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Block F: Defence > W4P2 > Flashcards

W4P2 Flashcards

1
Q

Trick for epidermis layers?

A

Come Let’s Get Sun Burned

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2
Q

Which skin layer has the hair follicles and the nerve?

A

Reticular layer of the dermis

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3
Q

Burn effects on other organs

A

Lungs: leads to broncho constriction
Cardio: edematous, a lot of water loss. so keep hydrated

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4
Q

The Parkland Formula*

  • what type of fluid is given?
A

Formula: 4 cc/kg/%TBSA

  • this does NOT include first degree burns
  • first half is given in the first 8 h
  • second half is given in the next 16 h

Most commonly used method for estimating total amount of fluid to be administered in the first 24 h post burn.

Fluid given: Ringer’s lactate
- NOT NS (due to risk of hypercholeremia acidiosis)

  • ** formula only provides an estimate of fluid req
  • clinically: monitor urine output by means of Foley catheter and titrate fluids to achieve a urine output of 30 cc/h in adults and 1 cc/kg/h in children.
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5
Q

Degrees of burns, best to worse

A

first degree: superficial

third degree: not good, deep, serious

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6
Q

Based on the Parkland Formula at what percentage can you give oral fluids only?

A

Burns <20% TBSA in adults and <10-15% TBSA in children can be treated with oral fluids only.

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7
Q

Burn Size Assessment

A

Quantifying the degree of injury is an important initial step in the treatment of burns as it affects decisions regarding resuscitation, transfer, and surgical debridement.
- average overestimate of 75% by referring physicians

Should be performed with a standardized Lund-Browder diagram for 2nd and 3rd degree burns

The simpler rule of nines is helpful for rapid assessment but is less accurate

The patients palm, including the fingers, is often used to estimate 1% TBSA (variable accuracy)

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8
Q

What is a 1st degree burn

A

like a sun burn
it DOES not go into the dermis
painful, the nerves aren’t cut off, they still sensate skin

if you DON’T have blisters then you know its epidermal or hypodermal

(blisters= indicate it is in the dermal level. scars only form if the dermis is involved)

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9
Q

2nd degree burns

A

two types:
a. superficial: you can see the blistering that occurs. this is above the reticular layer. so they are SENSATE, the nerves are intact. good capillary refill. they will heal without surgery

b. deep burn: change in colour- more red. less feeling of pain… not a good sign, infiltrated reticular layer. must watch closely, might need surgery so it doesn’t progress and scar.

burns evolve over time

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10
Q

Third degree burn

A

full thickness, charred appearance

these NEED surgery

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11
Q

Burn Center Referral Criteria

A

Early transfer to a burn center should be arranged following the secondary survey if the patient’s injuries meet the burn center referral criteria set forth by the American Burn Association

Following criteria means you REFER:

  1. 3rd degree burns: refer
  2. 2nd degree burn over 10% BSA, if the patient is <10 or >50 yrs old
  3. 2nd or 3rd burn over 20% in other groups
  4. burns to genitalia, face, hands, feet, any functional parts– refer*
  5. Electrical burn
  6. Inhalation burn
  7. Circumferential burns
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12
Q

The oral Mucosal Immune System

A

This is a part of the MALT: Mucosal associated lymphoid tissue

At three different sites:

  • The oral mucosa
  • Salivary glands
  • Gingival Crevice
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13
Q

Oral Mucosa

A
  • Mechanical barrier formed by the squamous epithelium and lamina propria
  • Intraepithelial DC/langerhans cells sample the environment
  • Ab, especially IgA are secreted
  • Pro-inflammatory cytokines can be secreted by epithelial cells as well as immune cells in the oral mucosa
  • the DC and T cells will decide whether to release a regulatory/tolerant/non responsive out put or to activate immune system
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14
Q

Salivary glands and Saliva

A

Saliva acts as a mechanical flush
Contains IgA, Lactoferrin, lysozyme, complement, leukocytes among other antimicrobial elements
IgA function inpart to inhibit attachment of bacteria and viruses to the oral epithelium

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15
Q

Gingival Crevice

A
  • Neutrophils continuously traffic from gingival capillaries into the sulcus
  • Leukocytes accumulate in response to plaque
  • Neutrophils in the gingiva are activated by local cytokine production and co-receptors and are able to phagocytose and kill microorganisms
  • Neutropenia results in gingivitis and loss of peridontal attachment (if chronic)
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16
Q

Oral Health and Disease

  • recall hyper IgE case
A

poor oral health is associated with disorder of the innate immune system.

hyper IgE syndrome caused by mutations in an important messenger protein, STAT 3 result in peridontal disease as well as failure to exfoliate the primary teeth.

