
142
What is the hilum?
Point of entry and exit to lung
143
What is located within root and hilum of lung?
``` Pulmonary artery 2 pulmonary veins Main bronchus Bronchial vessels Nerves Lymphatics ```
144
Describe division of the trachea
``` 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 ```
145
Describe the features of alveoli that make them efficient at gas exchange
Thin cell wall | RBCs in close contact
146
Define ventilation
Movement of air in/out of lungs (breathing)
147
What are the boundaries of the upper respiratory system?
Nasal cavity to start of oesophagus and trachea
148
Define inspiration and expiration
Inspiration: pressure around elastic alveoli made low by expanding chest Expiration: pressure increased by decreasing size of chest, compressing gas in lungs
149
Describe the flow of air
Only flow from high pressure to low pressure
150
What do lung muscles control?
Diameter of airways
151
What muscles control respiration?
Respiratory muscles - generate pressure differences
152
In quiet breathing which process is the only active part?
Inspiration
153
Explain expiration in quiet breathing
Passive result of elastic recoil of lungs - pull lungs and diaphragm back to resting position
154
What is the diaphragm?
Major respiratory muscle (not essential however)
155
What nerves innervated the diaphragm?
Phrenic | Cause diaphragm to flatten, descend creating negative pressure, drawing air into chest
156
What is the role of the intercostal muscles?
2 movements: increase diameter of chest, draw air into lungs by reducing pressure Stiffen chest during inspiration preventing it being sucked in
157
Describe the 2 movements of the external intercostals
Pump-handle: anterior end of each rib elevated | Bucket-handle: diameter of chest increases by rib on either side raised from horizontal position
158
What nerves innervated the inner and innermost intercostals?
Segmental
159
What happens when the inner intercostals contract?
Pull ribs down, reduce diameter of chest | Reinforce spaces between ribs to prevent chest from bulging out during expiration
160
When do abdominal muscles contribute to expiration?
Only during heavy exercise
161
How to the abdominal muscles contribute to expiration?
Squeeze contents of abdomen up against the diaphragm, force up chest thus expelling air
162
Define intrapleural pressure
Pressure in small amount of liquid between parietal and visceral pleurae Usually negative with respect to atmosphere
163
How are the lungs expanded?
By creation of negative pressure outside inflating lungs
164
Describe the interaction between the lungs and chest wall
Chest wall elasticity causing to spring outwards, lungs causing to collapse thus are locked together and expand/contract as single unit
165
What happens to the lungs if the thorax is punctured?
Air enters pleural space, pressure will increase causing lungs to collapse
166
What are the elastic properties of lungs caused by?
Elastic fibres and collagen in tissues, surface tension caused by alveolar-liquid interface
167
What is lung compliance (CL)?
Measure of easily lungs can be stretched
168
What is the compliance equation?
Change in V/change in pressure
169
How can diseases effect compliance?
Kyohoscoliosis: progressive spine deformity Emphysema: destruction of elastic fibres, collagen causing increased compliance but lungs don't deflate as easily
170
Define airway resistance (Raw)
Resistance to the flow of gas within the airways of the lung
171
What are the 3 types of obstructive pulmonary disease?
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
172
What are the types of airway flow?
Laminar: parallel, orderly, streamlined Turbulent: chaotic
173
What are the main sites of airway resistance?
Vocal cords of larynx, open during inspiration, close during expiration Nose (inflammation, cold) Reduced resistance through mouth (exercise)
174
Using Poiseuille's law explain resistance in lower respiratory tract
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
175
Explain resistance in bronchi and bronchioles
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
176
What are the 2 circulatory systems?
Pulmonary | Circulatory
177
Describe the systemic circulatory system
High pressure developed in systemic arterial system provides driving force to perfuse all body tissues (except lungs) Pressure: 120/80mmHg
178
Describe the pulmonary circulatory system
Output of right side of heart Serves low pressure pulmonary circuit (lungs) Pressure: 20/8mmHg
179
What is unusual about the pulmonary artery?
Only artery in body to carry deoxygenated blood
180
Why is the pulmonary circulatory system low pressure?
As the membrane separating capillaries and alveoli is very thin High pressure would rupture membrane causing fluid to leak into alveoli
181
Describe the relationship between trachea division and diameter
Each time trachea splits into 2 diameter rapidly increases | Pulmonary vessels also double up to supply greater number of alveoli
182
Compare the flow of systemic and pulmonary circulation
Pulmonary flow is much greater than systemic
183
What are the 2 respiratory functions of pulmonary circuit?
Re-oxygenate blood | Remove CO2
184
What are the non-respiratory functions of pulmonary circuit?
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
185
What is the blood flow at rest in alveolar capillary and explain the length
0.8s - 3x longer than gaseous transfer | During exercise when flow rate increased can still completely re-oxygenate blood
186
What is the function of distension in pulmonary blood vessels?
Keeps pressure low when cardiac output increases without damaging tissue
187
What are the 2 mechanisms that can lower pulmonary blood pressure?
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
188
What can happen to pulmonary arteries if alveolar pressure increases too much?
Can increase resistance and reduce blood flow as alveoli inflated so much constrict capillaries
189
Explain the pressure change between pulmonary artery and capillary
Small change | As small change in venous pressure can make a considerable change to driving force
190
Explain the function of pulmonary circulation as a blood reservoir
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
191
Describe the function of bronchial circulation
Part of systemic circulation that supplies structures of lung including upper respiratory tract Doesn't reach terminal or respiratory bronchioles/alveoli
192
What is a pulmonary embolism and how does it effect circulation?
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
193
How is perfusion and ventilation matched?
Fraction of alveolar ventilation is matched to fraction of cardiac output per fusing that alveolus
194
What is the ideal ventilation/perfusion ratio of the lungs?
Between 0.8-1.0
195
How is distribution of blood flow affected in the lungs?
Gravity Alveolar gas pressure Hypoxia pulmonary vasoconstriction
196
In the systemic circulation what determines blood flow?
High resistance arterioles that regulate blood flow through capillary beds
197
Describe the effects of gravity on the upright lung
Ventilation: 2x greater in base than in apex Perfusion: 4x greater in base than in apex
198
What is the effect of alveolar gas pressure on capillaries?
If BP less than alveolar gas pressure capillary will be compressed
199
Explain how hypoxic pulmonary vasoconstriction promotes optimum V/Q
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
200
Describe the effect of Symp innervation on pulmonary vessels
Release NAdr acts on a1 and a2 receptors a1: vasoconstriction a2: vasodilation
201
Describe the effect of vestigial M3 receptors on pulmonary vessels
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
202
What is minute ventilation? (VI)
Vol. of air passing through lungs each minute
203
On average how many breaths do we take a min and what is their vol.?
12 breaths/min, 0.5L
204
Define tidal volume (VT)
Vol. air displaced during normal (quiet) inhalation and exhalation
205
What is the net flow of tidal volume?
0 | Vol. breathed out = vol. breathed in
206
What are inspiratory reserve volume and expiratory reserve volume?
