Case 8 Flashcards

1
Q

Give a function of the epidermis

A

Waterproofs the skin and acts as barrier
Has keratinocytes here (produce keratin, a protective protein)
Merkel cells here, these detect fine touch and pressure

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2
Q

What the layers of the epidermis?

A
Strateum Corneum
Strateum Lucidium
Stratum Granulosum
Stratum Spinosum
Stratum Basale
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3
Q

What the the two types of epidermis, and where are they found?

A

Thick skin and thin skin
Thick skin on palms and soles, hairless
Thin skin everywhere else, has hair

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4
Q

Thick epidermis has 4/5 layers of epidermis, while thin epidermis has all 5. True or false?

A

False, thick has all 5

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5
Q

What type of cells makes up the epithelium?

A

Keratinised, stratified squamous (flattened, stacked)

All layers made from keratinocytes

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6
Q

Which layer of epidermis is present in thick epidermis that isn’t present in thin?

A

Strateum Lucidium - clear layer of dead skin cells

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7
Q

What is present in the Strateum Corneum?

A
  • Keratin
  • No nucleus
  • Barrier function
  • Corneodesmosomes: modified desmosomes that link adjacent cells in epidermis (adhesive structures)
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8
Q

What is present in the Stratum Granulosum?

A
  • Waterproof function

- Keratinisation of skin

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9
Q

What is present in the Stratum Spinosum?

A

Keratinocyte maturation

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10
Q

What is present in the Stratum Basale?

A
  • Single layer of cuboidal cells and melanocytes
  • Cells move from basale layer to surface
  • As cells move up, migration, differentiation and apoptosis happens
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11
Q

What is Sepsis?

A

A life threatening organ dysfunction caused by the disregulated host response to infection

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12
Q

Which infection leads to Sepsis

A

Any infection

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13
Q

Why has the definition of Sepsis changed in recent years?

A

Sepsis is rapidly acting (multi organ failure, septic shock, death)
If caught early, can be treated well
If caught a few hours later, can be fatal
Changed criteria for spotting sepsis, so it can be detected earlier

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14
Q

What is bacteraemia?

A

Bacteria in blood

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15
Q

What is infection?

A

Inflammatory response to microorganisms or invasion of

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16
Q

What is septic shock?

A

As a subset of sepsis which particularly profound, circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone.

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17
Q

Give the risk factors for sepsis

A

Very young or very old (under 1 or over 75)
Immunocompromised
Having a chronic disease like diabetes or cancer

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18
Q

What bacteria cause sepsis?

A
  • S.aureus
  • pseudomonas S.pp
  • E.coli
  • Klebsiella
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19
Q

Where can bacteria enter to cause infection?

A
  • Respiratory tract (most common)
  • Abdomen (after surgery)
  • Bloodstream after wound
  • Genitourinary tract (elderly more likely to get UTI’s)
  • Skin infection
  • Catheter related
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20
Q

What are Langerhans cells?

A

Dendritic cells - migrate to lymph nodes upon activation

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21
Q

Describe the layers of the skin

A
  • Epidermis
  • Dermis
  • Hypodermis/subcutaneous
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22
Q

What are the layers of the dermis?

A
  • Papillary layer

- Reticular Layer

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23
Q

What cells are present in the Papillary layer of the Dermis?

A
  • Fibroblasts (make collagen)
  • Adipocytes
  • Blood vessels
  • Phagocytes
  • Lymphatic capillaries
  • Nerve fibres
  • Meissner Corpuscles (touch receptors)
  • Dermal papillae, these are projections of dermis into Stratum Basale of Epidermis
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24
Q

What is in the Reticular layer of the Dermis?

A
  • Dense, irregular connective tissue (collagen and elastin)
  • Well vascularized (blood supply)
  • Rich sensory and sympathetic nerve supply
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25
Q

What is the function of the subcutaneous layer?

A

Connects the skin to underlying fascia (fibrous tissue) of bones and muscle

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26
Q

What structures are in the subcutaneous layer?

A
  • Fat (though this varies in some areas) - for insulation and cushioning
  • Well vascularised = blood vessels
  • Loose, areolar connective tissue
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27
Q

What structure would you expect to find in the hypodermis of the head and neck that you wouldn’t find in other parts of the body?

A
  • Platysma (very broad muscle)

- Muscles for facial expression

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28
Q

The clitoris, penis and eyelids have no adipose tissue is their hypodermis. True/False?