Apthous ulcers are associated with autoimmune syndromes such as Behcet’s disease, although the complete mechanisms are to be elucidated

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17
Q

What are some DDx for 30 year old female presents with multiple dental caries, despite a good routine of oral hygiene and previous low rate of caries formation

A

GERD,
eating disorder w vomitting
micronutrient deficiency: diets

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18
Q

GI tract defense mechanisms

A
  • Mucosal barrier with tight junctions, cilia*, IgA and commensal organisms are first line of defense
  • Recognition of potential pathogens is mediated by innate receptors, such as TLR’s and NOD molecules
  • Mutations in NOD receptors are associated with the development of the autoimmune inflammatory bowel disease, Crohn’s disease

we need most of the response to be PRIMARILY immunoREGULATORY*

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19
Q

Peyer’s patches

A
  • Principal sites of mucosal responses are the Peyer’s patches found in SI, the appendix, and in lymphoid follicles of the large intestine
  • These contain specialized epithelial cells, M cells, which interact directly with molecules and particles of the gut lumen
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20
Q

Function of the M cells

A

found in Peyer’s patches

M cells are interspersed between enterocytes and in close contact with subepithelial lymphocytes and DCs

They take up antigens from the gut lumen by endocytosis

Ag are released beneath M cellsa nd taken up by APCs (DC/T cells)

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21
Q

what are gut homing effector T cells

A

Gut derived lymphocytes will enter the mucosal and lymphatic circulation will be also “home” to mucosal sites

Gut homing effector T cells bind to MADCAM1 on epithelium

Gut epithelial cells express chemoknines specific for gut-homing T cells

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22
Q

What cells protect the gut?

A
  • Specialized T cells (the homing ones) can preferentially kill infection cells
  • Intraepithelial lymphocytes play roles in minimizing gut inflammation and facilitating repair
  • IgA neutralized toxin and prevents adherence of viruses and bacteria to epithelial cells
  • Most gut immune responses result in tolerance
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23
Q

What gets activated when your gut cells get infected?

A

Infection signals synthesis of a series of stress induced proteins

infected cell expresses two atypical class I molecules MIC-A and MIC-B

T cells bearing the NK receptor bind to MIC-A and MIC-B

The infected epithelial cell is killed by induction of apoptosis and replaced by adjacent healthy cells

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24
Q

How does IgA defend the gut?

A

Polymeric IgA is transported into the gut lumen through epithelial cells at the base of the crypts

Polymeric IgA binds to the mucus layer overlying the gut epithelium

IgA in the gut neutralizes pathogens and their toxins

so prevents the toxin from even entering the cell

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25
Q

Role of Commensal Flora/ the microbiome

A

it is important/protective

  • Antibiotic use affects commensal flora and can result super-infection by opportunistic organisms such as Clostridium difficile and Candida spp.
  • Some bacteria penetrate the gut epithelial layer by entering through M cells and dendritic cells.
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26
Q

Probiotics

  • purpose
  • function
A

are marketed to help replace/augment intestinal flora

does it help…

they are not the same as the bacteria in your gut or something. so it doesn’t REALLY help.

studies have shown the probiotic use during antibiotics results in disturbance of the normal flora, delayed reconstitution of patients own flora pattern and increased inflammatory changes in the gut wall

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27
Q

IPEX

A

failure to produce regulatory T cells,
presents as early onset colitis

  • covered in a different lecture…
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28
Q

Helicobacter infection results in:

A

In response to Hb, gastrin secreted by G cells stimulates excess acid production, which destroys gut tissue = ulceration

In some cases, chronic inflammation develops leading to atrophy of the stomach wall and occasionally malignant outgrowths

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29
Q

inflammatory bowel disease: how are immune cells involved in its pathogenesis

A

IBD results from pathogenic T cells in the lamina propria

The disease can be treated by transfer of CD4 CD25 T reg cells which home to mesenteric lymph nodes and the colon

CD4 CD25 Treg cells proliferate and inhibit the pathogenic effector T cells

After inflammation resolves, CD4,CD25, Treg cells remain in clusters with dendritic cell and pathogenic effector

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30
Q

Choosing wisely is about…

A

A campaign to help clinicians and patients engage in conversation about unnecessary tests, treatment and procedures