IVR: max. vol. inspired above VT (2/3L>VT) EVR: max. vol. expired after VT expiration (1-1.5L>VT)
207
Define vital capacity (VC)
Total vol. air can be moved in 1 breath from full inspiration to full expiration
208
How is VC calculated?
VC = VT + IRV + ERV
209
What is functional residual capacity (FRC)?
Vol. air remaining in lungs after quiet expiration | Usually 3L
210
What is residual volume (RV)?
Vol. air remaining in lungs after full expiration Cannot be expired 1.5L
211
What 3 factors influence static volumes?
Anatomy (size) Elasticity of lungs, chest wall - exercise increases Strength of respiratory muscles - exercise increases strength
212
What do changes in lung volume indicate?
Lung disease - early indicator
213
What is spirometry and what 2 things does it measure?
Most common pulmonary function test (PFT) measures lung function Vol. and/or flow of air than can be in/exhaled
214
What is pulmonary ventilation?
Normal breathing | Air flowing into lungs during inspiration and out during exhalation
215
What 3 pressures are involved in pulmonary ventilation?
1. Atmospheric 2. Intra-alveolar 3. Intrapleural
216
What is alveolar ventilation?
Vol. of gas per unit time that reaches alveoli and takes part in gaseous exchange
217
What is the importance of alveolar ventilation?
Insufficient ventilation (hypoventilation) and excess ventilation (hyperventilation) occur in many lung diseases
218
Define anatomical dead space
Vol. air in upper respiratory tract (mouth, pharynx, trachea, bronchi up to terminal bronchioles) that cannot be exchanged Expired unchanged
219
What is alveolar dead space?
Vol. of air in alveolar with insufficient blood supply to effectively respire Increases with age and disease
220
What is the physiological dead space?
Anatomical + alveolar dead space
221
What factors influence physiological dead space?
VL - determined by age, sex, training | Breathing pattern - high-freq. artificial respiration still ventilates alveoli
222
How is alveolar ventilation calculated?
(VT - anatomical dead space) * respiratory rate = alveolar ventilation L/min
223
What is the respiratory exchange ratio (respiratory quotient) (R)?
CO2 output/O2 uptake
224
What is the importance of the respiratory exchange ratio?
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
225
What factors can affect RQ?
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)
226
What are the 2 key tasks for the control of breathing?
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)
227
What are the 3 centres of the pons?
1. Pons 2. Apneustic 3. Pneumotaxic
228
What is the function of the pons?
Influence, modify activity of medullary centres | Smooth out inspiration, expiration transitions
229
Describe the function of the apneustic centre
Inspiratory cut-off info. from pneumotaxic centre and vagus integrated before projected onto DRG
230
What is the function of the pneumotaxic centre?
Act as cut-off neurons for inspiration | Stimulation causes earlier termination of inspiration, higher respiratory freq. reduced VT
231
Describe the dorsal respiratory group (DRG)
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
232
Explain the sensitivity of chemoreceptors
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
233
What are the 2 types of chemoreceptors?
1. Central | 2. Peripheral
234
Describe central chemoreceptors
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
235
Where are peripheral chemoreceptors found?
Carotid sinus | Aorta arch
236
Describe type 1 (glomus) chemoreceptors
Responsive to local changes in PO22, PCO2, pH Prominent cytoplasmic granules Associated with un/myelinated afferent fibres
237
Describe type 2 (sustenfacular) chemoreceptors
Interstitial cell wrapped around T1 and nerve endings | Function unclear
238
Explain how O2 can influence respiration
``` Substantial drop (<60mmHg) If CO2 not removed, chemoreceptors will become unresponsive to PCO2 ```
239
Describe how pH can affect respiratory rate
Decreased pH, increases ventilation | Mediated by peripheral chemoreceptors
240
What are the 3 types of mechanoreceptors in lungs and airway?
Slowly adapting Rapidly adapting C-fibre endings
241
Describe pulmonary stretch receptors
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.
242
What are the 2 types of rapidly adapting stretch receptors (irritant receptors)?
Pulmonary C-fibres | Bronchial C-fibres
243
Describe pulmonary C-fibres
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
244
Describe bronchial C-fibres
Present in conducting airways Sensitive to inflammation products - causes bronchoconstriction and inc. airway vascular permeability Stimulation causes hyperponea and reflex laryngeal constriction
245
What are the 2 examples of upper airway irritant receptors?
Nasal receptors | Pharyngeal and laryngeal receptors
246
Describe nasal receptors
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
247
Describe pharyngeal and laryngeal receptors
Afferent pathway in laryngeal and glossopharyngeal nerves Aspiration/sniff/swallowing reflexes -be pressure induced abduction - ensure UAW patency during inspiration
248
Describe joint proprioceptors
Costovertebral joints contain mechanoreceptors sensitive to rib displacement Sensation of dyspnoea arising from absence of chest movement when holding breath
249
Describe muscle stretch receptors
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
250
What is a polymer and how are the made and broken down?
Long molecule consisting of many similar monomers Built up in condensation reaction Broken down by hydrolysis
251
What is the difference between nucleotides and nucleosides?
Nucleotides made of phosphate, sugar, base whereas nucleosides have no phosphate
252
What name is given to nucleotides with ribose or deoxyribose sugars?
Ribonucleotides | Deoxyribonucleotides
253
What are the 7 nitrogenous bases that can generate nucleosides?
3 purines: adenine, guanine, hypoxanthine 3 pyrimdines: cytosine, thymine, uracil Nicotinamide
254
Describe the structure of purines
2 rings: 1 5 membered ring fused to 6 member ring
255
Describe the structure of pyrimdines
1 6 membered pyrimidine ring
256
How are nucleosides made and how can they form nucleotides?
Made by attaching base to a deoxy/ribose ring | Form nucleotides by phosphorylation with specific kinase
257
What are the 2 main roles of nucleotides?
1. Short-term carriers of chemical energy (ATP) | 2. Storage and retrieval of biological info. (nucleic acids - DNA)
258
What is Lesch-Nyhan Syndrome (LNS) and what does it cause?
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
259
What is the function of hypoxanthine-guanine phosphoribosyltransferase?
Salvages purines from degraded DNA for purine synthesis
260
What is gout?
Painful condition caused by deposition of uric acid as needle like crystals in joints and/or soft tissue
261
What is asthma?
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
262
Describe lung morphology in asthma
Bronchial inflammation Oedema(build up of fluid), mucus plugging Bronchospasm (sudden constriction) Obstruction Over inflation/Atelectasis (collapse of lung) COPD
263
What 2 divisions is asthma separated into?
Extrinsic - antigen dependent | Intrinsic - exercise etc. (unclear)
264
Asthma is the interaction between what 3 components?
Cells: mast, eosinophils, macrophages Mediators: histamine, prostaglandins, cytokines Neuronal pathways: autonomic, sensory
265
Describe ParaNS innervation of the lungs
Muscarinic receptors Bronchoconstriction Inc. mucous secretions Inc. ion transport
266
Describe SympNS innervation of the lungs
B2 receptors Innervates blood vessels and glands NOT bronchial SM Cause by circulating Adr (hormone), NAdr (NT) Bronchodilation Red. glandular secretions Vasoconstriction
267
Describe non-adrenergic non-cholinergic innervation of the lungs
Mediator NO - bronchodilation
268
Describe sensory nerve innervation of the lungs
Non-myelinated C-fibres Neurokinin A: bronchoconstriction Substance P: inc. microvascular leakage/mucous secretion Calcitonin gene-related peptide: vasodilation
269
Describe the activation of mast cells
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
270
What 3 processes does mast cell activation lead to?
