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Pathophysiology

Musculoskeletal System Review

Integumentary System Review

Neurology System Review

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- Stroke

- Headache/Migraine
 Musculoskeletal Physiology
Define differences between bone cells
Bone Cells About
Osteoblasts Bone forming cells. Bone makers. Become osteocytes that are imbedded in bone. Form
new bone & synthesize osteoid (un-mineralized portion of bone matrix → mature
bone)
Osteoclasts Bone resorbing. Bone breakers. They’re attached to integrins by podosomes—which
helps bind to bone. Secretes HCl & protease enzyme → resorption of bone (dissolves
bone minerals & collagenase). They “rest” when they’re not resorbing.
Osteocytes Bone maintaining. These coordinate osteoblast & clast function. They respond to PTH.

• Osteoblasts are important in The formation of new bone.

• Osteocytes are important in bone maintenance.
• Osteoclasts are important in bone resorption.
Understand difference between compact and spongy bone
• Compact – “cortical bone”. This is the main part of skeleton. Solid & strong. Consists of Haversian
system (structural unit).
• Spongy – “cancellous bone”. Filled w/ red marrow. No haversian system—Trabeculae: plates or bars
instead. (Epiphysis = red marrow)
• Diaphysis – contains yellow marrow.

• What is the importance of the bone element, ground substance? Diffusion of substances between the
bond and blood vessels.
• Which part of the bone contains the yellow marrow? Diaphysis.
Understand basics of bone remodeling and bone repair
• Bone heals itself.
• Remodeling – periosteal & endosteal surfaces are remodeled to size/shape of bone before injury.
o Phases: activation, resorption, formation of new bone (aka secondary bone) – 3-4 mos.
• What is the final step in formation of bone? Mineralization.
Describe different joint classifications
• 1. Movement based:
o Synarthrosis – immovable
o Amphiarthrosis – slightly movable (Amphi = both)
o Diarthrosis – freely movable
• Which of the following joint types is classified as an immovable joint? Synarthrosis
• 2. Structure based:
o Fibrous – bone to bone. Ex sutures in skull. Directly connected to bone by dense fibrous connective
tissue.
o Cartilaginous – connected by fibrocartilage or hyaline cartilage
▪ Symphysis – Ex symphysis pubis & intervertebral disks. Bones are connected by pad/disk of
fibrocartilage
▪ Synchondrosis – Ex joints btwn ribs & sternum. Bones are connected by hyaline cartilage
(costal cartilage)
o Synovial – moveable, complex, diarthrosis (synovial fluid – lubrication/moveable)
• Articular cartilage – reduces friction in joint & distributes forces of weight bearing. Has NO blood
vessels, lymph vessels, or nerves (insensitive to pain & regenerates slowly after injury)
• Which of the following is TRUE regarding the articular cartilage? Has no blood vessels

Define muscle fiber differences and types

• Each muscle fiber is a single muscle cell surrounded by a membrane that can excite/send an impulse
• Myofibrils – functional unit of contraction
• White muscle – type II fibers – FAST
• Red muscle – type I fibers – sloooooow
 • Muscle membrane:
o Sarcolemma – spreads impulse
o Basement membrane – keeps cell’s shape

Understand basics of muscle contraction

• Ryanodine receptors (RyRs) are the primary ion channels that control Ca2+ release in muscles
• Phases:
o Excitation – AP travels from nerve terminal → NMJ → initiates electrical impulse (muscle fiber AP).
This triggers receptors in t-tubule wall → opening RyR channels & Ca2+ release
o Coupling – Ca2+ is released so now actin can bind w/ myosin
o Contraction – actin slides toward myosin to form cross-bridge → muscle shortening. “All or
nothing”.
o Relaxation – cross-bridge detaches. Sarcomere lengthens as Ca2+ pumps back into SR.

Understand basics of types of muscle contraction and muscle movement

Isometric Isotonic
Static/holding contraction Lengthening (eccentric) or shortening
(concentric) contraction
Muscle maintains a constant length as Muscle maintains constant tension as it
tension increases moves
Muscle contract, limb does not move Muscle contracts, limb moves
• Agonist – prime mover, contracts
• Antagonist – reciprocal muscle, relaxes
• Ligaments – attach bone to bone
• Tendons – attaches muscle to bone
• Ligaments attach bone to bone.
Describe what happens with aging of the m/s system
• Bones – loss of bone, stiff, brittle, dec. strength, lengthened bone remodel time, slow mineralization,
osteoporosis, inc. bone resorption
• Joints – cartilage is more rigid/fragile, ROM is dec.
 • Muscles – apoptosis, sarcopenia (age-related loss of muscles), dec. strength & bulk, dec. O2 intake,
dec. basal metabolic rate & lean body mass
• Exercise – improves muscle strength, inc. bone mineral density, improves balance, coordination,
mobility, & lean body mass. Dec. risk for falls
Musculoskeletal Patho
Define types of fractures and in which populations they are most prevalent

• Complete – bone is broken all the way through

• Incomplete – bone is damaged, but still in 1 piece
o Closed/simple – skin is intact
o Open/compound – skin is broken
• Comminuted – bone breaks into more than 2 fragments
• Linear – Fx runs parallel to long axis of bone
• Oblique – Fx of shaft of bone is slanted
• Spiral – encircles bone
• Transverse – straight across bone
• Greenstick – perforates 1 cortex & splinters spongy bone – common in children
• Torus – cortex buckles BUT does not break
• Bowing – longitudinal force is applied to bone
• Pathologic – break happens at site of pre-existing abnormality
• Stress – fatigue/insufficiency
• A NP is reading a report of a humerus x-ray and reads that there is a comminuted transverse fracture
of the distal humerus. What does this mean in regards to the characteristics of the fractures? The bone
is fractured in more than 2 pieces, and the break is straight across the bone.
Understand basic patho of bone fracture
• Inflammatory phase → Repair phase → Remodeling phase
o Inflammatory – 3-4 days. Bone tissue destruction. Triggers inflammatory response. Hematoma
forms.
o Repair – several days. Capillary ingrowth, mononuclear cells, fibroblasts form hematoma →
granulation tissue. Osteoblasts w/ in procallus make collagen & matrix which → callus
o Remodeling – mos. – yrs. Callus is reabsorbed (no longer necessary). Trabeculae are formed. Now
bone can w/ stand norm. stress
 • What is the first thing that happens when a bone fracture to begin the healing process? Hematoma
formation
• What is the correct term used when a fracture heals in a nonanatomic position? Malunion
Describe Support structure injuries, subluxation, and dislocation
• Patho: inflammatory exudate forms btwn torn ends. Granulation tissue grows inward. Collagen forms
3-4 days after injury. Vascular fibrous tissues fuse new & surrounding tissues into 1 mass. Healing
tendon/ligament doesn’t have strength to w/ stand strong pull for 4-5 wks. After injury.
• Dislocation – temp displacement of bone from joint
• Subluxation – partially lost contact btwn bones in the joint

• Strain – tear/injury to tendon (attaches muscle to bone) – Strain = tendon

• Sprain – tear/injury to ligament (attaches bone to bone)
• Avulsion – complete separation of tendon or ligament
• The correct term to describe an injury to the ligament is Sprain.

