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BPT 17 - Geriatric > 11 - IMMUNE SYSTEM PATHOLOGY > Flashcards

11 - IMMUNE SYSTEM PATHOLOGY Flashcards

1
Q

Pathologies of immune system

A

Hypersensitivity reactions
Autoimmune disorders
Immunodeficiencies

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2
Q

DESCRIPTION: antigen

A

substance triggering immune reaction

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3
Q

Description: antibodies

A

specific binding to antigen facilitate phagocytosis

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4
Q

Descripton: B cells

A

produces antibodies

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5
Q

Function macrophages

A

Phagocytosis

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6
Q

Description of cytotoxic T cells (CD8)

A

immune cell destroying infected cells (viruses) & cancer cells

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7
Q

Description: Helper T cells CD4

A

boost activity of B cells & macrophages

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8
Q

Description: Dendritic cells

A

antigen presentation

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9
Q

fct neutrophils

A

kill bacteria, do phagocytosis & degranulation

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10
Q

Description complement system

A

set of plasma protein: inflammation, kill cells, facilitate phagocytosis

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11
Q

Description mast cells

A

release histamine, trigger inflammation

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12
Q

Definition of hypersensitivity

A

disproportionate reactivity to antigen

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13
Q

Definition of hypersensitivity reactions

A

immune responses to harmless antigens causing symptoms upon re-exposure

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14
Q

Definition of hypersensitivity disease

A

persistent & recurrent reaction to innocuous antigen

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15
Q

Type 1 HS: features

A

Mediated by Ig E antibodies triggering mast cells
Immediate hypersensitivity: response within minutes

Many allergic reactions: reaction to common environmental allergens
Harmless substances that can be:
- Inhaled: pollen, dust misters
- Injected: venom from bees or wasps
- Contact allergies: metals, latex
- Eaten: nuts, shellfish

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16
Q

type 1 HS: 2 steps reactions

A

1) First exposure = sensitization
Dendritic cell bring allergen to lymph nodes & show it to T helper cells
IL-4: stimulate B cells to produce antibodies (IgE)
IgE antibodies binds to mast cells (airways, GI tract, dermis)

2) Subsequent exposure
Allergen bind to mast cells: degranulation
* Release of pro-inflammatory mediators (histamine)
* Bronchospasm
* Vasodilation & increase permeability

17
Q

Type 1 hs: symptoms (mild & other)

A

Mild symptoms
Urticaria
Asthma
Eczema
Allergic rhinitis: most common 10-30% of population globally

Other symptoms
Runny or stuffy nose
Sneezing
Red, itchy & watery eyes
Swelling around eyes

18
Q

Anaphylaxis: type of HS, def & causes

A

Type 1

Definition
= life-threatening emergency & requires immediate intervention with injected epinephrine to restore blood pressure, strengthen heartbeat & open airways

Exposure to large quantity of allergen
Wide spread release of histamine: increase vasodilation + airways constriction
Not enough oxygen to vital organs

Causes
Insect bites & stings (ants, bees)
Food ingestion (peanuts, seafood)
Medication (penicillin, aspirin)

19
Q

Type 1 HS: treatment

A

Anti-histamines: counteract histamine effects
Corticosteroids: reduce inflammation
Epinephrine: induces vasoconstriction (prevent anaphylactic shock)

20
Q

Type 2 HS: 2 types

A

Cytotoxic hypersensitivity
Myasthenia gravis

21
Q

Cytotoxic hypersensitivity type 2 : def, features & steps

A

Definition
= antibody mediated destruction of healthy cells

Features
IgG antibodies recognize cell surface or matrix antigens
Tissue specific
Timing: 2-24h

Steps
1) Phagocytosis

2) Activation of complement system
- Recruitment of neutrophils & degranulation
- Lytic death of host cells

3) Cellular dysfunction

22
Q

Myasthenia gravis: type of HS, def, symptoms & def of myasthenia crisis

A

Type 2

Definition
= antibody directed against nicotinic receptors

Nerve impulse of motor neuron fail to pass neuromuscular junction & stimulate contraction
Fluctuating weakness & fatiguability of skeletal muscle (cranial muscles = first affected)
85% of patients generalized weakness affecting muscles of limbs (later onset)

= slow progressive disease with daily & longer term fluctuations in symptoms

Infections can lead to exacerbation of symptoms

Symptoms
Double vision & dropping eyelid
Fatigue while chewing
Open jaw
Difficulty swallowing
Trouble talking & walking

Myasthenia crisis
= life-threatening medical emergency due to weakening of respiratory muscles & requiring ventilatory assistance

23
Q

Type 3 HS: 2 types

A

Cytotoxic hypersensitivity
Systemic lupus erythematous

24
Q

Cytotoxic hypersensitivity type 3: def, features, An-Ab complex

A

Definition
= antibody mediated destruction of healthy cells

Features
IgG antibodies recognize soluble antigens
—> Formation of antigen-antibody complexes
Systemic
Timing: hours, days or even weeks

Antigen-antibody complexes
Less immunogenicity, difficult to trigger phagocytosis
Deposit on basal lamina of blood vessel

Activation of complement system
—> Inflammation: edema
—> Recruit neutrophils: degranulation & tissue damage

Results: vascular is
Most happening in skin, kidneys, joints, pleura & pericardium

25
Q

Systemic lupus erythematous: type of HS & def

A

Type 3

= defects in apoptotic clearance can be associated with onset of SLE

26
Q

Type 4 HS: description & name 1

A

T-cell mediated hypersensitivity: damage to tissue through CD4 or CD8
Delayed type hypersensitivity: 24-72h from exposure
CD8+ mediated: directly kills target cells (perforin & granzymes)