Degranulation Phospholipid metabolism Gene transcription
271
Describe macrophages
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
Describe the activation of T-lymphocytes (Th2 cells)
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
Describe basophils
Protein receptors on surface that bind IgE | Degranulate to release histamine, heparin, secrete lipid mediators (leukotrienes, cytokines)
274
Describe eosinophils
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
What are the 5 ways in which the airways are remodelled?
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
What are the 3 treatment areas of asthma?
1. Prevent mediator release 2. Relax contracted bronchial SM 3. Reduce inflammatory response
277
Name a drug that can inhibit mediator release and explain its action
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
Describe drugs that relax SM
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
Where are B2 receptors found?
SM, epithelial, mucous glands, vascular endothelium, mast, cells of inflammation
280
Describe theophylline
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
Describe the anticholinergic drug ipratropium bromide
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
Describe the anti-inflammatory beclomethasone dipropionate
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
What are leukotrienes?
Mediator released by mast, eosinophils, basophils Associated with bronchoconstriction, inc. vascular permeability, inc. mucous secretion, attract and activate inflammatory cells
284
Describe montelukast and zileuton and their effects
Montelukast: leukotriene D4 receptor comp. antagonist, maintenance treatment of asthma Zileuton: 5-lipoxygenase inhib., inhib. leukotriene synthesis Effects: inhib. bronchoconstriction, anti-inflammatory effects
285
Name and describe an immunomodulator
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
What is a possible side effect of omalizumab?
Anaphylaxis - systemic vasodilation, inc. microvascular leakage, bronchoconstriction, drop in BP
287
How is vascular permeability inc.?
Inc. size of fenestrations
288
At which generation of division does respiration begin?
17 - respiratory bronchioles
289
BOB Obstructed the Overseeing COPs
Lung morphology of asthma ``` Bronchial inflation Oedema, mucus plugging Bronchospasm Obstruction Over inflation/atelectasis (collapse) COPD ```
290
Treacle Syrup Always Beats Maple
Asthma remodelling of airways ``` Thickening of subbasement membrane Subepithelial fibrosis Airways SM hypertrophy, hyperplasia Blood vessel proliferation, dilation Mucous gland hyperplasia, hypersecretion ```
291
ASTHMA
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
What are the 4 specialities of RBCs specific for its function?
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
What is RBC count?
Number of red blood cells in 1 microlitre whole blood
294
What is haematocrit?
Percentage of RBCs in centrifuged whole blood
295
What is the diameter of RBCs?
7.8 micrometres
296
Explain cooperativity in haemoglobin
O2 binding to 1 subunit causes conformation change that increases subunit 2 affinity for O2, increases 3 and so on...
297
Define allosterism
Change in activity and conformation of an enzyme resulting from binding of compound to allosteric binding site (not active site)
298
What are the 2 haemoglobin states?
Tense (T) and relaxed (R)
299
Compare the T and R states of haemoglobin
R higher affinity for O2 | In absence of O2 T more stable, in O2 R stable so make conformation change
300
What is the name for haemoglobin when no O2 is bound?
Deoxyhaemoglobin
301
What is the name for haemoglobin when O2 is bound?
Oxyhaemoglobin
302
What is the name for haemoglobin when Fe is oxidised and no O2 is able to bind?
Methaemoglobin
303
Compare the affinities of CO, NO and O2 for Fe2+
CO, NO higher affinity so can displace O2 | Accounts for toxicity
304
What is the RBC count in M and Fs?
M: 4.5-6.3 million F: 4.0-5.5 million
305
What is the haemoglobin content for M and F?
M: 14-18 g/dL F: 12-16 g/dL
306
What is the haematocrit of M and F?
M: 40-54% F: 37-47%
307
What is the most important factor in determining saturation of Hb?
O2 partial pressure
308
What is important about the saturation level at resting tissue O2 partial pressure?
75% saturation means there is reserve capacity
309
Define homotropic and heterotropic effectors
Effectors: small molecules that influence O2 binding to Hb Homotropic: +ve effector Heterotropic: -ve effector
310
Give an example of a heterotropic effector and explain how it works
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
When is 2,3-BPG conc. inc.?
Hypoxia: inc. amount of O2 dissociated to tissue
312
Explain the physiological importance of HbF having a greater affinity for O2 than HbA
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
Describe the effects of pH, PCO2 and temp. on O2 binding
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
What 3 ways is CO2 transported in the blood and by what %?
Dissolved - 7% Carbamino compounds - 23% Bicarbonate - 70%
315
Describe external respiration/pulmonary respiration
O2: diffuse from alveolar air to pulmonary capillaries CO2: diffuse from pulmonary capillaries into alveolar air
316
Define O2 carrying capacity, O2 content and O2/haemoglobin saturation
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
What 4 things is rate of gas diffusion dependent on?
1. Partial pressure difference 2. Distance 3. Surface area 4. Molecular weight and solubility
318
Why is arterial PO2 slightly lower than alveolar PO2?
Physiological shunt | Blood from bronchial circulation enters pulmonary vein
319
Explain the Haldane effect
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
Describe gas exchange in the pulmonary capillaries
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
Describe gas exchange in systemic capillaries
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
What is the mediastinum?
Space between pleural cavities, occupies centre of thoracic cavity
323
What is the pericardium?
Fluid filled sac that surrounds the heart and great vessels 2 layers Serous: thin, 2 parts Fibrous: rough CT outlayer
324
What are the 2 parts of the serous layer of pericardium?
Parietal: lines inner surface of fibrous pericardium Visceral: adheres to heart, forms outer covering
325
What are the 4 function of the pericardial fluid?
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
What is the difference between the L and R ventricle wall size? Why is it important?
L ventricle wall much thicker as requires much larger pressure to pump blood around whole body
327
What are sulci?
Grooves on the surface of the heart due to the partitions that separate the heart into 4 chambers
328
What are the 3 sulci of the heart?
1. Coronary sulcus: circles the heart, separates atria from ventricles 2. Ant. and post. interventricular sulci: separate ventricles
329
Describe the structure of the heart
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
What is the function of chordae tendinae?
Stabilise heart and prevent back flow of blood | When contracted, close valve preventing prolapse and back flow
331
What are the 4 heart valves and what types do they fall under?
Semilunar: pulmonary, aortic Atrioventricular: mitral, tricuspid
332
What is the function of heart valves?
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
What are the heart sounds causes by?
Closure of valves
334
What are the 2 heart sounds and how are they caused?
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
What are 3 common valve diseases and what are their characteristics?
Incomplete: blood flows back into chamber Stenosis: restricted valve impedes flow from chamber Calcified aortic valve: narrowed and densely calcified
336
What is the cardiac skeleton and what is its function?