Describe Epicondylitis, tendinopathy, bursitis

• Epicondylitis – inflammation of tendon where it attaches to bone Ex tennis elbow (lateral) or golfer’s
elbow (medial)
• Tendinitis – inflammation of tendon
• Tendinosis – painful wearing down of collagen fibers
• Bursitis – bursa inflammation (synovial fluid sacs) d/t repeated trauma. Septic bursitis is d/t a wound
infection.
• A patient presents with soreness of the lateral hip. The NP suspects inflammation of the greater
trochanteric bursa. What would the NP document as the diagnosis in the chart? Bursitis.
Define Myositis ossificans (heterotopic ossification)–patho and manifestations
• Patho: Complicated local muscle injury → Inflammation of muscle tissue → calcification & ossification
of muscle.
o Calcification = think hardening
• Ex: “rider’s bone” in equestrians, “drill bone” in infantry soldiers, thigh muscles in football players
• When the muscle becomes hard like bone condition is called? Myositis Ossificans

Define Rhabdomyolysis – patho, manifestations

• Patho: severe muscle trauma (compartment syndrome, crush syndrome) → quick breakdown of
muscle → releases intracellular contents (myoglobin) into bloodstream → muscle cell loss (life-
threatening)
• S/s: muscle pain, weakness, & dark urine from myoglobin
• In Rhabdomyolysis what is the substance that is released that can be found in the urine? Myoglobin
Define Compartment syndrome patho and manifestations
• Compartment syndrome can → rhabo
• Patho: complication of Fx → inc. Venous pressure → dec. arterial flow → not enough blood flow to
affected area → ischemia & edema
 • S/s: (5P’s) pain (much more than initial injury should have caused), paresthesia, pallor, pulselessness,
paralysis (late)
• A patient presents to the provider with no pulse in their hand, pallor, and weakness/paralysis of their
thumb after experiencing an ulnar fracture. The provider would document which diagnosis in the
chart? Compartment syndrome
Describe Osteoporosis “Porous bone” – Basic OPG/RANKL/RANK system, patho and manifestations, be able
to describe risk factors and different causes
• Def: dec. bone mass/density; imbalance of bone resorption & formation
• **RANKL = Ligand that’s released by osteoblast → activators receptor – RANK (on the osteoclast).
RANKL suppresses apoptosis → osteoclasts survive longer = more bone breaking than bone making.
RANKL is blocked by OPG.
• Causes/patho: (types depend on cause)
o Dec. estrogen/testosterone, dec. activity level, dec. Vit D, Ca2+, Mg
o Alterations in osteoprotegerin (OPG), receptor activator of nuclear factor kappa B (kB) ligand
(RANKL), & receptor activator of nuclear factor kB (RANK): OPG/RANKL/RANK system
o Post-menopause; Glucocorticoids (inc. RANKL, inhibits OPG production → dec. bone density)
• S/s: pain, bone deformity, Fx, kyphosis, dec. height. Treatment = Denosumab.
• What is RANK? Receptor on osteoclasts – know this!!!!!
• One of the theories behind the pathophysiology of osteoporosis is that there is an alteration of the
RANK/RANKL/OPG normal system. How does estrogen play an important role with this system and in
the development of osteoporosis in the post-menopausal female? Decreased estrogen decreases OPG
secretion from osteoblasts

Define Osteomalacia = soft bones – patho and manifestations

• Patho: dec. Vit D → dec. absorption of Ca2+ from intestines → slow/inadequate mineralization →
osteoid formation BUT calcification doesn’t happen → soft bones
• S/s: pain, bone Fx, vertebral collapse, bone malformation, waddling gait
Define Osteomyelitis – patho and manifestations
• Cause: staphylococcal infection. Infection spreads under periosteum & along bone shaft or into bone
marrow
• S/s: acute/chronic inflammation, fever, pain, necrotic bone (Sequestrum)
Describe Paget disease (osteitis deformans) – basic patho and manifestations
• Patho: state of inc. metabolic activity in bone. TOO MUCH bone resorption/formation → large/soft
bones (usually axial skeleton)
• S/s: brain compression, impaired motor function, deaf, optic nerve atrophy
• The basic pathophysiology of which disease process is characterized by excessive bone resorption and
bone formation? Paget’s disease

Differentiate between inflammatory and noninflammatory joint disease

• Noninflammatory – NO synovial membrane inflammation, NO systemic s/s, normal synovial fluid
o OA
• Inflammatory – inflammatory damage/destruction in synovial membrane or articular cartilage. Does
have systemic s/s (fever, inc. WBC, malaise, anorexia, hyperfibrinogenemia). Can be infectious or
noninfectious.
o RA
• Which of the following is one of the things that differentiates inflammatory joint disease from non-
inflammatory joint disease? In inflammatory joint disease there are prodromal symptoms
• Prodromal symptoms = early symptoms that signals onset of disease/illness (so in inflammatory there
are symptoms that signify a flare up is coming)
OA (osteoarthritis) and RA (rheumatoid arthritis) – patho, manifestations
• OA (also DJD) – noninflammatory
o Patho: loss of articular cartilage, sclerosis (hardening) of underlying bone, new bone spurs
(osteophytes)
o S/s: local areas of damage & loss of articular cartilage, new bone forms of joint margins, joint
capsule thickens; pain, stiffness, joint gets bigger, deformed, swelling
 • RA – inflammatory
o Patho: systemic autoimmune destruction of synovial membrane & joints. Synovial membrane is
destroyed 1st → articular cartilage, joint capsule, & surrounding ligaments/tendons
o S/s: RA or RF test -- will have antibodies IgG & IgM. Systemic s/s, symmetric joint
swelling/deformities, stiffness 1 hr. after rising, rheumatoid nodules in organs; Caplan syndrome =
pulm. Nodules + pneumoconiosis

Basics of bone tumors

• Bone tumors may originate from bone cells, cartilage, fibrous tissue, marrow, or vascular tissue
• All tumors have s/s of pain & swelling
Type About Picture
Osteosarcoma Contain masses of
osteoids. Common in
young ppl. Usually occurs
around the knees.

