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PA2203- Final > Inflammatory Diseases + Immune Deficiencies > Flashcards

Inflammatory Diseases + Immune Deficiencies Flashcards

1
Q

what is IBD and what are the 2 types

A

chronic, relapsing inflammation in the digestive tract

  1. Ulcerative colitis-inflammation and ulcers in the mucosa/submucosa (superficial) of Large intestine/Rectum- continuous
  2. Chrons Disease- Inflammation in the bowel walls (mucoa to serosa). Any area from mouth to anus- patchy
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2
Q

symptoms of IBD

A

Abdominal pain, diarrhea, rectal bleeding, severe internal cramps and weight loss

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3
Q

IBD risk factors

A 
Diet- high animal pro
fam hx (NOD2 mutation)
Cigarette smoking
Northen climate
Age (>65)
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4
Q

IBD pathogenesis

A

inappropriate inflammatory response to normal gut microflora in ppl with a genetic predisposition (NOD2)
-defective immune signalling fails to clear invading commensal bacteria which trigger inflammation leading to damage

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5
Q

What innate cells primarily mediate the inflammatory response in IBD

A

macrophages/neutrophils

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6
Q

What can ulcetieris collitis and churns disease lead to (s/s)

A

-difficulty absorbing nuts, abdominal pain, diarrhea

UC- toxic megacolon, increased incidence of cancer
CD- Fitsula which connects the intestine to another organ or tissue

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7
Q

tx of IBD

A

biologics- anti TNF a monoclonal antibodies
immunomodulators
corticoster

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8
Q

overall picture of Gout

A

recurring inflammatory arthritis

  • chronic deposition of uric acid crystals in jt tissues
  • inflammatory response of host tissue to deposited uric acid crystals
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9
Q

where is gout mc

A

1st metatarsophalangeal jt

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10
Q

gout risk factors

A
  • hyperuricaemia (high bmi, kidney disease)
  • diet (alcohol)
  • genetics
  • M>F
  • > 35
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11
Q

s/s of gout

A
  • jt inflammation
  • gout flares
  • asymetrical arthritis
  • nodules
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12
Q

pathogenesis of gout (steps)

A

uric crystals interact w macrophages and activate NLRP3 inflammasome

-NLRP3 catalyzes activation of caspase 1 which generates inflammatory cytokines IL1B IL18

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13
Q

Pathogenesis of OA

A
  • exfoliation of cartilage fragments leading to delimitation and exposure of underlying bone
  • DAMPS/Alarmins activate local macrophages (produce inflammatory factors)
  • monocytes and neutrophils recruited
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14
Q

How does atherosclerosis damage the epithelium of blood vessels (3)

A

hypertension: trauma from turbulent blood flow

Hyperlipidemia: diet (LDLs), genetics

Chronically elevated blood glucose levels

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15
Q

Pathogenesis of athersclerosis

A
  1. LDLs accumulate in the innermost layer of vessels (intima)
  2. monocytes enter intima and engulf LDLs
  3. Die and form Foam cells
  4. plauques continue to develop and eventually hardens and encroaches the arterial lumen impeding blood flow
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16
Q

S/S of athersclerosis

A
  • CVD leading cause of death worldwide

- Occlusion, plaque rupture, thrombosis (leading to coronary symptoms, angina, stroke etc)

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17
Q

Risk factors of atherosclerosis

A
  • genetics
  • high BP
  • elevated blood lipids
  • diabetes
  • BMI
  • Smoking
  • sedentary lifestyle
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18
Q

tx of atherosclerosis

A
  • Lipid lowering meds
  • Diet/life mods
  • BP meds
  • Blood thinners
19
Q

What is sepsis and what causes it

A

inflammatory response to microbial products in the blood (systemic)

-primaily induced by bac in blood

20
Q

General pathogenesis of sepsis

A

innate cells induce pro inflammatory state (complement, free rads etc) than an antiinfammatory state occurs to try to combat it (IL 10, poor phagocytosis etc)

21
Q

Consequences of sepsis

A
  • mito dysfunction
  • apoptosis and necrosis
  • endothelial dysfunction
  • metabolic acidosis
  • capillary leakage (hypotension)*
  • Disteminated intravascular coagulation*