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
When and how do the coronary vessels fill w/ blood?
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
How is blood flow regulated?
By need: inc. O2 consumption and cardiac activity inc. in coronary blood flow proportionate to inc. in O2 consumption
339
What 2 molecules can regulate coronary blood flow?
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
What is angiogenesis and what is its importance?
Inc. number of new parallel blood vessels Red. vascular resistance within myocardium New vessels and collateralisation of vessels inc. coronary blood flow
341
What is Ischemic heart disease?
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
What is the clinical relevance of Ischemic artery disease?
Patients may present w/ jaw/toothache | Treatment may provoke symptoms or acute complications
343
How is the heart muscle supplied with blood?
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
Describe the structure of cardiac muscle
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
What is the role of cardiac muscle?
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
What is the resting potential of cardiac muscle cell?
-85mV
347
Describe the flow of K+ in a cardiac muscle cell
Flows out down conc. gradient | Flows in down electrical gradient
348
Why is K+ the greatest influencer of RMP in cardiac muscle?
Substantial K+ gradient | Membrane relatively permeable
349
Describe the 5 phases of an AP in a ventricular myocyte
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
What is the absolute refractory period?
Period when new AP cannot be generated as Na channels remain inactivated after closing at end of phase 0
351
What is the relative refractory period?
From about -50mV to RMP, AP can be triggered but requires greater stimulation
352
Describe the 3 phases of sinoatrial node AP
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
What are the main differences between SAN and ventricular APs?
SAN generated by Ca rather than Na No phase 1 or 2 No plateau, need AP to fire
354
Describe the transmission of AP throughout the heart
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
Explain the main waves of a electrocardiogram
P: AP through atria, depolarisation SAN QRS complex: AP through ventricles, depolarisation T: repolarisation of ventricles
356
What is the function of the cardiovascular system?
1. Rapid supply of O2 and nutrients 2. Rapid waste removal 3. Control: body temp, hormone distribution
357
Define flow rate and velocity
Rate: volume per unit time Velocity: distance per unit time
358
Compare total flow and flow volume
Total: constant throughout CVS | Flow volume: constant between serial segments
359
What 2 things is resistance in blood caused by?
1. Between blood and internal surface of vessel | 2. Between blood constituents (viscosity)
360
What is the importance of Poiseulle's law?
Resistance inversely proportional to 4th power radius | 50% dec. in diameter will cause 16 fold inc. in resistance
361
What is the important of the pressure differences between arteries and veins?
Causes blood to flow
362
What maintains the pressure difference between arteries and veins?
Heart maintains high pressure in arteries | Vessels maintain low pressure in veins
363
How is pressure regulated?
Proportional to resistance | If resistance inc. pressure will drop proportionally to maintain blood flow
364
What is blood flow proportional to?
4th power radius
365
What are the 2 types of blood flow?
1. Laminar | 2. Turbulent
366
Describe laminar flow
All particles flowing parallel to vessel wall | Particles in centre flow fastest
367
Describe turbulent blood flow
Irregular path, may develop whirlpools in vessels | Causes vibrations heard as murmurs
368
What is the critical velocity?
Velocity at which blood flow transitions from laminar to turbulent
369
What 4 factors inc. the likelihood of turbulent flow?
1. Flow velocity inc. 2. Vessel radius inc. 3. Blood density inc. 4. Blood viscosity dec.
370
How is blood viscosity determined?
By the haematocrit: percent blood volume which is RBCs
371
What are the 3 layers of blood vessels?
1. Tunica intima 2. Tunic media 3. Tunica adventitia
372
Describe the tunic intima
Inner layer Endothelial cells Acts as barrier between blood and vessel Filtration controls passage of WBCs
373
Describe the tunica media
2 layers of elastic tissue: internal and external sandwich layer of SM Mechanical strength SM allows altering of diameter
374
Describe the tunica adventitia
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
Compare large and small arteries
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
Describe arterioles
SM major component, contraction regulated
377
Describe capillaries
Single layer of endothelial cells No tunica media or adventitia Site of exchange of nutrients and waste between blood and interstitial fluid
378
Describe venules
Endothelial lining and small amount of fibrous tissue
379
Describe veins
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
What 4 factors influence venous return?
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
Explain how the skeletal muscle pump inc. venous return
Veins in limbs located between muscle blocks and contain valves When muscle contracts pinches vein pushing blood back to heart
382
Explain how the abdomino-thoracic pump inc. venous return
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
Describe the control of cardiac output
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
How does regulation of CO change during exercise?
Mild exercise: small changes in CO achieved by changes in HR and stroke vol Heavy exercise: further inc. CO achieved by inc. HR
385
Describe how SNS innervation controls HR
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
Explain how PSNS fibres controls HR
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
Define end-diastolic volume and end-systolic volume
EDV: blood in ventricle prior to contraction ESV: blood remaining in ventricle post contraction
388
What 3 factors influence EDV?
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
What 4 factors influence ESV?
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
Define inotrope
NT/hormone/drug that alters force of contraction of heart | +ve: inc. contractility
391
Describe right sided heart failure
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
Describe L sided heart failure
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
What 2 things does maintaining BP require?
1. Cooperation of heart, blood vessels and kidneys | 2. Supervision of brain
394
What are the 3 main factors affecting BP?
1. CO 2. Peripheral resistance 3. Blood vol
395
Define intrinsic and extrinsic autoregulation
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
What is the Frank-Starling law?
Within physiological limits, the heart pumps all blood that comes into it w/o allowing accumulation of blood in vessels
397
Describe short and long term control of BP
Short Mediated by NS and blood borne chemicals Counteract fluctuations in BP by altering CO and PR Long Regulate blood vol.
398
Describe short term neural controls of BP
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
Describe the short term vasomotor controls of BP
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
Describe the baroreceptor-initiated reflexes in short term control of BP
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
Describe the chemical controls for short term BP control
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
Describe the long term controls of BP
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
What are the 4 effects beta stretch receptors have?
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
What are 4 chemicals that inc. BP?
Adrenal medulla hormones: NA, AD ADH: vasoconstriction in extremely low BP Angiotensin II: intense vasoconstriction Endothelium derived factors: endothelin, vasoconstriction
405
Describe the anatomy of the microcirculation
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
Describe the capillaries
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
Describe capillary beds
Arise from single metateriole Vasomotion: intermittent contraction and relaxation Throughfare channel: bypass capillary bed
408
Describe the 4 active function of capillary endothelium
1. Prostacyclin: relaxation of vascular SM 2. NO: relaxation 3. CO: relaxation 4. Endothelin: contraction
409
What is the passive function of capillaries?
Exchange of CO2, O2, H2O, nutrients between blood and interstitial fluid by osmosis, diffusion and filtration
410
What are the 3 types of capillary?
1. Continuous 2. Fenestrated 3. Sinusoidal
411
In which 6 locations are continuous capillaries found?
1. Skin 2. lung 3. fat 4. muscle 5. heart 6. brain
412
Describe continuous capillaries
Endothelial cell and basal lamina do not form openings
413
In which 2 locations is fenestrated capillaries found?