Chondrosarcoma Makes
cartilage/chondroid.
Common in middle-
age/elderly. Usually in
spongy bone of long
bones. Causes erosion
that → soft tissues

Fibrosarcoma Firm, fibrous masses of

collagen. Usually affects
femur/tibia. Lung mets is
common. This mass you
can actually feel.
 Myelogenic Develop from bone
tumors Marrow cells. Giant cell
tumor → mass bone
resorption. Found in
femur, tibia, radius, or
humerus. Slow &
relentless growth rate.
Limited movement.
Myelogenic = Marrow

• From which cells do collagenic tumors arise? Fibroblast

Describe Ankylosing Spondylitis -patho and manifestations
• Patho: chronic inflammatory joint disease of spine/sacroiliac joints → inflammatory cells infiltrate &
erode fibrocartilage → repair w/ scar tissue that ossifies & calcifies → stiffening & fusion of joints.
There is uncontrolled bone formation.
• Gene HLA-B27 association.
• S/s: low back pain, stiffness, pain, restricted motion, “bamboo” spine, kyphosis
• Which disease process is characterized by the infiltration of inflammatory cells into the fibrocartilage
and eventually erodes it, which leads to fusion of the bones? Ankylosing Spondylitis

Describe Gout – patho, stages, and manifestations

• Patho: R/t purine metabolism. Metabolic disorder that disrupts body’s control of uric acid
production/excretion → HIGH uric acid levels → crystallized uric acid → deposit in connective tissue
b/c purine synthesis/breakdown is inc. or uric acid is poorly secreted by kidneys.
• Stages:
o Asymptomatic hyperuricemia – urate level is high, but NO s/s
o Acute gouty arthritis – attacks are here
o Tophaceous goat – tophi appear in cartilage, synovial membranes, tendons, & soft tissues
• S/s:
 o Pain in great toe (worse QHS), hyperuricemia, recurrent attacks of monoarticular arthritis, renal
stones
o Tophi: small, white visible nodules
Understand differences between Contracture physiologic vs. pathologic
• Physiologic – muscle fiber shortens W/ OUT an AP. Temporary.
o Cause: failure of SR (Ca2+ pump) even though ATP is available
• Pathologic – muscle fiber shortens d/t muscle spasm/weakness. Permanent.
o Cause: Lots of ATP. Contracture occurs even though there’s a normal AP.
Define Chronic Fatigue syndrome (myalgic encephalomyelitis) basic patho and manifestations
• Patho: profound fatigue, neuro energy production, immune impairments. Can be caused by CNS
dysregulation, heart/immune probs, chronic proinflammatory cytokines, cellular energy metabolism
probs, ion transport probs
• S/s: unrestful sleep. Debilitating fatigue made worse by physical/mental exercise; muscle pain,
noninflammatory joint pain, HA, flu-like s/s, memory/concentration probs.
Disuse atrophy – patho and manifestations
• Patho: prolonged inactivity → dec. muscle cell size.
• Causes: BR, trauma, casting, or nerve damage. Oxidative stress → dec. protein synthesis & inc.
proteolysis.
• Which disease process is the result of a mutation in the SCN4A gene? Periodic paralysis
Fibromyalgia – patho and manifestations
• Patho: chronic, widespread joint & muscle pain, fatigue, & tender points. CNS dysfunction → amplified
pain transmission & interpretation
o May be d/t the flu, chronic fatigue syndrome, HIV, Lyme disease, meds, physical/emotional trauma
• S/s: vague. Inc. sensitivity to touch, no inflammation, fatigue, sleep probs. Diffuse, chronic pain. Must
have tenderness in 11 of the 9 pairs (18 total) of tender points.

Poly/dermatomyositis basic patho and differences

• Patho: autoimmune inflammation of connective tissue & muscle fibers
• Symmetric proximal muscle (pelvic & shoulder girdle) weakness & myalgia that develops over wks. –
mos.
• Polymyositis – generalized muscle inflammation. Mediated by T cells.
• Dermatomyositis – polymyositis PLUS skin rash. B cell mediated.
Integumentary
Aging changes of the skin
• Skin becomes thinner, drier, wrinkled, changes in pigmentation. # of capillary loops shorten & dec. Less
melanocytes & Langerhans cells. Sebaceous, eccrine, & apocrine glands atrophy.
 • Temp. regulation is not as good. Pressure/touch receptors dec. in # → dec. sensory perception. Dec.
protective functions. Infections inc. Delayed wound healing.
• Neural innervation of the skin is the function of the sympathetic by way of alpha adrenergic receptors.
Basic differences in lesions; primary and secondary
Primary Lesions
Wheal Elevated, weird shaped area of cutaneous edema. Solid & transient.
Diameter is varied.
Nodule Elevated, firm, circumscribed lesion. Deeper than papule.
Tumor Elevated, solid lesion. Deeper in dermis.
Vesicle Elevated, circumscribed, superficial lesion. Does not extend into dermis.
Filled with serous fluid.
Bulla Vesicle that measures > 1 cm
Pustule Elevated, superficial lesion. Like a vesicle but filled w/ purulent fluid.
Cyst Elevated, circumscribed, encapsulated lesion. Is in dermis/subcutaneous
layer. Filled w/ liquid or semisolid.
Telangiectasia Irregular red lines. Produced by capillary dilation.