A

True

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29
Q

What accessory structures of the skin begin in the dermis?

A

Nails, endocrine glands, and hair

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30
Q

How is the surface area of the skin divided around the body?

A

Use the ‘9’ rule

  • Head is 9%
  • Upper limb is 9%
  • Lower limb is 18%
  • Abdomen is 18% (abdomen and front of thorax, abdomen and back of thorax)
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31
Q

What are melanocytes?

A

Cells which produce melanin

Specifically, cytoplasmic projections that transfer melanin granules (proteins) into granulocytes

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32
Q

Where are melanocytes found?

A

Basal layer of epidermis

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33
Q

What does melanin do?

A

Absorbs light/ UV-B = acts as protection for skin

Needs to be stimulated by UV-B or ACTH (adrenocorticopic hormone, produced by pituitry gland and regulates cortisol)

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34
Q

Describe the mechanism of a Meissner Corpuscle

A

Mechanoreceptor (sensory, responds to mechanical pressure)
Stimulus (nudge)
- Meissner Corpuscle made of disks (specialised epithelial cells)
- disks move and Na+ can leak into disk below
- do this until bottom reached (where afferent nerve fibre is)
- Transmit Action Potential to afferent nerve fibre
- goes to CNS = response
- goes to efferent nerve fibre
*Meissner Corpuscles require constant changing stimuli

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35
Q

What is the function of a Meissner Corpuscle?

A

Detects ‘light touch’

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36
Q

What is the function of a Pacinian Corpuscle?

A

Mechanoreceptor

Detect vibration pressure in hairless skin

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37
Q

What is the structure of a Pacinian Corpuscle?

A

‘onion’ shaped, many rings of connective tissue built around nerve ending = reduces mechanical sensitivity of nerve ending

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38
Q

Describe the mechanism of a Pacinican Corpuscle

A

Significant stimuli (push from finger)

  • layers begin spinning
  • Na+ and other ions enter the ring
  • Ions go to the middle of rings
  • Reach afferent nerve fibre at centre
  • AP generated
  • Goes to CNS = response
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39
Q

Name all the infection types that S.aureus causes

A
  • Toxin mediated

- Suppurative (produce pus)

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40
Q

How does S.aureus cause disease from releasing toxins?

A

-S.aureus enter body
-Grow and colonise
-Release toxins
-Toxins acts as Superantigens (SAgs)
-Superantigens stimulate non-specific T cell response
-Polyclonal T cell and cytokine release
This is a defence mechanism against immune system

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41
Q

What are the toxin mediated diseases caused by S.aureus?

A
  • Scalded skin syndrome (bacteria grows in dermal layers, skin falls off)
  • Food poisoning
  • Toxic shock syndrom
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42
Q

What are the suppurative diseases caused by S.aureus?

A
  • Impetigo
  • Empyema
  • Pneumonia
  • Osteomyelitis
  • Endocarditis
  • Septic arthritis
  • Folliculitis
  • Carbuncles
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43
Q

What is the treatment for septic arthritis?

A

Admission and IV antibiotics

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44
Q

What are the pathogenicity factors of S.aureus?

A
  • Capsule
  • Protein A
  • Fibronectin binding protein
  • Cytolytic exotoxins
  • Panton-valentine leucocidin
  • Superantigens exotoxins
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45
Q

How does the Capsule of S.aureus aid it in infection?

A

Prevents phagocytosis by protecting the bacteria from being engulfed

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46
Q

How does Protein A of S.aureus aid it in infection?

A

Surfaceproteinoriginally found in the cell wall of the bacteria Staphylococcus aureus.
Binds to IgG = exerting anti-opsonisation effect

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47
Q

How does Fibronectin binding protein of S.aureus aid it in infection?

A

Aids binding to host cell
The protein is a cell-surface bound protein that binds to fibronectin (involved in general cell adhesion) and Fibrinogen (involved in clotting).

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48
Q

How do Cytolytic proteins of S.aureus aid it in infection?

A
  • Produced from gram negative bacteria

- Act as Haemolysins (lipids and proteins which break down cell walls of RBC’s) = destroy red blood cells

49
Q

How does Panton-valentine leucodine of S.aureus aid it in infection?

A
  • Beta pore forming toxins

- Lyses Polymorphonuclear lymphocytes (immune cells)

50
Q

What are the types of superantigens exotoxins?

