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Mechanism of Disease > Infectious and Skin Diseases > Flashcards

Infectious and Skin Diseases Flashcards

1
Q

Clinical Presentation of Immune Response:

Clinically, histologically, impt mediator, etc

A

Clinically: redness, swelling, pain
Histologically: edema
Pyogenic: pus production
Granuloma: macrophages surrounded by T cells
Tumor necrosis factor (TNF): important mediator

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2
Q

When does the immune response end?

A

when phagocytes clear all antigen
Lack of T-cell stimulation results in apoptosis

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3
Q

Acute vs. Chronic Inflammation

Acute Inflammation

A

Dilaton of small blood vessels
Increased microvasculature permeability
Migration and activation of immune cells

More WBCs

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4
Q

Acute vs. Chronic Inflammation

Chronic Inflammation

A

Infiltration by macrophages, lymphocytes, plasma cells
Increased tissue destruciton
Attempts at healing

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5
Q

Meningitis - Infectious Disease

What are the 3 layers of the Meninges?

Meninges protects CNS

A
  1. Dura mater (tough mother)
  2. Arachnoid (and subarachnoid)
  3. Pia mater (tender mother)
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6
Q

Meningitis - Infectious Disease

Dura mater

A

Outermost covering
Dense CT

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7
Q

Meningitis - Infectious Disease

Arachnoid

A

Middle layer
Subarachnoid space is fluid filled with many projections
Large blood vessels

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8
Q

Meningitis - Infectious Disease

Pia mater

A

Innermost covering (immediately next to the nerve tissue)
Loose CT and small blood vessels

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9
Q

Meningitis - Infectious Disease

Meningitis

What is it? General Presentation?

A

Bacterial or viral infection
Acute onser fever
Headache
Stiff neck
Photophobia (light sensitiviy)
Confusion

Usually inflammation of subarachnoid space

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10
Q

Meningitis - Infectious Disease

How does Meningitis cause Neuronal Injury?

A

Inflammation in subarachnoid space
substantial infiltration bvy neutrophils
May breach blood-brain barrier and cause localized inflammation in neural tissue
Damage to blood vessels can cause hemorrhage into the brain

Most damage is due to increases pressure

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11
Q

Meningitis - Infectious Disease

Meningitis Pathogenesis

A
  1. Coloization of nasopharynx
  2. Evade Opsonization in the bloodstream
  3. CSF access through endothelium of Blood-brain barrier
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12
Q

Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against colonization or mucosal invasion (stage 1)

A

Secretory IgA (IgA protease secretion)
Ciliary Activity (Ciliostasis)
Mucosal Epithelium (Adhesive pili)

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13
Q

Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against intravascular survival (stage 2)

A

Complement (Evasion of alternative pathway by polysaccharide capsule)

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14
Q

Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against Crossing of blood brain barrier (stage 3)

A

Cerebral endothelium (adhesive pili)

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15
Q

Meningitis - Infectious Disease

Host Defense (Pathogen Strategy) against Survival within CSF (stage 4)

A

Poor opsonic activity (Bacterial replication)

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16
Q

Meningitis - Infectious Disease

Pathogen Strategy: Immunoglobulin A (IgA)

Where does it come from? What is it? What does it do?

A

Produce dby plasma cells associated with mucosa
First line of defense
Opsonization
Primarily acs through exclusion, bindng, and crosslinking
Extensive glycosylation to prevent degredation by proteases

Not an inflammatory Ig

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17
Q

Meningitis - Infectious Disease

Pathogen Strategy: Ciliostasis

A

Prevent movementof bacteria out of bronchial tubes
Attachment of bacteria to cilia impedes movements
Toxins - may damage axoneme or deplete ATP

18
Q

Meningitis - Infectious Disease

Pathogen Strategy: Adhesive Pili

A

Pili bind non-ciliated mucosal cells allowing them to cross the epithelium and basement membrane

Infection occurs most easily in simple epithelia (Nasopharynx, intestines)

19
Q

Meningitis - Infectious Disease

Pathogen Strategy: Bacterial Toxins: Exotoxins

A

Secreted by living bacteria
Highly antigenic (antitoxin neutralizes)
Highly Toxic (fatal in microgram quantities)
Usually do not induce fever
Usually bind to specific receptors

20
Q

Meningitis - Infectious Disease

Pathogen Strategy: Bacterial Toxins: Endotoxins

A

Secreted when bacteria cells are killed
Weakly immunogenic
Toxic at 10-100s micrograms
Induce fever
no specific receptors

Part of cell wall then released

21
Q

Parasitic Diseases

How do parasitic diseases cause damage?

Can be caused by single celled and multicellular organisms

A

Damage can be caused by consumption by parasite (parasite is consuming something the host organism needs)
Damage may actually result from immune response to parasite

22
Q

Parasitic Diseases: Trichinosis

Trichinosis

What causes it? What does it do?