Secondary Lesions
Scale Heaped up, keratinized cells. Flaky skin & weird shape, can be thick or thin.
Dry or oily.
Lichenification Rough, thickened epidermis caused by rubbing, itching, or irritation.
Keloid Weird shaped, elevated progressively enlarging scar. Grows beyond
wound. Caused by too much collagen formed during healing.
Scar Thin-to-thick fibrous tissue. Replaces norm. skin after injury/laceration
Excoriation Loss of epidermis. Linear, hollowed-out, crusted area
Fissure Linear crack/break from epidermis to dermis. May be moist/dry.
Erosion Loss of part of epidermis. Depressed, moist, glistening. Happens after
rupture of vesicle or bulla.
Ulcer Loss of epidermis/dermis. Concave.
Atrophy Thinning of skin surface. Loss of skin markings.
Pressure ulcers; patho, manifestations, stages
• Patho: d/t unrelieved pressure on skin (shearing forces, friction, moisture) → capillary blood flow
occlusion → underlying tissue damage (like ischemia or necrosis)
• Decubitus ulcer – d/t lying/sitting in same position for too long on a bony prominence
Stage I Non-blanchable erythema of intact skin
Stage II Partial-thickness skin loss. Involves epidermis or dermis.
Stage III Full-thickness skin loss. Involves damage/loss of SubQ tissue.
Stage IV Full-thickness skin loss w/ damage to muscle, bone, or supporting structures.
• What is the outermost layer of the skin? Epidermis.
• A patient presents with partial thickness skin loss that involves epidermis only. What stage is this
patient’s pressure ulcer? Stage II

Describe Pruritus patho

• Pruritus = itching. Most common s/s of primary skin disorders.
• Itch = specific unmyelinated C nerve fibers. Regulated by CNS.
• Neuropathic – r/t pathologic condition
• Psychogenic – psych prob.
Different types of dermatitis or eczema patho and manifestations
• S/s: pruritus, lesions w/ indistinct borders, epidermal changes. Chronic eczema – thickened, leathery,
hyper-pigmented skin from recurrent irritation/scratching
• Allergic contact dermatitis – T-cell mediated or delayed hypersensitivity (Type IV). Allergen comes in
contact w/ skin, binds to carrier protein → sensitizing antigen is formed → Langerhans cells process
antigen → carry it to T cells → sensitization
• Which cells of the skin are important in immunity? Langerhans cells
• A skin disorder that is the result of a type IV hypersensitivity reaction is known as Allergic contact
dermatitis.
• Irritant contact dermatitis – non-immunologic inflammation. d/t chemical irritation from
acids/prolonged exposure to irritants.
• Atopic dermatitis – d/t family Hx of allergies, hay fever, inc., IgE
• Stasis dermatitis – happens in legs d/t venous stasis, edema, vascular trauma.
 • Seborrheic dermatitis – chronic skin inflammation that involves scalp, eyebrows, eyelids, nasolabial
folds, axillae, chest, & back (cradle cap in babies). Greasy, scaly, white, or yellowish plaques.
• A skin lesion that is elevated, firm, rough, and has a flat top. Plaque.

Differentiate between Psoriasis and pityriasis; define patho and manifestations of both
Psoriasis Pityriasis Rosea
Chronic, relapsing, proliferative skin disorders Benign, self-limiting inflammatory disorder
Patho: T-cell autoimmune-mediated skin Patho: D/t a virus
disease
S/s: scaly, thick, silvery, elevated lesion, S/s: Herald patch – circular, demarcated,
usually on scalp, elbows, or knees salmon-pink

Systemic complications: arthritis & heart

disease
• An autoimmune skin disorder that results in scaly, silvery lesions with evidence of dermal and
epidermal thickening is Psoriasis.
Lichen planus patho and manifestations
• Patho: auto-inflammatory disorder of skin & mucous membranes. Origin is unknown, but it involves T
tubules, adhesion molecules, inflammatory cytokines, & antigen-presenting cells
• S/s: lesions are non-scaling popular violet-colored w/ itching on wrists, ankles, lower legs, & genitals
• A benign T cell mediated auto-inflammatory skin disorder that results in violet colored lesions is Lichen
planus.
Acne basics; differentiate between different types, basic patho, manifestations
• Acne vulgaris – inflammatory disease of pilosebaceous follicles. Hypertrophy of sebaceous glands &
telangiectasia. Common during adolescence.
• Acne rosacea – skin inflammation of middle-aged adults. Lesions are erythematotelangiectatic,
papulopustular, phymatous, & ocular. R/t chronic, inappropriate vasodilation → flushing & sun
sensitivity

DLE, basic patho and clinical manifestations

• Lupus erythematosus
o Inflammatory, autoimmune, systemic disease w/ cutaneous s/s
o Types: Skin (discoid), Systemic (SLE)
• Discoid (cutaneous) lupus erythematosus
o Acute, subacute, chronic. Restricted to skin.
o Patho: altered immune response w/ new T & B cells formed, dec. # of regulatory T cells, & inc. pro-
inflammatory cytokines. Tissue damage d/t autoantibodies & immune complexes.
o S/s: photosensitivity, butterfly pattern, can → SLE

Erythema multiforme; differentiate between types; basic patho

• Patho: immune complexes formed & deposited around dermal blood vessels, basement membranes, &
keratinocytes. Affects mouth, air passages, esophagus, urethra, & conjunctivae

• S/s: “Bull’s eye” or target lesion, erosions/crusts form when lesions rupture.
 • Steven-Johnson syndrome – cause is unknown but involves an immune mechanism r/t drug
administration → severe blistering

Pemphigus basic patho and manifestations

• Patho: autoimmune, chronic, blister-forming disease of skin & oral mucous membranes. Caused by
circulating IgG autoantibodies that work against surface adhesion molecules in the epidermis.
• S/s: blisters can be deep or superficial to the epidermis.

Types of bacterial infections and viral infections; HSV, herpes zoster patho and manifestations
Infection Bacterial About Picture
or Viral
Folliculitis Bacterial Infection of hair follicles from
a staph infection

Furuncles Bacterial Boils (inflammation of hair

follicles) that develop from
folliculitis from staph
infection

Carbuncles Bacterial Collection of infected hair

follicles. Painful, swollen &
red w/ systemic s/s

Cellulitis Bacterial Infection of dermis & SQ

tissue from staph or group B
streptococci infection
Necrotizing Bacterial Inflammation that spreads
fasciitis quickly to fascia, muscles, &
SQ fat → skin

Erysipelas Bacterial Superficial form of cellulitis

Impetigo Bacterial Superficial lesion from staph

HSV-1 Virus Cold sores

HSV-2 Virus Genital

Herpes Virus Caused by varicella-zoster
zoster virus.
(shingles)