(Example: type I diabetes)

CD4+ mediated: effector T helper cells activate macrophages
—> Secrete pro-inflammatory cytokines that damage tissues

Multiple sclerosis

27
Q

Multiple sclerosis: def, symptoms, subtypes

A

Definition
= primary T-cell mediated inflammatory disorder

Inflammation
Demyelination: neurons more susceptible to apoptosis (lesions)
Irreversible axon loss & cell death (neurons & oligodendrocytes)
Brain atrophy

Symptoms
Fatigue
Pain
Weakness & balance problems
Sensory loss (paraesthesia or dysesthesia)
Visual dysfunction (optic neuritis)
Spasticity & spasms
Coordination issues (ataxia) & tremors
Depression
Bladder & bowel symptoms

Subtypes
Clinically isolated syndrome
Relapsing-remitting MS
Secondary progressive MS
Primary progressive MS

28
Q

Autoimmune diseases: causes, treatment & etiology

A

Causes
Loss of tolerance towards self-antigens

Treatment
Corticosteroids & NSAIDs to reduce inflammation & suppress immune reaction
Physical therapy: if disease impacts bones, joints & muscles

Etiology
Often unknown
Mix genetic predisposition, hormonal factors & environmental factors

29
Q

Immunodeficiency diseases: types & leads to

A

Primary immunodeficiency: congenital conditions
—> Mutation to genes affecting functioning of immune cells

Secondary immunodeficiency: acquired
—> Various factors reduce effectiveness of immune response in intrinsically normal immune system

Immunodeficiency lead to
Frequent & unusual complications of common infections (pneumonia)
Opportunistic infections (Candida, CMV)
Increase prevalence of tumors

30
Q

Immunosuppressive drugs & adverse effects

A

Corticosteroids: to decrease inflammation
—> One of the most common used drugs

Adverse effects
Related to dosage & chronic use
=> Present in 90% of patients after 60 days
Osteoporosis & fracture: impairment of bone matrix mineralization
Adrenal suppression: inadequate cortisol production
Cushingoid features: weight gain & redistribution of adiposity
Diabetes & hyperglycaemia: most common cause of drug induced diabetes
Myopathy: muscle weakness & atrophy
Glaucoma: increase in intraocular pressure
Psychatric disturbances: psychosis, insomnia, euphoria, depression
Immunosuppression: predispose patients to fungal & viral infections

31
Q

Infectious disease: name one

A

HIV infection

32
Q

% of infected people & routes of transmission of HIV

A
  • 0,7% of population infected with HIV
  • Routes of transmission: unprotected sexual intercourse & sharing needles
33
Q

HIV: life long infection: human immunodeficiency virus

A

Human immunodeficiency virus:
2 copies of ssRNA
Capside
Enzymes (retrotranscriptase, integrase)
Envelope
Envelope glycoprotein (gp120)

HIV = retrovirus —> genome integrated in DNA of CD4 T-cells
Infected T-cells will produce new HIV viruses

34
Q

Killing CD4 T cell: cases of CD4 infected & non infected

A

CD4 helper cells infected by HIV can die:
- Integrase cause DNA damage => apoptosis
- Viral protease cleaves caspases => apoptosis
- CD8 cytotoxic T cells recognize viral protein on surface => apoptosis
- Antibodies recognizing viral protein on surface => apoptosis

Building up of viral RNA => Pyroptosis: highly inflammatory cell death

CD4 T helper cells not infected by HIV can also die:
- Exposure to HIV: move to lymph nodes
- Building up of viral RNA => pyroptosis: highly inflammatory cell death
- Release of inflammatory cytokines
- Death of non infected CD4 T cells through pyroptosis

Chronic inflammation & disease progression

35
Q

HIV: clinical manifestations: types & description of each

A

1) Acute infection
- Initially high viral load
- Production of antibodies (3-6 weeks)
- Reduction of circulating virus

Symptoms:
Flu like symptoms
Lymphoadenopathy

2) Latent period: asymptomatic HIV disease (CD4 count > 500 cells/mm3)
- No clinical symptoms
- Positive antibody test for HIV
- Without treatment it can last anywhere between 1 to 20y

3) Early symptomatic HIV disease
- Persistent generalized lymphadenopathy
- Oral lesions (candida infections)
- Reactivation of varicella-zoster virus (shingles)
- Haematological disturbances (thrombocytopenia, anaemia)

4) Advanced HIV disease or AIDS (CD4 count < 200 cells/mm3)
- Neurological manifestations (AIDS encephalopathy)
- Weight loss
- Opportunistic infections (tuberculosis)
- Malignancies (lymphomas, kaposis’ sarcoma)
- Fatigue
- Dermatological conditions

36
Q

HIV treatment

A
  • Highly active antiviral therapy. (HAART): usually started in early symptomatic HIV disease
    => Suppress HIV replication
    => Undetectable levels of HIV in blood
37
Q

HIV prognosis

A
  • Manageable chronic illness for patients having access to treatment & adhere to treatment
  • Leading cause of death is now kidney or liver failure, due to medications
38
Q

HIV: standard precautions

A
  • Use protective barriers (gloves, eye shields, gowns), when handling blood, body fluids & infectious fluids
  • Wash hands, skin & mucous embraces immediately & thoroughly if contaminated by blood or other body fluids
  • Prevent needle or scalpel sticks
  • Any health care worker with open wounds or skin lesions should not treat clients or handle equipment until lesion heals

BPT 17 - Geriatric (11 decks)

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