A

Obtained by ingestion of undercooked meat, usually pork
Infects skeletal muscle

23
Q

Parasitic Diseases: Trichinosis

Symptoms of Trichinosis

A

Fever
Myalgia (muscle pain)
Periorbital edema

24
Q

Parasitic Diseases: Trichinosis

Life Cycle of Trichinella spiralis

A
  1. Adult in intestines produce larva
  2. Larva infiltrate blood
  3. Exit blood vessels in skeletal muscle
  4. Adults die and muscle fiber calcifies
25
Q

Parasitic Diseases: Trichinosis

Enteric Phase of Trichinosis

A

Strong immune response to larvae: T helper cells produce cytokines, Eosinophil and Mast cell activation

Increases intestinal mobility: T helper cytokines, mast cell granules, expel larvae from gut in animal models

Inflammatory response to larvae elsewhere can cause widespread destruction

26
Q

Parasitic Diseases: Trichinosis

Muscle Phase of Trichinosis

A

Muscle cell is co-opted as a nurse
Disruption of myofibrils
Enlarged/central nuclei
Collagen capsule formation

27
Q

Parasitic Diseases: Trichinosis

Clinical Presentation of the Enteric Stage

A

Typical of enteric disease
Diarrhea and nausea
Vomiting, pain, low grade fever (immune response)

28
Q

Parasitic Diseases: Trichinosis

Clinical Presentation of Muscle Stage

A

Typical of infection/muscle damage
Myalgia and paralysis
Fever, headache, skin rash
Edema and conjuctivitis

29
Q

Integumentary Disorders

What are the two types of disorders of the skin?

A

Growths: Cyst, Malformation, Begnin/malignant neoplasm
Dermatitis (rashes): non-neoplastic

30
Q

Integumentary Disorders: Psoriasis

Psoriasis

A

Inflammatory skin disease
Scaling skin condition
Reddness, swelling, edema

31
Q

Integumentary Disorders: Psoriasis

Pathology of Psoriasis

A

Thickened epidermis (elngated rete ridges)
Neutrophil infiltration
Excessive epidermal proliferation (shortned cell cycle, 2X peoliferative population)
Accmulation of nucleated cells in the stratum corneum (parakeratosis)
Endothelial cell proliferation

32
Q

Integumentary Disorders: Psoriasis

Pathogenesis of Psoriasis

A

Immunologic abnormalities:
* T helper lymphocytes (MHCs)
* cytokine overexpression (TNF, IFNy, IL-2)
* Presence of unique dendritic cells
* Genetic link to HLA-C
* Sensitized T cells accumulate in epidermis (IFNy)
* Can be induced by localized trauma

33
Q

Integumentary Disorders: Psoriasis

What is the relationship between Angiogenesis and Psoriasis

A

Angiogenic facors can be found in psoriatic lesions
TNFa
TGFb
IL8
VEGF

34
Q

Integumentary Disorders: Psoriasis

VEGF

A

Released from keratinocutes
Stimulate epidermal hyperplasia, vascular growth, leukocyte infiltration
Regulates psoriatic keratinocyte activity

35
Q

Integumentary Disorders: Verrucae

Verrucae (warts)

What causes it? What does it do?

A

Squamoproliferative
Caused by HPV
Generally regress (self limited)
Virus transmitted by contact
Viral typing can confirm if problematic infection (poor prognosis -> cancer)

36
Q

Integumentary Disorders: Verruca

Verruca Pathology

A

Epidermal hyperplasia is uneven
Cytoplasmic vacuolization (halos)
Increased keratohyalin granules
Eosinophilic keratin aggregates in cells

37
Q

Integumentary Disorders: Verruca

Verruca Development

A

HPV viral proteisn in keratinocytes
E6 of HPV may interfere with maturation

38
Q

Integumentary Disorders: Pemphigus

Blisters

What are they

A

Acantholysis
Dissolution of intercellular bridges

Which ones determine where blister forms

39
Q

Integumentary Disorders: Pemphigus

What are the three types of blisters?

A

Subcorneal:
Suprabasal:
Subepidermal:

40
Q

Integumentary Disorders: Pemphigus

Pemphigus

A

Autoimmune formation of blisters
Autoantibodies attack the intracellular junctions: inepidermis or mucosa

41
Q

Integumentary Disorders: Pemphigus

Types of pemphigus

A

Foliaceus: subcornal lesion
Vulgaris: suprabasal lesion
Bullous Pemphigoid: subepidermial, nonacantholytic lesion

Eosinophils, lymphocytes, and sometimes neutrophils seen in lesion

42
Q
A

Mechanism of Disease (11 decks)

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