Varicella - Virus
chickenpox
 Wart Virus Benign lesions caused by HPA

• A child presents with lesions superficially on the skin. The provider knows that this disorder is causes to
Staphylococcus? Impetigo
Fungal infections; describe different types
• Tinea is caused by dermatophytes Tinea capitis, tinea pedis, tinea corporis, tinea cruris, tinea unguium
• Candidiasis – caused by Candida albicans found on skin, GI, vagina.
o S/s: thin-walled pustule that produces a whitish-yellow curd-like substance
Hives (Urticaria); describe basic patho of manifestations
• Patho: Type I hypersensitivity Rxn. Histamine release → endothelial cells of skin to contract → fluid
leaks from vessels
• S/s: itchy area of raised erythema w/ central pallor; wheals, welts
• Urticaria is the result of which type of hypersensitivity reaction? Type I
Scleroderma; describe basic patho and manifestations
• Patho: sclerosis (hardening) of skin → muscles, bones, & internal organs.
o T helper cells & their cytokines: fibroblast proliferation & fibrosis d/t multiple autoantibodies
• S/s: Skin is hard, hypo-pigmented, taut, shiny, & tightly connected to underlying tissue
Ticks and Lyme disease; patho, manifestations, and stages
• Ticks
o Patho: ticks embed their heads into pts skin so they can get blood. They gorge on blood and get
huge. Then they release their toxins/transmit microorganisms.
• Lyme disease
o Patho: tick that spreads infection Borrelia burgdorferi
o Stages:
▪ Localized – 3-32 days w/ erythema migrans w/ or w/ out fever, fatigue, malaise, myalgia,
arthralgia
▪ Disseminated infection – secondary erythema migrans, arthralgia, meningitis, neuritis,
carditis
▪ Late persistent infection – yrs. After. Arthritis, encephalopathy, polyneuropathy, HF
Skin cancers; patho and manifestations
Tumor type Benign vs. About Picture
Malignant
Seborrheic Benign Proliferation of cutaneous
keratosis basal cells that produce
smooth/warty elevated
lesions

Keratoacanthoma Benign Tumor of squamous cell that

comes from hair follicles
 Actinic keratosis Benign Premalignant lesion made of
aberrant proliferations of
epidermal keratinocytes
caused by too much UV light

Nevi (moles) Benign Pigmented or not. Lesions

that form from melanocytes.
Can transition to malignant
melanomas
Basal cell CA Malignant Surface epithelial tumor.
Mutation of TP53 & PTCH1
genes

Squamous cell CA Malignant Tumor of epidermis: in situ

or invasive. Mutation of TP53
gene

Malignant Malignant Tumor of skin that comes

melanoma from melanocytes.

Kaposi sarcoma Malignant Vascular malignancy. D/t

herpes virus. Common in
immunosuppressed pts
(post-transplant, AIDS)

• A patient presents with a skin lesion with crusting and ulceration that is invading the epidermis. The
provider would suspect which type of skin cancer? Squamous cell carcinoma
• ABCDE rule as a guide (listed under malignant melanoma)
o Asymmetry
o Border irregularity
o Color variation
 o Diameter > 6 mm
o Elevation that includes raised appearance/rapid enlargement

Cold injuries basics

• Injury from extreme cold that affects fingers, toes, ears, nose, cheeks
• Alternating cycles of vasoconstriction/vasodilation → Burning Rxn
• S/s: white/yellowish, waxy, firm to touch
Differentiate between different burn types
• Partial thickness injury
o Only epidermis.
o Local pain w/ erythema. No blisters until 24 hrs. after injury.
• Superficial partial-thickness injury
o Thin-walled, fluid-filled blisters form minutes after injury.
o Painful!
• Deep partial-thickness injury
o Entire dermis. Spares skin appendages like hair follicles & sweat glands
o Waxy, white skin. Can distinguish after 7-10 days btwn deep partial & full when hair or skin buds
reappear
• Full-thickness injury
o Entire epidermis, dermis, & underlying SQ are destroyed. Painless d/t destroyed nerve endings.
o Burn color is white, cherry red, or black; wound is dry or leathery
• Which type of burn is associated with injury to the epidermis only and all skin barrier are intact? Partial
thickness injury
Understand basics of burn shock
• Burn shock in immediate (acute) phase is d/t hypovolemia, heart issues, cellular issues
• Capillary seal = end of burn shock
• Ebb phase – heart contractility is dec. during 1st 24 hr. b/c blood is shunting away from liver, kidney, &
gut.
 Neurology
Describe Types of nervous cells
• Neuron (see below)
• Neuroglial cells (neuroglia) = “nerve glue”
o Astrocytes – fill spaces btwn neurons & surround CNS blood vessels
o Oligodendroglia (Oligodendrocytes) – store myelin in CNS. Counterpart of Schwann cells. Schwann
cells form individual myelin sheaths around axons in the PNS, while oligodendroglia form multiple
myelin sheaths on separate axons in the CNS.
o Ependymal cells – line CSF filled cavities of CNS
o Microglia – phagocytosis in CNS (they get rid of debris)
o Schwann cells (neurolemmocytes) – wrap around & cover axons in PNS. They form & maintain the
myelin sheath.

Understand Basics of the neuron

• How the NS communicates. Needs glucose for fuel.
• 3 components
o Cell body (soma)
▪ Located mainly in CNS.
▪ Have densely packed cell bodies: CNS = nuclei, PNS = ganglia/plexuses
o Dendrites – carry nerve impulses toward cell body
o Axons – carry nerve impulses Away from cell body
▪ Myelin – insulated layer formed/maintained by the Schwann cells.
▪ Nodes of Ranvier – spaces in btwn Schwann cells
▪ Saltatory conduction – ions flow btwn myelin segments (instead of the entire length of the
axon) → makes the impulse travel faster!!!
▪ Conduction velocities depend on myelin coating & axon diameter.
▪ The larger the axon, the faster the travel

• Functional classification
 o Sensory – Afferent. Sends impulses from sensory receptors → CNS
o Associational (interneurons) – sends impulses from neuron → neuron
o Motor – Efferent. Sends impulses from CNS → effector organ
• Motor neurons are classified as Efferent which means they transmit impulses away from the CNS.

• The end processes form a complex NMJ (in skeletal muscle).

Describe Nerve injury and regeneration
• When an axon is severed (injured) → Wallerian degeneration = deterioration of nerve fiber that has
been separated from its nutritive source (by injury or disease)
• Schwann cells & macrophages play a key role
• Process is limited to myelinated axons
• Regeneration depends on the location/type of injury, inflammatory response, & scar tissue formed
• In the axon distal (below) cut – myelin sheath shrinks/disintegrates. Axon portion deteriorates &
disappears. Myelin sheaths reform into Schwann cells that line up btwn the cut & effector organ.
• Proximal to the injury – similar changes but only as far back as far as the next node of Ranvier (cells
inc. metabolic activity, protein synthesis, & mitochondrial activity; new terminal sprouts project from
the proximal segment 7-14 days after injury)
• The closer the cell body of the nerve – more likely it will die & not regenerate
• Crushing injury to nerve allows recovery more fully than a cut injury
• Nerve regeneration is limited to which type of nerves? Myelinated peripheral nerves
Describe Synapses basics; synaptic boutons; neurotransmitters
• Nerve impulse: Neurons make & conduct electrical/chemical impulses by selectively changing the
electrical portion of their plasma membranes & influencing other nearby neurons by the release of
neurotransmitters.
• Synapses – region btwn adjacent neurons. Impulses are transmitted across the synapse via chemical &
electrical conduction. Neurotransmitters are formed in the neuron.
o Presynaptic neurons (toward) – next to synapse. Relays impulses toward synapse.
o Postsynaptic neurons (away) – farther away from synapse. Relays impulses away from
synapse.

