Y2 W1,2,3,

Front 1

What are the main cells of the immune system and what is their primary function?

Back 1

Lymphocytes, T-cells, B-cells, NK cells, Macrophages, Dendritic cells... recognition of foreign antigen

Front 2

Where are the typical locations of T-cells?

Back 2

Paracortical areas of lymph nodes. Thymus. Bone marrow. Peripheral blood. PALS (spleen).

Front 3

What are some T Cell surface characteristics

Back 3

antigen-specific T cell receptor (TCR)
CD3 protein surface marker.
CD4+ helper/inducer cells.
CD8+ suppressor/cytotoxic cells

Front 4

CD4+ Th1 + Th2 secrete which cytokines?

Back 4

Th1: IL-2, IFN-gamma
Th2: IL-4, IL-5

Front 5

Typical location of B-cells?

Back 5

Superficial cortex of lymph nodes. Germinal centers and mantle zone of stimulated lymph nodes. Follicles of WP (spleen). MALT. Bone marrow and peripheral blood.

Front 6

The following characteristics describe what immune cell?
Antigen specific surface IgM.
When stimulated by Ag, it forms plasma cells that secrete Ag-specific immunoglobins

Back 6

B Cells

Front 7

Which MHC is present on all nucleated cells? What is it recognized by?

Back 7

MHC Class I, recognized by CD8+ cytotoxic Tcells w/ TCR specific for Ag peptide.

Front 8

Which MHC is present only on APC's? What is it recognized by?

Back 8

MHC Class II, recognized by CD4+ helper Tcells.

Front 9

What is an allergen?

Back 9

Antigen that elicits a hypersensitivity reaction.

Front 10

Name the Hypersensitivity reaction:
Release of vasoactive and spasmogenic mediators of inflammation.

Back 10

Type I : Immediate

Front 11

What are Type I Hypersensitivity:
Reactant?
Antigen?
Effector Mxn?
Examples?

Back 11

IgE
Soluble Ag
Mast Cell Degranulation
Examples: Asthma, Hay fever, anaphylxs

Front 12

What are Type II Hypersensitivity:
Reactant?
Antigen?
Effector Mxn?
Examples?

Back 12

IgM,IgG
Fixed Ag
Lysis by complmt/phagocyt; Ab-mediated cellular dysfxn
Examples: Transfusion rxn, Haemolytic anaemia (Drugs), Pernicious Anaemia, Pemphigus vulgaris, Myasthenia Gravis

Front 13

What are Type III Hypersensitivity:
Reactant?
Antigen?
Effector Mxn?
Examples?

Back 13

Immune Complex (III things stuck together)
Soluble Ag
IC formation/deposition elicits imflammation.
Examples: Glomerulonephritis, Serum Sickness, Arthus Rxn, Rheumatoid Arthritis, SLE

Front 14

What are Type IV Hypersensitivity:
Reactant?
Antigen?
Effector Mxn?
Examples?

Back 14

Delayed: CD4+ Th1/Th2
Soluble Ag
Macrophage and eosinophil activation
Contact dermatitis, TB rxn

Direct: CD8+ CTL
Fixed Ag
Cytotoxicity
Contact Derm

Hint 14

No Ab involved!
4T's (Touching, TB skin tests, Transplant rejection, T-cells)
DM1, GVH, MS, Guillain Barre

Front 15

What is graft vs. host disease?

Back 15

Occurs when donor T-cells recognize the recipient's HLA antigens as foreign and react against them.

Front 16

How does tolerance develop?

Back 16

Deletion of clones of self reactive lymphocytes. Centrally in thymus and bone marrow or in peripheral tissues.

Front 17

List 5 DDx for Sudden Collapse

Back 17

Cardiac arrhythmia, MI, Seizure/Neuro disorder, Metabolic disorder, Intoxication

Front 18

What is the management of an anaphylactic reaction?

Back 18

Administer IM adrenaline
(0.01 mg/kg w/ max dose of 0.5mg into vastus lateralis)
Resus w/ IV saline
Support airway/ventilation
Supplementary O2

Front 19

What is atopy?

Back 19

Predisposition to develop localised immediate hypersensitivity rxns to a variety of inhaled/ingested antigens.

Front 20

What are "serum" characteristics of atopic individuals?

Back 20

Higher serum IgE
Incr in IL-2 producing Th2 cells
Incr in eosinophils
50% have +ve family hx

Front 21

What three events happen due to complement activation?

Back 21

Opsonisation (C3b)
Cytolysis (MAC)
Inflammation (Incr perm + attr of phagocytes)

Front 22

what are bacterial endotoxin properties that provide serum resistance?