1. Kidney | 2. Gut
414
Describe fenestrated capillaries
Endothelial cell body forms small openings | Allows components of blood and interstitial fluid to bypass endothelium
415
In which 3 locations are sinusoidal capillaries found?
1. Liver 2. Spleen: breakdown of red blood cells 3. Red bone marrow
416
Described sinusoidal capillaries
Formed by fenestrated endothelial cells and incomplete basal lamina From large, irregular vessels Found where free exchange of substances/cells is advantageous
417
What are the 3 methods of transport across the capillary bed?
1. Diffusion: most important 2. Transcytosis 3. Bulk flow
418
Describe diffusion across capillary bed
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
Describe transcytosis in capillary bed
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
Describe bulk flow in capillary bed
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
Describe the flow of molecules in filtration and reabsorption
Filtration: from capillaries into interstitial fluid Reabsorption: from interstitial fluid into capillaries
422
Compare fluid flow at the arterial and venous end of capillaries
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
What can happen if ECF levels are not regulated?
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
How is blood flow controlled?
All flow to particular vascular bed controlled by size of arterioles which is controlled by SM contraction
425
What are the 2 areas circulation can effect and how?
1. Local: regulates blood flow to tissue | 2. Central: affects BP by acting on total peripheral resistance; affects central blood vol
426
What are the 2 types of vascular smooth muscle control?
1. Intrinsic: located in tissue | 2. Extrinsic: hormones and nerves from outside tissue
427
What are the 3 intrinsic control factors of VSM?
1. Local temp 2. Transmural pressure 3. Local metabolites, autacoids, endothelium derived factors
428
Explain how local temp can control VSM
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
Explain how transmural pressure can control VSM
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
What are 5 local metabolites that act as vasodilators?
1. K ions 2. Adenosine 3. Acidosis 4. Hypoxia 5. Inc. interstitial osmolality
431
Explain local metabolite control of VSM
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
What is inflammation?
Inc. permeability of the microcirculation
433
What 4 autocoids can control VSM?
1. Bradykinin 2. Histamine 3. Serotonin (5-HT) 4. Arachidonic acid derivatives
434
When are autocoids released and what are their 5 effects?
From cells and tissues in response to inflammation 1. Redness 2. Pain 3. Loss of function 4. Heat 5. Swelling
435
Explain how endothelium factors can cause vasodilation
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
What are endothelins?
Endothelium derived contraction factors | Proteins that effect vasoconstriction of blood vessels and BP
437
Describe endothelin A receptors
Found in SM of blood vessels | Cause vasoconstriction, retention of Na resulting in inc. BP
438
What is the function of Endothelin B receptors and how do they work?
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
Where is the shared location of endothelin receptors and what is their function there?
Nervous system | May mediate neurotransmission and vascular function
440
Describe the effect of sympathetic vasoconstrictor nerves on peripheral circulation
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
What are the 3 effects of inc. sympathetic vasoconstriction on peripheral circulation?
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
Describe the effects sympatho-adrenal activation in regulation of peripheral circulation
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
Describe the effects of angiotensin II and ADH on peripheral circulation
General vasoconstriction of VSM causes inc. resistance and BP
444
What are 3 paracrine regulators produced by endothelium that promote relaxation?
1. NO 2. Bradykinin 3. Prostacyclin
445
What is the importance of NO and how can levels be inc.?
Involved in setting resting tone of vessels Inc. by PSNS activity Vasodilators drugs (nitroglycerin) act through NO
446
What is endothelin 1?
Vasoconstrictor produced by endothelium
447
Describe myogenic autoregulation of circulation
Intrinsic to VSM VSM contracts when stretched and relaxes when not Dec. arterial pressure causes cerebral vessels to dilate
448
Describe metabolic autoregulation of circulation
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
Describe the skeletal muscle pump
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
Explain the role of the thoracic cavity in venous return
Inspiration creates -ve pressure allowing veins to dilate making route to heart easier, inc. venous return
451
Why is standing up a problem for BP?
Gravity causes blood pooling in lower body preventing blood from reaching brain Orthostatic/postural hypotension
452
How does the baroreceptor reflex return BP to normal?
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
What are the changes in CO, HR and SV during exercise and how are these accomplished?
CO: 6.0-20 l/min HR: 80-190 bpm SV: 75-105 ml Large inc. sympathetic nerve activation Redistribution of CO
454
How do sympathetic vasoconstrictor nerves cause circulatory changes during exercise?
Varicosities secrete NA @ nerve endings can red. blood flow through resting muscles to 1/3 normal
455
How does inc. blood flow through muscle capillaries affect circulation during exercise?
Inc. SA for exchange allowing greater O2 and nutrient supply
456
How is blood flow through skeletal muscle changed during exercise?
Dec. O2 in muscle enhances flow and causes release of local vasodilators
457
What is the most important vasodilator? What are 4 others?
Adenosine 1. K+ 2. CO2 3. ATP 4. Lactic acid
458
What is shock?
Generalised severe red. in blood supply to body tissues | Inadequate perfusion leads to cellular hypoxia and tissue damage
459
What is hypovolemic shock?
Condition in which rapid fluid loss results in multiple organ failure due to inadequate perfusion
460
What are the 4 causes of hypovolemic shock?
1. Trauma 2. Vomiting/diarrhoea 3. Burns 4. Haemorrhage
461
What are the 4 systems the body activates in response to hypovolemic shock?
1. CVS 2. Neuroendocrine 3. Haematological 4. Renal
462
How does the CVS respond to hypovolaemic shock?
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
How does the renal system respond to hypovolaemic shock?
Kidneys stim. secretion of renin from juxtaglomerular apparatus Angiotensinogen -> angiotensin II Vasoconstriction of arteriolar SM, stim. aldosterone release by adrenal cortex
464
How does the neuroendocrine system respond to hypovolaemic shock?
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
How does the haematological system respond to hypovolaemic shock?
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
After a 20% haemorrhage what are the immediate responses?
Activation of CV reflexes: baroreceptor reflex | Maintenance of blood flow to heart and brain
467
After 20% haemorrhage, what are the 3 intermediate responses? (Mins-hrs)
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
After 20% haemorrhage, what are the 3 long-term responses? (Days-weeks)
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
What are the 4 effects of 20-40% haemorrhage?
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
What are the 6 effects of >40 haemorrhage?
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
What are the 6 functions of the kidneys?
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
Why is control of body fluid vol. important?
Required for CVS | Many metabolic functions sensitive to pH: maintained by buffers in fluid, activity of kidneys and lungs
473
What 4 products are excreted by the kidneys?
1. Urea: from AAs 2. Uric acid: from nucleic acids 3. Creatinine: from muscle creatine 4. Haemoglobin and hormone metabolism end products
474
What organs make up the upper and lower urinary system?
Upper: kidneys Lower: bladder, urethra
475
Describe the excretion of urine
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
What does the renal vein drain into?
Inf. vena cava
477
What is the minimum required daily urine production?
500-600ml
478
Describe the structure of the kidneys
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
Described the blood supply of kidneys and pyramids
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
What are the 2 types of nephron?