• Synaptic knobs (boutons) store neurotransmitters. Neurotransmitters are released across the synaptic
cleft (space btwn neurons) when the AP in the presynaptic neuron causes the synaptic vesicles to
release 1 or more NT’s. The NT binds to receptor sites on the plasma membrane of the postsynaptic
neuron.

• Neurotransmitters (norepi, acetylcholine, histamine, GABA, dopamine, serotonin) have effects on

postsynaptic neurons:
o Excited – depolarized. Acetylcholine, norepi, glutamate
o Inhibited – hyperpolarized. Dopamine, GABA, glycine, serotonin
Describe function of Reticular formation
• Reticular formation – maintains wakefulness. network of connected nuclei that regulate vital reflexes
(like heart & lung func.).
• RAS (reticular activating system) = reticular formation + cerebral cortex

Describe Lobes of forebrain and basic function of each

• Forebrain = anterior part of the brain, including cerebral hemispheres, the thalamus, & hypothalamus.
• Cerebrum (pictured below are the cerebrum’s lobes)
o Gray matter (nuclei) – cell bodies & dendrites of neurons in cerebral cortex. Receive, integrate,
store, & transmit info
 o White matter (numerous trats) – beneath cerebral cortex. Composed of myelinated nerve fibers.

• Frontal lobe
o Prefrontal – goal-oriented behavior. ST memory
o Premotor – programs motor movement
o Primary motor area – primary voluntary motor area
o Broca speech area – motor aspect of speech
• What is the area of the brain that controls motor aspects of speech? Broca’s area
• Parietal lobe – somatic sensory input
• Occipital lobe – visual cortex
• Temporal lobe – primary auditory cortex. Wernicke area = reception/interpret speech. LT memory
• Corpus callosum – connects 2 cerebral hemispheres
• Limbic system – primitive behavioral responses, expression of affect (emotional/behavioral states),
consolidation of memory
• Diencephalon – processes incoming sensory data made up of epithalamus, thalamus, hypothalamus, &
subthalamus
Understand Function of different parts of brainstem

• Midbrain – relay center for motor & sensory tracts. Center for auditory & visual reflexes. Cerebral
aqueduct (carries CSF)
• Hindbrain
o Cerebellum – balance & posture. Damage is characterized by ipsilateral loss of equilibrium,
balance, motor coordination
o Pons – controls RR’s
o Medulla oblongata – controls reflex activities (HR, RR, BP, coughing, sneezing, swallowing,
vomiting)
• The area of the brain that is responsible for maintaining balance and coordination is the Cerebellum.
Define Cranial nerves, what each is, does, and whether motor, sensory, or both
• Cranial nerves – project from brain & pass through foramina in skull. 12 pairs (sensory, motor, &
mixed).
 • Mnemonic for nerves: Oh Oh Oh To Touch And Feel Very Good Velvet Ahh Such Heaven
• Mnemonic for sensory, motor, or both: Some Say Marry Money But My Brother Says Big Brains Matter
More

1. Olfactory (S) – smell

2. Optic (S) – vision
3. Oculomotor (M) – pupil reaction, EOM
4. Trochlear (M) – EOM. Superior oblique muscles (rotates laterally & intorts [twists in & out] eye)
5. Trigeminal (M, S) – mastication, face sensation
6. Abducens (M) – EOM. Lateral rectus; abducts the eye
7. Facial (M, S) – facial expression; taste on front of tongue
8. Vestibulocochlear (S) – hearing
9. Glossopharyngeal (M, S) – motor fibers work on pharynx & salivary glands; tastes on back on tongue
10. Vagus (M, S) – motor & sensory for pharynx; parasympathetic motor fiber (supplies smooth muscle of
abd organs)
11. Spinal accessory (M) – shrugs your shoulders
12. Hypoglossal (M) – tongue muscles
https://www.youtube.com/watch?v=FtJtYMRVw7A (watch this!!!)
• Which cranial nerve would you be most concerned about if on examination you found that the patient
was unable to abduct their left eye? Abducens nerve
Understand Basics of spinal cord anatomy
• Cord is in vertebral canal & is protected by vertebral column
• Spinal cord connects the brain & body, conducts somatic & autonomic reflexes, provides motor pattern
control centers, & modulates sensory & motor function
• Conus medullaris = end of spinal cord
• Cauda equina = nerve bundle at end of spinal cord (“horse’s tail”)
 • Gray matter
o Posterior/dorsal horn is composed of sensory neurons
o Lateral horn contains cell bodies involved w/ ANS
o Anterior/ventral horn contains cell bodies for efferent pathways leaving spinal cord by way of
spinal nerves (motor)
• The posterior horn of the spinal cord is primarily composed of sensory neurons.
• White matter
o Spinal tracts are named after their beginning & end point (Ex spinothalamic tract)
o Afferent tracts = sensory (carry impulses to CNS & away from organs/receptors)
o Efferent tracts = motor (carry impulses away from CNS & to organs)

Upper and lower motor neurons; basic differences and manifestations

• Upper motor neurons
o Disruption of UMN’s → initial paralysis → partial recovery
o Pathways are completely w/ in CNS
o Efferent pathways relay info from cerebrum → brain stem/spinal cord
• Upper motor neurons are located where? CNS
• Lower motor neurons
o Destruction of LMNs → PERMANENT paralysis
o Neurons have direct influence on muscles
o Cell bodies originate in gray matter of spinal cord but their axons extend into PNS
Describe Meninges structure and function
• Protective membrane that surrounds brain & spinal cord. Composed of dura mater, arachnoid, & pia
mater.
• Subdural space – btwn dura & arachnoid. Has bridging veins.
• Subarachnoid space – btwn arachnoid & pia matter. Contains CSF.
• Epidural space – btwn dura & skull.
• Arterial supply to the meninges is in which dural space? Epidural space