A
  • Enterotoxins (A,B,C,D,E,G)
  • Toxic Shock Syndrom Toxins
  • Exfoliatin toxins
51
Q

What do enterotoxins do?

A

These are half of all S. aureus isolates cause vomiting and diarrheas
(This s. aureus grows in food)

52
Q

What do Toxic Shock Syndrom Toxins do?

A
  • Can happen in men and women
  • Symptoms are: high temperature (fever) of 39C (102.2F),headache, chills, muscle aches, asore throatand acough, feeling and being sick, diarrhoea, awidespreadsunburn-like rash, the whites of the eyes, lips and tongue turning a bright red, dizzinessorfainting, breathing difficulties, confusion, drowsiness
53
Q

What do Exfoliatin toxins do?

A

Blistering of the skin known as staphylococcal scalded skin syndrome, usually in infants.

54
Q

What is MRSA?

A

Methicillin Resistant S. aureus (MRSA)
Antibiotic resistant strain of S.aureus
Common cause of nosocomial infections (hospital spread)

55
Q

What is given to treat MRSA?

A

-Flucloxacillin will not work
-Give Glycopeptides e.g. Vancomycin
Weakens walls of bacteria, killing it
-Tetracycline
Different antibiotics needed means increase in cost and resources

56
Q

What are PSMs?

A
Peptides of S.aureus
Allows bacteria to attach to cell walls
Cause neutrophils to lyse
Help biofilm formation
*Good target for drugs
57
Q

How can bacteria enter the body?

A
  • Skin breaks
  • Catheter
  • Surgical wound
  • Immunocompromised = can’t fight off infection
58
Q

How does bacteraemia happen?

A

The biofilm forms

Spores of this drops off into the blood

59
Q

What is the first step in identifying Strep?

A

Blood culture

60
Q

What would you expect to see in a blood culture of alpha haemolytic strep?

A

Haemoglobin changes colour

61
Q

What would you expect to see in a blood culture of beta haemolytic strep?

A

RBC lysis

62
Q

What would you expect to see in a blood culture of gamma haemolytic strep?

A

No change

63
Q

What are the subgroups of beta haemolytic strep?

A
  • Pyogenes (Group A)

- Agalactae (Group B)

64
Q

What bacteria species is beta haemolytic strep?

A

Gram positive cocci

65
Q

What is the bacteria usually responsible for UTIs and uncomplicated wound infections?

A

Enterococcus

66
Q

What is Strep Throat/Pharyngitis?

A

Inflammation of the pharynx =

scratchiness in the throat and difficulty swallowing

67
Q

What is the difference between viral and bacterial Pharyngitis?

A
Viral - can treat at home, will see red, swollen tonsils and throat
Bacterial - Need urgent care. 
Swollen uvula, tonsils and throat. 
White spots
Tongue is grey and furry
68
Q

What is erysipelas?

*What are the symptoms?

A

Bacterial infection of upper skin, caused by group A strep
*Symptoms: fever, chills, malaise, a red, swollen, and painful area of skin with raised edge blisters on the affected area
swollen glands

69
Q

What is scarlet fever?

*What are the symptoms?

A

Toxin mediated disease of group A strep
Rapidly fatal
*Symptoms: sore throat, fever, headaches, swollen lymph nodes, and a characteristic rash. The rash is red and feels like sandpaper and the tongue may be red and bumpy.

70
Q

What is Necrotizing fasciitis?

*What are the symptoms?

A

Flesh-eating disease, infection from group A strep that results in the death of parts of the body’s soft tissue. It is a severe disease of sudden onset that spreads rapidly.
*Symptoms include red or purple skin in the affected area, severe pain, fever, and vomiting. Have to remove all of infected tissue

71
Q

What diseases does group A strep cause?

A
Pharyngitis – Rheumatic fever
Impetigo
Scarlet fever
Erysipelas
Cellulitis
Necrotising fasciitis
Puerperal sepsis
Invasive group A streptococcal disease
Streptococcal toxic shock syndrome
Sepsis
72
Q

Describe how group A strep spreads

A
  • Germ is invasive and opportunistic, meaning infection happens when this germ is where it shouldn’t be
  • Inhaled through droplets or direct contact
  • Reservoir is skin or nasopharynx
  • Bind to pharyngeal mucosa through Protein Fm, Lipotechoic acid or M antigen (binds specifically to epithelial wall)
  • Colonisation can be asymptomatic or symptomatic
73
Q

What are the Pathogencity factors of group A Strep?