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31
Q

What are the three principles of the choosing wisely campaign

A
  1. Shared decision-making
  2. Harm Reduction
  3. Resource stewardship
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32
Q

Define Unnecessary care

A

Is clinical activity - treatments or diagnostic interventions - “that have been shown by the evidence not to provide meaningful benefits”

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33
Q

Define Low Value care

A

Is a healthcare practice providing minimal benefit to recipients

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34
Q

EBM recommendation 1

A

Don’t suggest ordering the most invasive test or treatment before considering other less invasive options

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35
Q

EBM recommendation 2

A

Don’t suggest a test, treatment or procedure that will not change the patient’s clinical course

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36
Q

EBM Recommendation 3

A

Don’t miss the opportunity to initiate conversation with patients about whether a test, treatment or procedure is necessary

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37
Q

EBM Recommendation 4

A

Don’t hesitate to ask for clarification on tests, treatments, or procedures that you believe are unnecessary

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38
Q

Recommendation 5

A

Don’t suggest ordering tests or performing procedures for the sole purpose of gaining personal clinical experience

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39
Q

Recommendation 6

A

Don’t suggest ordering tests or treatments pre-emptively for the sole purpose of anticipating what your supervisor would want

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40
Q

What is overdiagnosis

A

When people without symptoms are diagnosed and then treated for a disease that won’t ever cause them any symptoms and …

when people whose symptoms or life experiences are given a diagnostic label which brings them more harm than good

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41
Q

How does overdiagnosis happen?

A
  • When asymptomatic people are screened
  • when diagnostic test is too broad
  • When definitions of disease are broadened (think of DSM, lowering of thresholds)
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42
Q

Popularity Paradox of screening

A

some people get screened, cancer is detected, and they get a good outcome. this encourages more people to get screened- even if they are not part of the population that meets the risk factors

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43
Q

What are the Four Questions to ask your health care provider

A
  1. Do I really need this test, treatment, procedure
  2. What are the downsides
  3. Are there simpler, safer options
  4. What happens if I do nothing
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44
Q

Vasculitis

A

Autoimmune process that is directly attacking the blood vessels. This is blood vessel inflammation

It can lead to:

  • Stenosis (due to clots and inflammation)
  • Occlusion
  • Aneurysm formation

Aneurysm: an abnormal bulge or ballooning in the wall of a blood vessel

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45
Q

How do you classify Vasculitis

A

Primary: occuring by itself, with etiology yet to be identified

Secondary: Occuring in association with another disease (SLE, RA, infection, cancer, toxic substances etc.)

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46
Q

Rheumatoid Arthritis

A

Rheumatoid arthritis, or RA, is an autoimmune and inflammatory disease that mainly attacks the joints, usually many joints at once

(synovial joints specifically?)

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47
Q

SLE

A

Systemic Lupus Erythromatosus

Systemic lupus erythematosus (SLE), is the most common type of lupus. SLE is an autoimmune disease in which the immune system attacks its own tissues, causing widespread inflammation and tissue damage in the affected organs. It can affect the joints, skin, brain, lungs, kidneys, and blood vessels. There is no cure for lupus, but medical interventions and lifestyle changes can help control it.

48
Q

Primary Vasculitis

A
  • Many different entities
  • Each affects blood vessels of a particular size
    • This will influence their clinical manifestations
    • This has been used for their classification
  • Differ in severity and risk of relapse
    • Some are self-limited and others are chronic
49
Q

What types of vessels are there for vasculitis

A

Large Vessels
Medium Vessels
Small Vessels

50
Q

What are examples of Large cell vasculitis

A

of the Aorta:

MOST COMMON type is: Giant Cell Arteritis
Second type: Takayasu Arteritis affects KIDS.

51
Q

Examples of Medium Vessel Vasculitis

A

Polyarteritis Nodosa
seen mostly with Hep B

has become more rare with vaccines

commonly associated with damage to nerves due to occlusion of blood supply to nerves

52
Q

Types of Small vessel Vasculitis

A
  1. Immune complex deposition based:
  2. Associated Small Vessel Vasculitis (non immune complex mediated, aka POSSY IMMUNE?)

There are three that are linked to ANCA an antibody

53
Q

What are examples of Immune Complex Small Vessel Vasculitis

A 
Cryoglobulinemic Vasculitis
IgA vasculitis (Henoch-Schonlein)
54
Q

What are examples of ANCA- associated small vessel vasculitis?

A

Microscopic Polyangitis
Granulomatosis with Polyangitis (Wegener’s)
Eosinophilic Granulomatosis with Polyangitis (Churg-Strauss)

55
Q

What are the affected Organs that tell you its a small vessel vasculitis?