Understand Basics of blood supply to brain and what part of the brain each supplies (ACA, MCA, PCA)
• CO2 regulates CNS blood flow!!!
• ACA – frontal & parietal lobes
• MCA – frontal, temporal, parietal lobes
• PCA – occipital lobe
• What is the main regular of cerebral blood flow? Carbon dioxide levels
• CO2 is a potent vasodilator. Inc CO2 → inc. ICP
Describe what the Blood brain barrier is, and what its function is
• Cellular structures that prevents harmful stuff from the blood from entering the interstitial spaces of
the brain & CSF. This matters b/c certain drugs are more likely to cross the BBB.
• Functions:
o Protects brain from foreign stuff in blood that can cause injury
o Proteins brain from hormones & NT’s secreted by other organs
o Maintains a constant biochemical environment for the brain
• Things that inc. permeability/break down BBB: HTN, dilutional hyponatremia, lots of anesthetics,
vasodilation, hypercapnia
Differentiate between the SNS and ANS
• Somatic nervous system – voluntary motor control of skeletal muscle
• Voluntary neural control is carried out by which functional category of the peripheral nervous system?
Somatic nervous system
• Autonomic nervous system – involuntary control of organ systems
o Located in both CNS & PNS
o Motor neuron component (PNS)
▪ Preganglionic (myelinated) – located in CNS (brain stem/spinal cord). In PNS the
preganglionic (efferent fibers) synapse (passing from one cell to another) w/ ganglionic
neuron located in PNS.
▪ Preganglionic neuron cell bodies of the autonomic nervous system are located in the
Central nervous system and are myelinated.
▪ Postganglionic (unmyelinated) – terminates on the effector organ

o Sympathetic Nervous System – Fight or flight.

▪ Receives innervation from Thoracolumbar division (T1-L2). Releases epi (vasodilates) &
norepi (constricts)
 ▪Effects of lesions interrupting sympathetic fibers include: blood vessel dilation (skin gets
warm/red), lack of sweating in involved area, constricted pupil on side of lesion, paralysis of
arrector pili muscles so “goose bumps” don’t happen when pt is cold.
▪ What is a lesion? It’s damage
▪ Horner’s syndrome – Injury to preganglionic sympathetic trunk or postganglionic
sympathetic neurons of cervical ganglion. W/ these pts you’ll see ipsilateral pupil
constriction (occurring on the same side), sunken Ipsilateral eyeball, ptosis of Ipsilateral eye
(drooping), no sweating on Ipsilateral side of face.
▪ Neuroreceptors: a-adrenergic & B-adrenergic receptors (alpha 1 is most common)
▪ Sympathetic postganglionic nerve fibers release which neurotransmitter? Norepinephrine
o Parasympathetic Nervous System – Rest & digest.
▪ “Rest-and-repose” response. Conserves & restores energy.
▪ Receives innervation from Craniosacral division (cell bodies in cranial nerve nuclei & sacral
region of spinal cord.)
▪ Cell bodies of the parasympathetic nervous system are located in which region of the spinal
canal? Cranial and sacral
▪ Neuroreceptors: cholinergic receptors (nicotinic type 1 & muscarinic). Nicotinic = muscle
contraction at NMJ. Can be found on cells of adrenal medulla.
Left = Craniosacral division (parasympathetic); Right = Thoracolumbar division (sympathetic)
Describe Neuroanatomy of pain, fibers, and how signal is transported
• Sensory pathways:
o Pain-temp. (spinothalamic tract)
o Proprioception; stereognosis; vibratory sense, fine touch in posterior column
o Vague light tough (anterior spinothalamic tract)
• Pathway for pain & temp enters spinal cord → immediately crosses over cord → travels to thalamus on
opposite side where it enters
• Pathway for proprioception & stereognosis; proprioception; vibratory sense stays on the same side of
the spinal cord until it reaches the brainstem
• Lesion of spinothalamic tract → loss of pain-temp. contralaterally below level of lesion (b/c of
immediate cross over in spinal cord)
• If there is an injury to the spinothalamic tract of the spinal cord what will you find on exam?
Contralateral loss of pain and temperature
• Lesion in posterior column → ipsilateral loss/dec. in stereognosis, vibratory sense, proprioception in
conscious pts (b/c there is NO cross over until the level of the brainstem)
• Light touch is carried in both tracts so it’s spared in unilateral spinal cord lesions (b/c there are
alternate routes)