*Describe what each factor does

A

-Streptolysin O and S
Lysis of Eukaryotic cells so bacteria can spread
-Hyaluronidase
Breaks down connective tissue
-Streptodornases
Breaks down DNA in lysed tissue/cells
-Streptokinase
Lysis of clots to allow spread of infection
-Pyogenic toxins
Superantigens (these trigger immune responses)
Responsible for many of the clinical manifestations e.g. scarlet fever
-C5A peptidase
cell-surface-localized serine protease that inactivates humanC5a (neutrophil chemoattractant produced during complement activation) = inactivates complement

74
Q

What is the danger of pharyngitis?

A

May develop Rheumatic fever and then Rheumatic heart disease

75
Q

How is strep throat diagnosed?

A

FEVERPAIN Index
Rapid antigen test - use to determine whether it is viral or bacterial. Sample of mucus exposed to antibodies - positive result if there is a reaction.

76
Q

What are the steps in the FEVERPain Index?

A

Fever over 38°C.
Purulence (pharyngeal/tonsillar exudate).
Attend rapidly (3 days or less)
Severely Inflamed tonsils
No cough or coryza (catarrhal inflammation of the mucous membrane in the nose)
1 point for each

77
Q

What are the results of the FEVERPain index?

A

0 or 1 is associated with a 13% to 18% likelihood of isolating streptococcus.

A score of 2 or 3 is associated with a 34% to 40% likelihood of isolating streptococcus.

A score of 4 or 5 is associated with a 62% to 65% likelihood of isolating streptococcus.

78
Q

What antibiotic should be given to someone with Pharyngitis/Strep throat?
*Is there a vaccine?

A

Phenoxymethylpenicillin - Penicillin or
Amoxicillin as alternative
*There is no vaccine

79
Q

How does Rheumatic fever happen after strep throat?

A

-S. pyogenes has M protein on cell envelope
-This has a cross reaction with human cell surface proteins
= autoimmune reaction which causes symptoms

80
Q

What are the symptoms of Rheumatic fever?

A

(1-5 weeks after streptococcal pharyngitis)
Fever
Rash
Carditis (inflammation of heart, can cause fibrosis of heart valves)
Arthritis
CNS manifestations (Sydenham chorea - rapid and involuntary movements of arms, legs and face.)
80% of symptoms increase within 10 weeks

81
Q

What are the symptoms of Rheumatic Heart disease?

A
Permanent damage to cardiac valve tissue
Dizziness
Chest pain
Shortness of breath
Tiredness
Heart Failure
82
Q

What is the likelihood of developing Rheumatic Heart disease?

A

1 in 3 with Rheumatic fever

83
Q

What type of S.aureus is S. pneumoniae?

A

alpha haemolytic

84
Q

What is the gram stain of S. pneumoniae?

A

Gram positive diplococci (in pairs)

85
Q

S. pneumoniae is a part of flora. True/False?

A

True

86
Q

What is meant by exogenous infection?

A

From outside agent e.g. droplet from carrier

87
Q

What is meant by endogenous infection?

A

From within e.g. own flora ends up in place where it shouldn’t during immunocompromised period

88
Q

What diseases does S. pneumoniae cause?

A

Bacterial Pneumonia - Leading Cause of CAP
Otitis media – ear infections
Pnuemococcal Bacteremia – systemic infection (in blood), very invasive form
Pneumococcal Sepsis
Pneumococcal Meningitis – 2nd leading cause in UK

89
Q

What are the Pathogenicity factors of S. pneumoniae?

A

-Capsule
Antiphagocytotic – invade innate immune system
-Pili
Enable attachment to cells of URT
-Choline binding protein
Facilitates binding to carbohydrate of cells in URT
-Autolysins – protein produced by strep
Facilitate breakdown of cell to allow release of pnuemolysin – damages eukaryote cells
-Pneumolysin – released when bacteria self destruct, helps bacteria around it
Breakdown of Eukaryotic cells

90
Q

What is given to treat pneumococcal meningitis?

A

Penicillin

91
Q

What are the beta lactam resistant strains of pneumoccal meningitis?

A

Cephalosporins

Vancomycin

92
Q

What is Prevanar 13?