A
  • Lung

- Kidney (glomerulonephritis

56
Q

What are the affected Organs that tell you its a Small and Medium vessel Vasculitis?

A
  • Skin: Small if superficial, Medium if its deeper
  • Peripheral Nerves: can be either, imaging will help
  • GI track
57
Q

Splinter Hemorrhage: what kind of vasculitis?

A

Small Vessel.

58
Q

Palpable Purpura: what kind of vasculitis?

A

Small vessel

59
Q

Digital Ischemia: what kind of vasculitis?

A

Small vessels

60
Q

Livedo Reticularis: what kind of vasculitis?

A

Medium Vessel

This looks like honeycomb markings on the skin with vessels inflammed and the center pale

61
Q

Skin Nodules: what kind of vasculitis?

A

Medium vessel

- happens in the dermis

62
Q

Mononeuritis Multiplex: what kind of vasculitis?

A

Small and/or Medium Vessels

the hand appears without form, limp

63
Q

What are the investigations done for Vasculitis?

A

CBC: expect anemia
Imaging
Auto-antibodies: ANCA
biopsy

64
Q

What does ANCA stand for?

A

Anti-Neutrophil Cytoplasmic Antibodies

65
Q

What are the types of ANCA?

A

cANCA

  • Cytoplasmic immunofluorescence
  • Directed against the neutrophil proteinase 3 (PR3)

pANCA

  • Perinuclear immunofluorescence
  • Directed against the neutrophil enzyme myeloperoxidase (MPO)

you use indirect immunofluorescence to detect if patient has ANCA or ELISA testing

66
Q

What are the specific diseases associated with the types of ANCA?

A

cANCA :
granulomatosis with polyangiitis (GPA)

pANCA:
Microscopic polyangiitis (MPA)
Eosinophilic Granulamatosis with polyangiitis (EGPA)

67
Q

Etilogy of ANCA vasculitis?

A

VERY RARE for all three individually
peak age of onset: 45-75
can present at any age
Male: Female ration of 1:1

contrast with lupus (9 women: 1 man)

68
Q

Granulomatosis with Polyangiitis (GPA)

A

type of cANCA, a small vessel vasculitis

Necrotizing granulomatous inflammation of the upper and lower respiratory tract (90%)
- nasal and sinus inflammation, septum perforation, saddle nose deformities
- pulmonary nodules, infiltrates
Necrotizing vasculitis of the small arteries and veins (80%)
- Renal failure, proteinuria, hematuria, cellular casts
- can be rapidly progressive

Arthritis
Purpura

69
Q 
Microscopic Polyangiitis (MPA)
- how to diagnose?
A

Necrotizing vasculitis no immune deposits affecting small arteries and veins

Many similarities with GPA

But occurs in older individuals and upper respiratory tract involvement much less frequent

pANCA positive
- biopsy must be obtained

70
Q

What are the cardinal features of MPA?

A

Glomerulonephritis
- necrotizing pauci-immune

Pulmonary Hemorrage

Mononeuritis Multiplex (multiple mononeuropathies)

71
Q

Eosinophilic Granulomatosis with polyangiitis (EGPA)

A

Eosinophil-rich and necrotizing granulomatous inflammation often involving respiratory tract, with necrotizing vasculitis small vessels.

Rarest of ANCA vasculitis, affecting all ages and gender equally

diagnosed with positive pANCA

72
Q

What is the EGPA characteristic triad?

A

Asthma
Eosinophilia
Systemic Vasculitis

73
Q

What are the three phases of EGPA

A
  1. Allergic Rhinitis and asthma X 10 years
  2. Peripheral Eosinophilia (>1500) and eosinophilic tissue infiltrates of multiple organs (lungs, GI tract)
  3. Vasculitic disease involving the nerves, lung, heart, GI tract, and kidneys
74
Q

What are the key clinical pearls of GPA?

A
  • ENT involvement frequent

cANCA (PR3) positive

75
Q

What are the key clinical pearls of MPA?

A

ENT usually absent

pANCA (MPO) positive

76
Q

What are the key clinical pearls of GPA and MPA?

A

pulmonary-renal syndrome

77
Q

What are the key clinical pearls of EGPA?