Back 22

long side chains project O-Ag away from bacterial surface.
LPS coat blocks cell receptors
O-Ag side chains mask bac-surface
O chains bind complmnt poorly and promote degradation of components.

Front 23

What are the important cytokines in pathogenesis of sepsis?

Back 23

TNF - fever, hem.necrosis
IL-1 - fever
IL-6 - fever
IL-10 - activates Th2 inhibits Th1

Front 24

Gm -ve bacteria induction of the inflammatory response

Back 24

CD14 + TLR4

Front 25

Gm +ve bacteria induction of the inflammatory response

Back 25

CD14 + TLR2

Front 26

What does a superantigen do?

Back 26

Bind directly to MHC II and TCR simultaneously (x-link TCR to MHCII), activating large numbers of Tcells to stimulate release of IFN-gamma and IL-1 IL-6 and TNF-alpha from macrophages.

Front 27

Endotoxin induces sepsis by which mechanisms?

Back 27

Activates mphages, complement, and hagemen factor

Front 28

When macrophages are activated by endotoxin what do they secrete

Back 28

IL-1 : Fever
TNF: Fever, Hem.Necrosis
NO: Vasodilator (Hypotension)

Front 29

what is the mechanism when complement is activated by endotoxin (alternate pathway).

Back 29

C3A: Hypotension, Edema
C5A: Neutrophil chemotaxis

Front 30

Sepsis occurs when...

Back 30

the balance between microbial virulence and host defense mechanism is disturbed.

Front 31

Define SIRS

Back 31

Syndrome of generalised and uncontrolled inflammation.
Defined by changes in temperature, WCC, RR, HR

Front 32

What may cause SIRS?

Back 32

Ischaemia, Inflammation, Trauma, Infection, or combination of insults.

Front 33

What is sepsis?

Back 33

Constellation of signs and sympmtoms assocated with a generalised and uncontrolled inflammatory response to systemic infection (Bacteraemia, viraemia, fungaemia, or parasitaemia)

Front 34

What is septic shock?

Back 34

Severe sepsis w/ persistent hypotensions (refractory to fluid resus) and resulting tissue hypoperfusion. (30% mortality rate w/ treatment!)

Front 35

What are the steps in wound healing?

Back 35

Haemostasis
Inflammation
Granulation Tissue
ECM deposition, remodelling, and wound contracture

Front 36

Healing by primary intention is?

Back 36

Clean, uninfected, small wound healing by rapid re-epitheliasiation w/ minimal scarring.

Front 37

Healing by secondary intention is?

Back 37

Larger wound w/ pronounced inflamm. response and extensive scar formation.

Front 38

Healing by tertiary intention is?

Back 38

Debrided, grafted wounds.

Front 39

What are the two common presentations of a rash?

Back 39

Morbilliform: Erythematous macule + papule
Scarlatiniform: Confluent blanching erythema

Front 40

This skin disorder has soft, cauliflower like lesions. Show epidermal hyperlasia, hyperkeratosis, koilocytosis. Caused by HPV.

Back 40

Verrucae

Front 41

Intensely pruritic wheals that form after mast cell degranulation.

Back 41

Urticaria (Hives)

Front 42

Normal number of melanocytes, Increase in melanin pigment.

Back 42

Ephiles (Freckle)

Front 43

Pruritic eruption, commonly on skin flexures. Often associated w/ asthma and allergies.

Back 43

Atopic Dermatitis (Eczema)

Front 44

Type IV hypersensitivity reaction that follows exposure to allergen.

Back 44

Allergic Contact Dermatitis

Front 45

Papules and plaques w/ silvery scaling, especially on knees and elbow.

Back 45

Psoriasis

Front 46

Acanthosis w/ parakeratotic scaling. Increase in stratum spinosum, decrease in granulosum.

Back 46

Psoriasis

Front 47

Flat, greasy, pigment squamous epithelial proliferation w/ keratin-filled cysts (horn cysts).

Back 47

Seborrheic keratosis.

Front 48

Common benign neoplasm of older persons. Lesions occur on head, trunk, and extremeties.

Back 48

Seborrheic keratosis

Front 49

Irregular areas of complete depigmentation. Caused by a decreased in melanocytes.

Back 49

Vitiligo

Front 50

Hyperpigmentation associated with pregnancy or OCP use.

Back 50

Melasma

Front 51

Very superficial skin infection. Usually from S.aureus or S.pyogenes. Highly contagious. "honey colored crusting"

Back 51

Impetigo

Front 52

Acute, painful spreading infection of dermis and subcut tissues. Usually from S.pyogenes or S.aureus.