1. Cortical | 2. Juxtamedullary
481
Describe cortical nephrons
Originate in outer 2/3 cortex
482
Describe juxtamedullary nephrons
Originate in inner 1/3 cortex | Have loops of Henle that pass deep into medulla
483
Describe the structure of nephrons
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
What is the renal corpuscle?
Bowman' capsule and glomerulus
485
What is the function of the renal corpuscle?
Formation of ultra-filtrate
486
What is the function of the PCT?
Bulk reabsorption of solutes and water, secretion of solutes (except K)
487
What is the function of the loop of Henle?
Establish medullary osmotic gradient | Reabsorption of water (descending) and NaCl (ascending)
488
What is the function of the DCT?
Fine-tuning of the reabsorption/secretion of small quantities of solute
489
What is the function of the collecting duct?
Fine-tuning reabsorption of water, reabsorption of urea
490
What are the 3 layers that glomerular filtrate has to pass through?
1. Fenestrated endothelium of capillary: filtering membrane 2. Continuous basal lamina of Bowman's capsule 3. Epithelial cells of capsule
491
How are mesangial cells in the basal lamina believed to be able to reduce glomerular filtration rate?
By contraction to red. SA available for filtration
492
What is glomerular filtration rate determined by?
Net filtration pressure
493
Describe the forces involved in net filtration pressure
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
Define glomerular filtration rate
Vol. fluid filtered from glomeruli into Bowman's capsule per unit time
495
Despite low NFP how are large vol. filtrate produced?
Glomeruli capillaries extremely permeable and have large SA
496
How is GFR regulated?
Via afferent arteries: constriction vs dilation
497
Describe the 2 types of GFR regulation
1. Extrinsic: sympathetic nerve | 2. Intrinsic: renal auto-regulation
498
Describe the 2 methods of auto-regulation of GFR
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
What 4 factors determine GFR?
1. Glomerular capillary pressure 2. Plasma oncotic pressure 3. Tubular pressure 4. Glomerular capillary SA
500
Define renal plasma clearance
Vol. plasma from which a substance is completely removed in 1min by excretion in urine
501
Define osmotic pressure
Hydrostatic pressure produced by difference in conc. between 2 fluids either side of a surface
502
Define osmolarity and osmolality
Osmolarity: moles of solute/litre of solution Osmolality: moles of solute/kg of solvent
503
How is water transported? What is this dependent on?
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
What are the 4 main hormones involved in regulating kidney function?
1. Angiotensin II 2. Aldosterone 3. ADH/vasopressin 4. Atrial natriuretic peptide
505
How does angiotensin II function?
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
How does aldosterone function?
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
Describe how ADH functions
Stimuli: inc. osmolarity ECF, dec. blood vol Mechanism: aquaporin-2 in apical membranes Effect: inc. facultative reabsorption of water, dec. osmolarity body fluids
508
How does atrial natriuretic peptide work?
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
Describe the process by which Na is absorbed by the proximal tubule
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
Described how Cl and water are absorbed by the proximal tubule
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
How are glucose and AAs absorbed by the proximal tubule?
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
What is the significance of reabsorption in the proximal tubule?
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
Why is hyper-osmotic urine more difficult to form compared to hypo-osmotic?
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
Describe reabsorption of NaCl in the thick-walled ascending limb of Loop of Henle
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
How does the descending limb of Henle form hypertonic solution?
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
What is the significance of NaCl reabsorption from the ascending loop on the osmolarity of the renal medulla?
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
What is the vasa recta?
Blood supply of the renal medulla | Surrounds collecting ducts, loop of Henle, convoluted tubules
518
What is the role of the vasa recta?
Supply medullary tissues w/ nutrients, O2 | Maintain hypertonicity of renal medulla: salt has to be retained; water, ions must be removed
519
What are inputs and outputs of water balance?
Input: food, water, oxidation Output: urine, stool, respiratory loss, sweat
520
What factors contribute to water balance?
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
Describe the distribution of water reabsorption in the kidneys
65% proximal tubule 20% loop Henle 15% fine tuned by hormones in distal tubule and collecting duct
522
What does the reabsorption of water in distal tubule and collecting duct depend on?
Circulating ADH | Inc. permeability to water allowing to achieve equilibrium w/ interstitial fluid of medulla
523
Describe the stimulation and mechanism of ADH
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
Describe how diabetes insipidus and and diabetes mellitus affect water balance
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
What is the juxtaglomerular apparatus?
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
What 3 factors can trigger renin release from juxtaglomerular apparatus?
1. Sympathetic stimulation 2. Fall in renal perfusion pressure @ afferent arteriole 3. Hyponatraemia (low Na)
527
How does renin function?
Cleaves angiotensin I from angiotensinogen then converted to angiotensin II by ACE Angiotensin II stim Na/H antiporters, inc. Na, water reabsorption
528
What is the overall effect of angiotensin and the 4 individual?
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
Why is acid/base balance important?
Many enzymes activity dependent on pH between narrow range
530
Compare volatile and non-volatile acids
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
What is the average plasma H conc. and pH?
Conc: 40nmol/L (0.00004mmol/L) pH: 7.36-7.44
532
What is a buffer?
Solution that resists/red. changes in pH
533
What is buffer capacity determined by?
1. Disassociate constant (pK): relationship between pK and pH determined by Henderson-Hasselbalch equation 2. Quantity of buffer
534
What is unique about the bicarbonate buffering system? Why is this important?
Remains at equilibrium w/ atmospheric air [HCO3-] controlled by kidneys PCO2 controlled by lungs
535
In what 2 regions in bicarbonate reabsorbed by the body?
Proximal and distal tubules | Most (85%) in proximal
536
Describe reabsorption of bicarbonate in PROXIMAL tubule
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
Describe the reabsorption of HCO3- in the distal tubule
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
What is the main difference between distal and proximal tubule bicarbonate reabsorption?
Proximal tubule has CA intracellularly and extracellularly whereas distal only intracellularly
539
Define acidosis and alkalosis
Acidosis: abnormal inc. in H+ blood conc., pH < 7.35 Alkalosis: abnormally high alkalinity of blood and fluids, pH > 7.45
540
What 3 mechanisms minimise disturbances to acid/base balance?
1. Buffering 2. Adjusting renal excretion: H+/HCO3- 3. Adjusting ventilation: blood PCO2
541
Describe respiratory acidosis
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
Describe metabolic acidosis
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
Describe metabolic alkalosis
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
Describe respiratory alkalosis
Caused by inc. ventilation (drugs stimulating respiratory centres) or hyperventilation (anxiety) High pH, red. PCO2 Red. acid excretion, red. HCO3- reabsorption
545
What are the 6 functions of the GIT?
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
What 6 organs make up the GIT? What are the 6 accessory structures?
1. Oral cavity 2. Pharynx 3. Oesophagus 4. Stomach 5. Small intestine 6. Large intestine 1. Teeth 2. Tongue 3. Salivary glands 4. Liver 5. Gall bladder 6. Pancreas
547
What are the 4 layers of the GIT from lower 1/3 oesophagus to anus?