A

asthma and eosinophilia

often, no ANCA, but if positive: pANCA (MPO)

78
Q

Disorders of Hypopigmentation

A

Vitiligo

Idiopathic Guttate Hypomelanosis

79
Q

Disorders of Hyperpigmentation

A

Post-inflammatory hyperpigmentation (PIH)
Pityriasis versicolor (can be hypopigmented or hyperpigmented)
Melasma

80
Q

Major determinant of skin color

A

is the activity of melanocytes, i.e. the quantity and quality of pigment/melanin production, not the density of melanocytes

81
Q

What is hypopigmentation (leukoderma)?

A

Skin that is lighter than the surrounding uninvolved skin

In DEpigmentation, there is total loss of skin pigmentation (e.g. vitiligo)

82
Q

What is hypomelanosis (more specific)?

A

Refers to hypopigmentation caused by either decreased melanocytes OR decreased melanin (see next slide)

Similarly, amelanosis refers to total absence of melanin in surrounding skin

83
Q

Hypopigmentation disorders can be divided into three categories

A

1) Melanocytopenic Hypomelanosis
- decreased / absent melanocytes
- e.g. vitiligo

2) Melanopenic Hypomelanosis
- normal melanocyte density BUT decreased/abnormal melanin
- e.g. nevus depigmentosus (misnomer not depigmented!)

3) Leukodermas without Hypomelanosis
- Normal melanocyte density and melanin; secondary to localized vasoconstriction
- e.g. nevus anemicus (can call this hypopigmented or leukoderma, but NOT hypomelanotic)

84
Q

Hypopigmentation, clinical features to be assessed

A

distribution pattern – circumscribed, linear, or guttate, diffuse

  • degree of pigment loss (hypo- vs de- pigmentation)
    characteristics on Wood’s lamp examination
85
Q

Wood’s Lamp

A

Any patient with a leukoderma can be examined using a Wood’s lamp (~365 nm)

Wood’s lamp exam is esp. useful in 1) circumscribed leukodermas, 2) individuals who have very lightly pigmented skin (phototypes I or II), 3) neonates

What it does: 1) accentuates epidermal pigmentation, 2) obscures dermal pigmentation & vascular lesions (differentiate hypo- vs a- melanosis)

if it fluorecses = depigmented*

86
Q

Vitiligo

A

Acquired condition characterized by autoimmune destruction of melanocytes, leading to circumscribed amelanotic macules and patches of skin > mucous membranes (can be a/w Koebner phenomenon)

Etiology:
Combination of genetic predisposition and environmental insults leading to autoreactive CD8+T cell-mediated destruction of melanocytes

87
Q

Leukotrichia

A

refers to white hair and can occur in vitiligo when hair follicle is involved

88
Q

Poliosis

A

refers to a patch of leukoderma with involvement of the hair follicles within it, leading to leukotrichia of the involved hairs

89
Q

Diagnosis of Vitiligo

A

Minimal Additional (if any) Testing Required – vitiligo is a clinical dx

90
Q

Vitiligo Management

A

Sun protection +++ (no melanin to protect from UV)
Topical: Corticosteroids, Calcineurin inhibitors (e.g. tacrolimus)
Light Therapy: (NB-UVB, PUVA)

91
Q

Nevus depigmentosus

A

same number of melanocytes/ melanin

NOT a depigmentation

no abnormalities in the melanocytes or melanin content

vascular phenomenon 2/2 decreased blood flow

disappears on Wood’s lamp examination

92
Q

Idiopathic Guttate Hypomelanosis

A

This case is an example where morphology is helpful in making the diagnosis

93
Q

Hyperpigmentation

A

A term used to describe disorders characterized by darkening of the skin; encompasses hypermelanosis

94
Q

Hypermelanosis

A

more specific term; denotes an increase in the melanin content of the skin
typically 2/2 increased melanin production
occasionally 2/2 increase in melanocyte density

95
Q

Melasma

A

Very common, acquired disorder characterized by symmetric, hyperpigmented patches with irregular borders; favoring face
irregular border/symmetric distribution = important clues!!