Back 52

Cellulitis

Front 53

Deeper tissue injury, usually from anaerobic bacteria and S.pyogenes. Results in crepitus from methane and CO2 production.

Back 53

Necrotising fasciitis

Front 54

Exotoxin destroys keratinocyte attachmens in the stratum granulosum only. Fever and generalized erythematous rash w/ sloughing of the upper layers of the epiderms.

Back 54

SSSS

Front 55

Potentially fatal autoimmune skin disorder w/ IgG antibody against desmosomes. +ve Nikolsky's sign.

Back 55

Pemphigus Vulgaris

Front 56

Immunofluorescence reveals Abs around cells of epidermis in a reticular or netlike pattern.

Back 56

Pemphigus Vulgaris

Front 57

Autoimmune disorder w/ IgG antibody against hemidesmisomes. -ve Nikolsky's sign. Eosinophils w/i blisters.

Back 57

Bullous Pemphigoid

Front 58

Immunofluorescence reveals Abs in a linear fashion below the epidermis.

Back 58

Bullous Pemphigoid.

Front 59

Pruritic papules and vesicles. Deposists of IgA at the tips of dermal papillae.

Back 59

Dermatitis Herpetiformis

Front 60

Associated w/ infections, cancers, and autoimmune diseases. Presents with multiple types of lesions.

Back 60

Erythema multiforme

Front 61

Fever, bulla formation, necrosis, sloughing of skin, and a high mortalitly rate. Usually associated with adverse drug reaction.

Back 61

Stevens-Johnson Syndrome

Front 62

Pruritic, Purple, Polygonal Papules. Sawtooth infiltrate of lymphocytes at dermal-epidermal jxn. Associated w/ hepatitis C.

Back 62

Lichen planus.

Front 63

Acute eczematous dermatitis conditions are characterised by

Back 63

Spongiosis

Front 64

Pathogenesis of acute eczematous dermatitis.

Back 64

1) Ag uptake by langerhans
2) migrate to draining lymph node
3)presented to naive CD4 Tcell
4) Tcells activated into effector and memory cells
5) Ag re-exposure -> memory Tcells migrate -> release cytokins, etc. -> recruit inflamm cells.

Front 65

T/F
Acute atopic dermatitis has an increase in Th2, where as Chronic atopic derm has increase in Th1

Back 65

True

Front 66

Pemphigus vulgaris produces which type of blister?

Back 66

Suprabasal acantholytic blister

Front 67

Bullous pemphigoid produces which type of blister?

Back 67

Subepidermal nonacantholytic blister

Front 68

Pruritic dermatosis caused by mite "sarcoptes ----- "
Often found in between webs of fingers hiding underneath the epidermis

Back 68

sarcoptes scabei
Scabies

Front 69

Firm, pruritic, pink/skin colored, umbilicated papules.
common lesions of children/adolescents.

Back 69

Molluscum Contagiousum

Front 70

Wedge-shaped perivascular infiltrate of lymphocytes, histiocytes, and eosinophils within the dermis.

Back 70

Arthropod causing lesion

Front 71

Epidermal hyperplasia (very undulant - looks like a crown) cytoplasmic vacuolization, keratohyaline granules

Back 71

Verrucae

Front 72

Which HPV subtypes cause:
1) condyloma acuminatum
2) cervical cancer
3) vulgaris/plantaris/palmaris

Back 72

1) HPV 6 + 11
2) HPV 16 +18
3) HPV 2 + 4

Front 73

This skin infection is characterised by spongiotic dermatitis, confined to the s.corneum, and shows red hyphae with acid-schiff stain

Back 73

Dermatophyte fungal inection

Front 74

MOA of corticosteroids as applied to inflammation

Back 74

Controls or prevents inflammation by controlling the rate of protein synthesis, suppressing migration of PMN's and fibroblasts, and reversing capillary permeability

Front 75

What are some treatment options for psoriasis?

Back 75

Local (Vit D, cortisones)
Light therapy (PUVA, UVB311)
Systemic therapy (MTX, cyclosporine)
Biologicals (mAb)

Front 76

Parkland formula

Back 76

weight (kg) x TBSA x 4mL

Front 77

How to determine the total body surface area burned

Back 77

Rule of Nines
Lund Browder charts
Hand rule (1%)

Front 78

Management of burns

Back 78

Fluid Resus (Parkland)
Pain Managment(keep cool, paracetamol +/- opiate, sedation)
Wound Management (Tetanus shot, clean/debride, non sticky dressing, topical antibiotics)
Supportive Care (maintain nutrition, body temperature, physiotherapy)