1. Mucosa 2. Submucosa 3. Muscularis 4. Serosa
548
Describe the mucosa of the GIT
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
Describe the submucosa
Highly vascular | Neuronal network: submucosal/Meissner's plexus; primarily control secretions, also SM and blood vessel tone
550
Describe the muscularis
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
Describe the neuronal control of the GIT
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
Define mastication
Breakdown of food mechanically and initial enzymatic digestion by ptyalin (alpha amylase)
553
What are the 3 stages of swallowing?
1. Oral: blows to back of OC; voluntary 2. Pharyngeal: involuntary 3. Oesophageal: involuntary
554
Describe the structures that control oral stage of mastication and their nerve supply
Muscles of mastication: mandibular of trigeminal Pterygoids, masseter, temporalis Tongue: hypoglossal Buccinator, orbicularis oris: facial
555
What muscles are involved in the pharyngeal stage of swallowing?
Cricopharyngeus: CN10, sympathetic; relax, aid movement Soft palate: CN5 7 9 12; close nasopharynx Pharyngeal: CN9 10; propel
556
What nerves control the oesophageal stage of swallowing?
CN10, sympathetic
557
Describe the waves of peristalsis in the oesophagus
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
What is the difference in peristalsis in oesophagus?
Upper part: peristaltic wave progresses rapidly | Lower 1/3: more sluggish
559
What are the differences in peristaltic wave caused by?
Upper part musculature is striated, lower part smooth
560
What are the 3 layers of the muscularis of the stomach?
1. Outer longitudinal 2. Middle circular 3. Inner oblique (at 45 degree to other layers)
561
What do the different layers of stomach muscularis allow for?
Movement in directions | Mix and churn food w/ acids/enzymes
562
Describe gastric pits and glands
Epithelial cells form narrow channel: pits | And columns of secretory cells: glands
563
What are the 3 exocrine glands of gastric glands? What do they secrete?
1. Mucus neck cell: mucus, HCO3- 2. Chief cells: pepsinogen 3. Parietal cells: HCl, intrinsic factor for B12 absorption
564
What are the 4 hormones secreted by enteroendocrine cells?
1. Gastrin 2. Secretin 3. Choleocystokinin 4. Gastric inhibitory peptide
565
Describe gastrin
Stimulated by peptides and AAs in stomach | Stimulates G cells to release gastric juice
566
Describe choleocystokinin
Stimulated by AAs, FAs in duodenum Stimulates Gall bladder: contract, release bile Pancreas: release pancreatic digestive enzymes into pancreatic fluid
567
Describe secretin
Stimulated by acidic chyme in duodenum | Stimulates pancreas to release HCO3- into pancreatic fluid
568
Describe gastric inhibitory peptide
Stimulated by glucose and fat in duodenum | Inhibits release of gastric juice
569
Describe cephalic regulation of the enteroendocrine
Sound, sight, smell Initiates reflex via medulla, hypothalamus, vagal output to stim. submucosal plexus Inc. gastrin, inc. peristalsis, inc. HCl
570
Describe gastric regulation of enteroendocrine
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
Describe intestinal regulation of enteroendocrine
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
Describe the vomit reflex
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
What are the 4 structures involved in the emesis?
1. Area postrema CTZ 2. Vestibular nuclei, N. tracts solitarius 3. Vomiting centre 4. Vagal nerve endings
574
Describe receptor, agonist and antagonists for area postrema emesis
D2 receptor Apomorphine, L-DOPA Antidopaminergic
575
Describe receptors, agonists, antagonists for vestibular nucleus and N. tractus solitarius
Vestibular: M, cholinomimetics (ACh, physostigimine), scopolamine N. tractus solitarius: H1, histamine, Dramamine
576
Describe receptor, antagonist, agonist for vomiting centre
M Cholinomimetic: bethanechol, atenolol, pyridostigmine, clonidine, propranolol Scopolamine
577
Describe receptor, agonist and antagonist for vagal nerve ending involved in emesis
5-HT3 Serotonin Ondansetron, granisetron, tropisetron
578
What are the 4 functions of the SI?
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
What are the 3 regions of the SI?
1. Duodenum 2. Jejunum 3. Ileum
580
Describe the mucosa and submucosa lining of the SI
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
Describe the control of SI motility
Neuronal Extrinsic and intrinsic (myenteric plexus) Hormonal factors
582
What are the 2 movements of SI?
Mixing contractions: segmentation | Propulsive movements: peristalsis
583
What is the migratory motility complex?
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
Describe the modulation of peristaltic activity
Gastroenteric reflex via myenteric plexus Hormonal inc.: gastrin, CCK, insulin, 5HT dec.: secretin, glucagon
585
What is the function of the ileocecal sphincter and valve?
Valve: prevent back flux of colon contents Sphincter: prevent rapid emptying of ileum Prevents contamination of SI by colonic bacteria
586
How do the stomach and ileocecal sphincter interact?
Reflexly via intrinsic nerve plexus Pressure build in cecum closes sphincter Pressure build in ileum opens
587
Describe the motility of the large intestine?
Proximal half concerned w/ absorption, distal 1/2 w/ storage Mixing: Haustrations Propulsive: mass movements
588
What are the 6 regions of the LI?
1. Cecum 2. Ascending colon 3. Transverse colon 4. Descending colon 5. Sigmoid colon 6. Rectum
589
Describe the ascending colon
Specialised for processing chyme | Short time compared to transverse colon
590
Describe the transverse colon
Specialised for storage and dehydration Chyme present for 24hrs Primary site of water and electrolyte removal, storage
591
Described the descending colon
Conduit between transverse colon and sigmoid | Accumulate for 24hrs an then instilled into caecum
592
How is faecal continence maintained?
Musculature of rectosigmoid region, anal canal, pelvic floor Puborectalis muscle and external anal sphincter functional unit to maintain continence
593
Describe the muscularis of LI
Internal circular muscle External longitudinal muscle thickened by 3 longitudinal bands called taeniae coli Colon gathers into sacs called haustra
594
What is the initiation of the propulsive movements of the LI?
Mass movements initiated by gastrocolic and duodenocolic reflexes initiated by distension of stomach and duodenum Associated w/ parasympathetic
595
Describe the Haustration movements
Ring-like circular contractions of circular muscle | Break up faeces, present portion to surface for water removal
596
Describe the muscle secretion and the absorption function of the LI
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
What are the functions of colonic bacteria?
Ferment carbs to H2, CO2, CH4 gas | Convert proteins to AAs
598
Describe the defecation reflex
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
Describe the structure of the liver
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
What are the 6 functions of the liver?
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
Describe the blood reservoir function of the liver
Normal blood vol. ~10% total Heart failure: inc. up by 1L Exercise/haemorrhage: dec. 30-40%
602
Describe the blood supply of the liver
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
What are hepatocytes?
Cells found in liver responsible for exocrine secretion, bile formation and endocrine products
604
Describe liver lobules
Hexagonal structures consisting of hepatocytes Hepatocytes radiate out from central vein At each corner of lobule is portal triad
605
What is in the portal triad?