A

Polyvalent vaccine introduced in 2010

Protects against 13 strains that cause 96% of infections

93
Q

Describe the mechanism of a Merkel cell

A
  • Stimulus (light touch)
  • NP (neucleopeptides) are released
  • These go to the NP receptor
  • Ion channels open
  • Na+ enters cell
  • Goes to afferent nerve = AP induced
  • AP goes to CNS = response
  • Goes to efferent nerve
  • need sustained/constant stimulus
94
Q

Describe the structure of a Merkel cell

A
  • Specialised keratinocyte
  • Oval shaped mechanoreceptors
  • Vesicle pockets with membrane around them
95
Q

Where are Merkel cells found?

A

In the stratum basale or papillary layer of thick skin (hairy and non hairy)

96
Q

Where are Pacininan Corpuscles found?

A

In the dermis of glabrous/hairless skin

97
Q

Where are Meissner’s corpuscles found?

A

In the papillary dermis of tips of fingers and lips (non hairy skin)

98
Q

What do Pacinian Corpuscles detect?

A

Vibration pressure

99
Q

Where are Ruffini corpuscles found?

A

Between dermal papillae and hypodermis

100
Q

What are Ruffini corpuscles?

A

Slowly adapting mechanoreceptors

101
Q

What is the function of Ruffini corpuscles?

A

Detect skin stretch - this helps with finger coordination

102
Q

Describe the mechanism of a Ruffini corpuscle

A
  • Stimulus (from finger)
  • Collagen shifts and is perturbed (Collagen is found in reticular dermis)
  • Ion channels on nerve channels open up
  • Na+ in extracellular matrix enters
  • Ions go along afferent nerve fibres = AP
  • AP goes to CNS = response
  • efferent nerve
103
Q

What are the ‘ridges’ on fingertips?

*why do we have them?

A

These are our “fingerprints”
Dermal papillae that forms epidermal/papillary ridges
They are used to amplify vibrations, assist in gripping, improve surface contact in wet conditions

104
Q

Name the two types of sweat glands

A

Apocrine

Eccrine

105
Q

Where are Apocrine sweat glands found?

A

Armpits and pubic area

106
Q

Where are Eccrine glands found?

A

-All over body, highest in palms and soles

107
Q

Where are Eccrine glands not found?

A
  • Eardrum (tympanic membrane)
  • Lip margins
  • Nipples
  • Inner surface of prepuce (foreskin), glans penis and labia minora
108
Q

Describe the mechanism of Apocrine glands

A
  • Secrete fatty sweat into gland tubule
  • Emotional stress
  • Tubule wall contracts
  • Fatty secretion is excreted on skin
  • Bacteria breaks down into odorous fatty acids = smell
109
Q

Describe the function of Eccrine cells

A

Thermoregulation

Cools the body down by secreting water onto skin

110
Q

What does ‘insensible water loss’ mean?

A

Water lost through evaporation

111
Q

What does the fluid secreted by Eccrine glands consist of?

A

99% water, NaCl, trace of other waste products

The solution is hypotonic

112
Q

What supplies the Eccrine and Apocrine glands?

A

Adrenergic fibres in the sympathetic nerves

113
Q

Where are Apocrine glands found?

A

-Start in dermis
-Travel up and fuse with hair follicle
OR
-Directly onto skin

114
Q

Where are Eccrine glands found?

A
  • Start in dermis

- Empties directly onto skin

115
Q

Describe the structure of of an Eccrine gland

A

-Simple coiled structure
-Made of cuboidal secretory cells (find in low reticular layer and hypodermis /subcutaneous layer)
-Intraepidermal spiral duct
-Dermal duct with a straight and coiled portion (2 layers thick - stains darkly and cells are clustered)
-Secretory tubule coiled deep in dermis of hypodermis
(See figures)

116
Q

What is the average amount of water lost to sweating?

A

300/400 ml

117
Q

Describe the structure of an Apocrine gland

A

-Coiled structure
-Bigger than Eccrine
-Have a large lumen for moving a viscous fluid
-Secretory products are stored at apex of cell in secretory regions
(See figures)

118
Q

Describe the mechanism of sweating

A
  • Eccrine innervated by sympathetic post-ganglionic fibre
  • Ach released and binds to receptors in membrane of clear eccrine gland cells
  • Secretion of colourless solution by coil in SC (secretory compartment)
119
Q

Where do the left and right coronary arteries branch from?

A

Ascending aorta