Epidemiology
Women (90%)&raquo_space; Men
+++ Darkly pigmented skin phototypes III-IV (Hispanics, Middle-Easterns, Asians)

96
Q

Causes of MElasma and Excacerbating factors

A

Etiology
Hyperfunctional melanocytes increased melanin production
UV likely has important role (sun exposed distribution + fades in winter)

Exacerbating factors:
Sun exposure
Hormonal factors (e.g. pregnancy, OCPs); often referred to as ‘mask of pregnancy’ when diagnosed during pregnancy
others: phenytoin, Autoimmune thyroid disease

97
Q

Melasma Management

A 
General Measures (for ALL patients)
Sun protection +++ (avoid sun exposure; sunscreen)
Discontinue causative drugs (if applicable)
Camouflage make-up
98
Q

Pityriasis Versicolor

A

Both hyperpigmented and hypopigmented forms are possible
occasional pink colored lesions (mild inflammation)
Residual pigmentary changes require weeks-months to resolve
Rate of recurrence very high (+++ hot humid climates)

99
Q

Cause of Pityriasis Versicolor

A

Pityriasis versicolor is a common yeastinfectionof the skin characterized by flaky (hypo/hyper- pigmented) patches appear on the upper trunk > neck, arms; worse in hot/humid climates (summer)
not considered contagious

Causative agent Malassezia spp. (furfur, globosa, restricta)
Hyperpigmented variant 2/2 induction of enlarged melanosomes by yeast
Hypopigmented variant 2/2 yeast digesting skin lipids and producing azelaic acid inhibits melanin synthesis (normal melanocyte density)

100
Q

spagetti and meatball microcope finding

A

Tinea Versicolor

101
Q

Acne Pathogenesis

Multifactorial, what are the 4 factors?

A

↑ Sebum production
Follicular Hyperkeratinization
Proprionibacterium acnes
Inflammatory response

102
Q

Follicular Hyperkeratinization

A

Sebum and keratin plug the hair follicle and accumulate leading to hyperkeratosis (comedone formation).

103
Q

increased sebum production

A

Influenced by the hormonal effect of androgen

104
Q

Proprionibacterium acnes

A

Abnormal proliferation of P. acnes (bacteria) in sebaceous follicle lead to cytokine release and inflammation

105
Q

Secondary acne lesions

A

Pigmentation

Scarring

106
Q

Management Moderate acne vulgaris

A

Papular/pustular/nodular: Oral antibiotic (e.g. tetracycline, doxycycline, and minocycline), topical retinoid ± BPO± topical antibiotic
Alternative: Oral isotretinoin or antiandrogens in female patients (e.g. oral contraceptives with cyproterone acetate or drosperidone or spironolactone

107
Q

Severe Acne Vulgaris Management

A

Acne conglobata/fulminans: oral isotretinoin, may require concurrent oral corticosteroid in acne fulminans

isotretinoin = acutane?

108
Q

Neonatal vs Infantile acne?

A

neonatal NOT true acne, no COMEDONES are seen. just an inflammatory response

infantile (2-12 months): true acne, resolves in a several months. transient androgen production

109
Q

Rosacea

A

A chronic inflammatory condition affecting skin mainly of the central face

Rosacea may look similar to acne, however, it can be differentiated by absence of comedones.

Common triggers:
Alcohol, sunlight, heat, hot beverages, spicy food, emotional stress.

110
Q

Hidradenitis Suppurativa

A

Hidradenitis Suppurativa (HS) is a chronic inflammatory skin disease characterized by persistent or recurrent flares of inflamed painful nodules, sinuses and scars in the axilla, groin, or both.

The prevalence of HS is estimated at 1% worldwide.

Prevalence is higher among females, Africans/African Americans, smokers and obese patients.

111
Q

What is Chronic Disease historically vs NOW

A

usually based on TIME

  • long and lingering
  • may lead to death or cure
  • may cause far more suffering than acute diseases or be more mild

NOW: not just various diseases but specific social problem that demands social action

112
Q

Epidemiological Transition

A

As infectious disease comes under control and more people live longer, the PROPORTION of non-infectious diseases (chronic) among adults increases.

over the last century, we have FOUND more chronic diseases as we started LOOKING for them

113
Q

What are some new BELIEFS about medicine?

A

a. Expectation with all the new technology that conditions should be cured/atleast SHOULD be treated in whatever way
b. That everyone has a right to proper medical care
c. That most diseases could be prevented

114
Q

Why do we find more chronic diseases?

A
  1. changing epidemiology (living longer)
  2. finding more because we are LOOKING for them
  3. Medicalization: regularly creating new diseases
115
Q

how Chronic disease has created a new body of care:

A

a. committed to healthy behaviours and preventions and self monitoring
b. required to do regular examinations and screenings
c. must treat risk factors by behaviour change, medication or both

116
Q

Chronic Care Model

A

informed activated patient interplay with prepared proactive practice team

GOAL;

  • to prevent chronic turning into acute hospitalizaiton
  • provide support for self treatment when possible (call reminders, home visits)
  • team treatment to have continuity of care to address comorbidities*

Block F: Defence (9 decks)

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