SEPTIC SHOCK- low BP

22
Q

tx of sepsis/septic shock

A
  • infection control (antibiotics)
  • Hemodynamic stabilization (control BP)
  • Modulation of septic response
23
Q

what is celiac disease and what is changed in individuals that are susceptible

A

Chronic inflammatory condition of the small intestine caused by immune response directed at gluten proteins

*modification of a gliadin by tissue transglutaminase (tTG) may make gluten more immunogenic

24
Q

what does the immune responses in celiac disease lead to

A

structural changes in the gut

  1. villous atrophy (flattening of the villi)
  2. Crypt hyperplasia (elongation of the crypts- malabsorption)
25
Q

s/s of celiac disease

A

diarrhea, fatigue, weight loss, bloating, gas etc

26
Q

pathogenesis of celiac disease (types of cells activated etc)-4

A
  1. Gluten antigens bypass tight junctions of gut epithelium (more apcs)
  2. APCs activate T cells (Th1, CTLs)

3, IEL numbers increase

  1. Inhibition of Treg function
27
Q

Which alleles lead to genetic suseptibility to celiac disease

A

HLA DQ2 and/or HLA DQ8

28
Q

What is the difference between celiac disease, gluten intolerance, wheat allergy

A

Celiac disease- T cells, IgG (structural changes)

Gluten intolerance- IgG

Wheat allergy- IgE

29
Q

What is an immunodeficiency disease + types

A
  • one or more components of the immune response are defective or lacking

Primary- caused by mutations in genes that are involved in immune system

Secondary- acquired because of another underlying illness/disorder

30
Q

Reoccurence of bacterial or fungal/viral infections indicate what type of immunodeficiency

A

bacteria- defects in antibody, complement or phagocytic function

Fungal/viral- defect in t cell responses

31
Q

Features of primary immunodeficiencies

A
  • most are x linked (males always show)

- failure in b cell development or antibody secretion

32
Q

Brutons X linked Agammaglobulinemia- cause and what occurs

A

Mutation in Brutons tyrosine kinase

-B cells can’t progress past pre b cell stage (absence in antibody)

33
Q

Hyper IgM syndrom- cause and what happens

A

Mutation in CD40L

Tcells can’t provide CD40L signal required for class switching- elevated IgM but no IgA IgG IgE

34
Q

Common variable immunodeficiency- cause and what happens (what type of inf)

A

mutations of a variety of genes that encode cell surface proteins and cytokine receptors

  • reoccuring bacterial inf
  • decreased lvls of IgG igA IgM
35
Q

Selective IgA deficiency- cause and what happens

A

B cells cannot secrete IgA

  • most common immunodeficiency disease in NA
  • recurring mucosal inf
36
Q

what does defects in C3 pro lead to

A

higher risks of reoccurring extracellular bac inf

37
Q

What is neutropenia

A

Deficiencies in neutrophil prod

38
Q

What is cyclic neutropenia and what causes it

A

neutrophil numbers fluctuate from near normal to very low every 21 days
-Mutatuons in neutrophil elastase (ELA2)

39
Q

what causes defects in phagocytic cell migration

A

Leukocyte adhesion deficiency- deficiency in b subunit of integrin molecules (LFA1) impairing diapedesis

40
Q

What is chronic granulomatous disease

A

Form granulomas as a result of inability to kill bacteria (defects in respiratory burst)

41
Q

What is SCID

A

Impairment of both arms of adaptive immunity (t and b cells)

-usually affected by severe bacterial, viral or fungal infections

42
Q

What causes X linked SCID and what does it result in

A

Mutations in the IL2 receptor

t cells/ NK cells fail to develop normally and B cell numbers normal but dysfunctional

43
Q

What causes Recombination activating gene deficiency SCID

A

Mutations in RAG1/2 enzymes resulting in arrested lymphocyte development due to inability to perform VDJ recombination

44
Q

Bare lymphocyte syndrome SCID and what does it result in

A

Defects in expression of MHC 1/2 molecules

-T cells can’t be pos selected and few develop, b cell dysfunction

PA2203- Final (11 decks)

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