Artery Vein Bile duct
606
Describe liver sinusoids
Wide blood vessels: single layered, have fenestrations, no basement membrane Blood makes contact w/ hepatocytes and is filtered/detoxified
607
Describe the metabolism of carbs in the liver
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
Describe protein metabolism in the liver
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
Describe fat metabolism in the liver
Carbs and proteins to fats Beta oxidation of FAs Synthesis of special lipids: lipoproteins, cholesterol, phospholipids
610
Describe the metabolism of RBCs
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
Describe the metabolism of bilirubin
Most from RBC metabolism and reticuloendothelial cells, some from breakdown of haem proteins Biliverdin formed from haem, red. to bilirubin (unconjugated)
612
Describe conjugated bilirubin
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
Describe the secretion of bile
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
What are the contents of bile?
Hydrogen carbonate ions Bile pigment and salts Cholesterol
615
What are the 2 methods by which bile acids are secreted?
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
Describe the metabolism of bile acids
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
What are the 2 important functions of bile?
1. Fat digestion and absorption by emulsifying fat globules | 2. Excrete waste products from blood: bilirubin, cholesterol
618
What is the function of the gallbladder?
Concentrate bile
619
Describe enterohepatic recirculation
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
Describe the control of gallbladder
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
Describe exocrine pancreas fluid
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
Describe the control of bicarbonate secretion from the pancreas
Stim: secretin, CCK, gastrin, CCK Inhib: atropine, somatostatin, pancreatic polypeptide, glucagon
623
Describe the enzyme secretions of the pancreas and their control
Acinar cells secrete isoenzymes: amylases, lipases, proteases Stim: CCK, ACh, secretin, vasoactive intestinal polypeptide
624
Describe the role of amylase secreted by the pancreas
Only exocrine pancreas enzyme secreted in active form Optimally active @ pH 7 Hydrolyse glycogen and starch to glucose, maltose
625
Describe the role of lipase secreted by exocrine pancreas
Optimally active pH 7-9 Emulsify and hydrolyse fat in presence of FAs
626
Describe the role of proteases secreted by exocrine pancreas
Essential for protein digestion Secreted as proenzymes and required activation for proteolytic activity
627
Describe the connection between the hypothalamus and pituitary gland
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
What are the 4 trophic hormones of the ant. pituitary?
1. Thyrotrophin (TSH) 2. Corticotrophin (ACTH) 3. Luteinising hormone (LH) 4. Follicle stimulating hormone (LSH)
629
What are the 6 hypothalamus factors that act on the ant. pituitary?
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
Describe the action and effect of TRH
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
Describe the action and effect of gonadotropin-releasing hormone (GnRH)
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
Describe the action and effect of corticotropin-releasing hormone (CRH)
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
Describe the action and effect of grown hormone-releasing hormone (GHRH)
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
Describe the action to growth hormone inhibiting hormone (somatostatin)
Inhibit release of growth hormone from somatotropes
635
Describe the action of prolactin inhibiting hormone (PIH)
Inhibit secretion of prolactin by lactotropes
636
Describe the feedback inhibition of the hypothalamus and ant. pituitary
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
Describe the -ve feedback inhibitor of thyrotrophin
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
Describe the -ve feedback inhibitor of corticotrophin
Short: corticotrophin inhib. hypothalamus Long: glucocorticoids inhib. CRH from hypothalamus and ACTH from ant. pituitary
639
Describe the -ve feedback inhibition of gonadotrophins
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
Describe the -ve feedback inhibition of growth hormone and what stimulates and inhibits its release
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
Describe the post. pituitary
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
What are the 2 post. pituitary hormones?
1. ADH | 2. Oxytocin
643
Describe the release of ADH from post. pituitary
Formed primarily in supraoptic nucleus Stim: high plasma osmolality (dehydration) Disorder: diabetes insipidus
644
Describe the release of oxytocin from post. pituitary gland
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
What are the 5 causes of peptic ulcers?
1. High acid and pepsin content 2. Irritation 3. Poor blood supply 4. Poor mucus secretion 5. Infection: H. pylori
646
What are the 3 divisions of gastric secretion?
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
What are the 3 major regions of the gastric glands?
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
What are the 5 cell types found in the gastric gland?
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
What is cimetidine? How does it work?
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
Describe the secretion of HCl in the stomach
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
What is omeprazole?
H/K ATPase blocker | Inactivates acid secretion and is effective agent in treatment of peptic ulcer
652
Explain the role of water in the inc. of blood plasma pH during digestion
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
How do peptic ulcers arise?
Imbalance in rate of secretion of gastric juice and degree protection afforded by: gastroduodenal mucosal barrier, neutralisation of gastric acid by duodenal juices
654
How is the duodenal protected from acidity?
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
What are the 2 feedback mechanisms that ensure neutralisation of gastric juice?
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
What are the 6 predisposing factors to peptic ulcers?
1. Chronic inflammation due to Helicobacter pylori 2. Non-steroidal anti-inflammatory drugs (NSAIDs) 3. Tobacco 4. Alcohol 5. Stress 6. Trauma
657
What is a secretagogue?
Substance that causes release of another substance
658
What are the 3 gastric secretagogues?
1. Gastrin 2. Histamine 3. ACh
659
Describe the role of gastrin as a secretagogue
Stim. H/K ATPase in parietal cells to release gastric acid (Ca dependent) Stim. histaminocytes to release histamine
660
Describe the role of histamine as a secretagogue
Stim. H/K ATPase in PCs to release gastric acid (cAMP dependent)
661
Describe the role of ACh as a secretagogue
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
What are parietal cell secretions inhibited by?
Prostaglandin E (PGE) and prostacyclin I2 (PGI2) via cAMP
663
Apart from ACh what 2 other secretagogue can stim. endothelial cells?
1. PGE2 | 2. PGI2
664
What is special about prostaglandins?
Cytoprotective - stim mucosal mucus and HCO3- secretion - inc. mucosal blood flow limits back diffusion of acid into epithelial of stomach
665
What are the 3 phases of H Pylori pathogenesis?
1. Active 2. Stationary 3. Colonisation
666
Describe the active phase of H pylori
Produce ammonia (dec. pH) by action of urease (enzyme) Makes conditions more favourable for self Optimum pH 7
667
Describe the stationary phase of H pylori
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
Describe the colonisation phase of H pylori
Well nourished bacteria detach from apical membranes, reproduce within mucus blanket Attach to sialic acid containing mucous proteins, re-enter active phase
669
What are the 8 characteristics of peptic ulcers?
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
What are the 4 types of drugs used to treat peptic ulcers?
1. Acid release inhibitors 2. Mucosal protection enhancers 3. Antacids 4. Antibiotics
671
What are the 4 acid release inhibitors used for peptic ulcer treatment?
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
What are the 4 mucosal protection enhancers used in peptic ulcer treatment?
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
What are the 4 antacids used in peptic ulcer treatment?
1. Magnesium hydroxide 2. Aluminium hydroxide 3. Sodium bicarbonate 4. Calcium salts
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What 2 antibiotics are used in treatment of peptic ulcers?
1. Clarithromycin | 2. Metronidazole

BDS 1 (11 decks)

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