Patho II Remediation Exam 1

Question 1

Describe what a polyp is and its histologic features.

Answer 1

Nasal Polyp

Recurrent rhinitis (repeated damage/blisters) → appear as focal protrusions of the mucosa

Histology – Edematous mucosa harboring hyperplastic or cystic mucous glands, infiltrated with neutrophils, eosinophils, and plasma cells with occasional clusters of lymphocytes

Question 2

Identify if the given clinical condition is acute/chronic otitis media and name the most common causes of each type of otitis media.

Answer 2

Acute Otitis Media

• -Less than 1 month
• -S.pneumoniae, H.influenzae, and M. catarrhalis

Chronic Otitis Media
–More than 12 weeks
–Pseudomonas aeruginosa, Staph. Aureus, or a fungus
Cholesteatomas (perforation)

→ Cranial Vault → temporal cerebritis or abscess
→ Spread into the mastoid spaces

Question 3

Explain the pathogenesis of polymyositis.

Answer 3

–Increased expression of MHC class I molecules on myofibers

–Activates CD8+ T-cells & attacks muscle fibers causing muscle damage

–No skin changes observed in polymyositis

Question 4

Fascia

Answer 4

• -A layer of thickened connective tissue that covers the entire muscle and is located over the layer of epimysium
• -Thick white portion

Question 5

Epimysium

Answer 5

–Connective tissue that wraps the whole muscle

–Specialized deep fascia

–Contains a lot of elastic fibers

–Where blood vessels and nerves enter muscle

Question 6

Perimysium

Answer 6

Fibrous sheath that surrounds each bundle of muscle fibers (fascicle)

Question 7

Endomysium

Answer 7

–Connective tissue that wraps each individual muscle fiber

–Rich in nerves & capillaries → supplies individual muscle fibers

Question 8

Sarcolemma

Answer 8

–The cell membrane that encloses each muscle cell

–Bilipid layer

–Plasma membrane of muscle cell

Question 9

Cause of GBS

Answer 9

–Acute-onset immune-mediated demyelinating peripheral neuropathy

–Damage to schwann cells or myelin with relative axon sparing → abnormal slow nerve conduction velocities

Question 10

Pathogenesis of GBS

Answer 10

–Associated with CMV, EBV, and mycoplasma pneumonia, zika virus, campylobacter infections or prior vaccination

–Result of a T-cell mediated immune response accompanied by segmental demyelination induced by activated macrophages

–Circulating immunoglobulins cross-react with components of peripherals nerves and cause demyelination

Question 11

Distinguish between type I and type II muscle fibers.

Answer 11

See pic

Question 12

Discuss the pathogenesis of DMD.

Answer 12

–X-linked recessive disease → caused by mutations in dystrophin

–Deletion or frameshift mutation which results in the absence of the dystrophin gene which plays a huge role in muscle generation

–Without dystrophin, muscles are susceptible to mechanical injury and undergo repeated cycles of necrosis & regeneration → even eventually muscle regeneration capabilities are exhausted/inactivated

Question 13

Explain the pathogenesis of dermatomyositis.

Answer 13

–Autoantibodies are produced against the capillary endothelial cells

–Complement C3 is activated as a result which forms the C5b-9 membrane attack complex

–The complement deposits induce swollen endothelial cells, vascularization, capillary necrosis, perivascular inflammation, ischemia, and destruction if muscle fibers

–T cells, macrophages and lymphocytes in the form of B cells and CD4+ cells are infiltrated into the muscle causing proximal muscle weakness and skin changes

Question 14

Explain the different pathways through which hyperglycemia can cause nerve injury.

Answer 14

See pic

Question 15

State the functions of glutamate, aspartate and GABA and relate their role in causing a seizure.

Answer 15

–Excess excitatory amino acid neurotransmitters → glutamate & aspartate

–Too few inhibitory amino acid neurotransmitters → GABA & glycine

Question 16

Clinical Features of MG

Answer 16

–An autoimmune disease associated with autoantibodies directed against Ach receptors (AchR)

–Starts at eyes and moves down

–Weakness worsens upon activity

–Post-synaptic issue

–Frequently manifests with ptosis (drooping eyelids) or diplopia (double vision)
→Due to weakness in the extra-ocular muscles

–Antibodies against MuSK (muscle-specific receptor tyrosine kinase)
→More focal weakness → neck, shoulder, facial, respiratory, and bulbar muscles

Question 17

Connection between thymus disorders and MG.

Answer 17

–Thymus contains myeloid cells that express the AchR antigen, antigen-presenting cells, and immunocompetent T-cells

–With thymic abnormalities (thymoma or thymic hyperplasia) there is an immune-mediated attack on the AChR