Differentiate between Types of acute pain

 Type About
Somatic – superficial Comes from connective tissue, muscle, bone, & skin. Pain is
sharp/well localized w/ A delta fibers. Pain is dull, aching, &
poorly localized w/ C fibers.
Visceral – internal Transmitted via sympathetic afferents. Poorly localized, dull.
Fewer nociceptors.
Referred Pain is somewhere other than its origin. Area of referred
pain is supplied by same spinal segment as actual site (Ex
MI).
Describe Chronic pain and neuropathic pain
• Chronic pain can be persistent/intermittent & sudden/gradual lasting 3-6 mos. Or more. Can lead to
behavior/psychological changes (unlike acute). Conditions include myofascial pain syndromes, chronic
post-op pain, low back pain, chronic pain w/ CA
• Neuropathic pain
o D/t trauma or disease of PNS/CNS. Usually chronic.
o Chronic neuropathic pain groups:
1. Peripheral – injured nerves are now hyper-excitable. Causes are trauma, DM, ETOH, CA,
HIV
2. Central – d/t lesion or dysfunction in brain/spinal cord. Causes are brain/spinal cord
trauma, tumors, vascular lesions, MS, post-herpetic neuralgia, phantom limb pain, reflex
sympathetic dystrophy
o S/s: paroxysmal w/ hyperesthesia & paresthesia (pins & needles), burning, shooting, stabbing;
“gnawing” & miserable
o Deafferentiation – neuropathies that are d/t lesions in PNS
o Hemiagnosia – paralysis & hypersensitivity on 1 half of body
o Phantom limb – pain felt in amputated limb after stump has healed
o Complex regional – 1-2 wks. After injury (Fx w/ out an identifiable nerve injury) OR injury to
brachial plexus or median, sciatic, or other peripheral nerves
• A patient presents with a herniated lumbar disc and they are complaining of pain in their right leg. The
NP knows that this is called radiculopathy.
Describe Temperature regulation
• Varies in response to location, activity, environment, circadian rhythm, & gender
• Regulation is mediated by hypothalamus
• Thermoreceptors:
o Peripheral = skin
o Central = hypothalamus
• Heat protection: chemical rxns of metabolism, skeletal muscle contractions (shivering), chemical
thermogenesis
• Conservation: vasoconstriction, voluntary mechanisms
• Loss: radiation, conduction, convection, vasodilation, dec. muscle tone, sweat evaporation, inc.
ventilation
Understand the Basics of fever
• Fever happens when there is a release of pyrogens from leukocytes/other cells in immune response
(endogenous pyrogens) & bacteria (exogenous pyrogens). Both are s/s of disease & norm. response to
disease.
• Hypothalamic thermostat is now reset to a high level. When fever breaks set point goes back to norm.
 • Benefits: kills microorganisms, fever helps infectious processes (dec. iron, zinc, copper that are needed
for bacteria to replicate), promotes lysosomal breakdown & apoptosis of cells, inc. lymphocytic
transformation & phagocyte motility, augments antiviral interferon production & phagocytosis
• Older pts: dec. or no fever in response to infection
• Kids: get higher temps. Than adults for minor infections & can have febrile seizures
Hyperthermia; heat cramps, heat exhaustion, heatstroke (accidental hyperthermias) patho and
manifestations
• Hyperthermia – not mediated by pyrogens. There is no resetting of the hypothalamic set point. At 41 C
nerve damage produces convulsions. At 43 C you die.
• Heat cramps – severe spasmodic cramps in ABD & extremities. Following prolonged sweating & Na+
loss. Happens to those not used to heat/strenuous activity in warm climates. S/s fever, fast HR, HTN w/
cramps
• Heat exhaustion – prolonged high temp. s/s dizziness, weakness, nausea, confusion, syncope →
stopping working, lying down, resting. Stopping activity dec. muscle work → dec. heat production.
Lying down redistributes vascular volume.
• Heatstroke – lethal d/t overstressed thermoregulatory center. Brain, heart, & thermoregulatory
centers don’t work w/ temps > 40.5C. S/s cerebral edema, degeneration of CNS, swollen dendrites,
renal tubular necrosis, death unless treated. Cooling too quickly → vasoconstriction → limits cooling
• A gardener is out working in the yard on a hot, humid summer day. They begin to feel dizzy, nauseated,
and weak. They find a shady place to lay down in the grass and then begin to feel better. The gardener
is likely experiencing which of the following? Heat exhaustion
Sleep; phases basics, sleep cycle, OSAS, patho and manifestations
• Hypothalamus is major sleep center
• Phases:
o Rapid eye movement (REM) – vivid dreaming. 90 min. 1-2 hrs. after falling asleep. Eyes flutter.
Breathing is irregular
o Non-rapid eye movement (NREM) – slow wave – most of the time is NREM. Stages evaluated by
EEG. Restorative & reparative. Growth occurs here.
• Sleep cycle: NREM has 3 stages
o N1 – right after you fall asleep (phase is only about 10 min.) Light sleep
o N2 – lasts 30-60 min. muscles relax, slow waves
o N3 – deep sleep. Lasts 20-40 min. Hard to wake up
• Dyssomnias – intrinsic & extrinsic sleep disorders & circadian rhythm sleep disorders
• Parasomnias – arousal & sleep-wake transition disorders & REM sleep disorders
• OSAS – trouble breathing while you sleep r/t upper airway obstruction & is r/t dec. O2 & inc. CO2
o Risk factors – obesity, males, age
o s/s: snoring, gasping, apnea 10-30 sec., fragmented sleep, daytime sleepiness
o Patho: obstruction d/t soft palate or base of tongue collapsing against the pharyngeal walls d/t
dec. muscle tone during REM sleep. Negative intrathoracic pressure wakes up pt.
o Systemic illnesses associated w/ OSAS – HTN, pulm. HTN, HF, nocturnal cardiac dysrhythmias,
MI, CVA
• People spend the most time in which stage of sleep? NREM sleep
Describe basic patho and clinical manifestations of Age-Related Macular degeneration (AMD)
• Drusen (retinal) waste products build up in deep retinal layers
• Wet AMD is the worst, dry is most common
• Wet = too many abnormal vessels → leak & bleed → retinal detachment
• Dry = loss of retinal pigment epithelium photoreceptors w/ overall atrophy of cells
Define Glaucoma; basic patho and clinical manifestations
• Intraocular pressure > normal pressure

• A patient with a defect of their central field of vision is diagnosed with Scotoma.
Differentiate between Types of hearing loss
• Conductive – impaired sound from outer to inner ear
• Sensorineural – impaired organ of Corti or its central connections
o Presbycusis – age related hearing loss (high frequencies)
• Mixed – conductive + sensorineural
• Functional – no reason but could be emotional/psychologic factors
Describe Vertigo; basic patho
• Spinning feeling that occurs from inflammation of ear’s semicircular canals
Differentiate between Arousal vs awareness (both are consciousness components)
• Arousal – state of being awake. Mediated by RAS
• Awareness – cognitive functions that embody awareness of self, environment, & mood. Content of
thought

Define Coma
• No verbal response to external environment or any stimuli. Noxious stimuli (deep pain, suctioning
produces movement)
• Light coma – purposeful movement w/ stimulation
• Deep coma – no response to any stimulus
Differentiate between Brain and cerebral death
• Brain death – brain will not recover & can’t maintain body’s homeostasis. State laws: entire brain,
brainstem, & cerebellum stop func. Brain autolyzes (self-digests)
• Cerebral death – cerebral hemispheres die but not brainstem or cerebellum. Brainstem may maintain
norm. resp. & cardiac functions, temp. control, & GI func.
Describe Seizure; types, patho, manifestations
• Patho: sudden, impermanent alteration of brain function caused by explosive, disorderly discharge of
cerebral neurons
 • Types:
o Generalized – neurons bilaterally (Ex absent, myoclonic, clonic, tonic-clonic, atonic)
o Partial (focal) – neurons unilaterally. Begins in specific region of cortex. (Ex simple, complex)
o Secondary generalization – partial → generalized
o Status epilepticus – emergency. Seizure lasts longer than 5 min., 2nd seizure occurs before LOC
is regained from 1st , or 1 seizure lasts longer than 30 min.
• A patient is diagnosed as having a partial seizure. The NP knows that this means that neurons
unilaterally were involved.
• S/s: depend on type of seizure
o Aura – partial seizure (weird sensation) → generalized seizure
o Prodromal – early s/s like malaise, HA, depression
o Tonic – contraction
o Clonic – relaxation
o Postictal – period immediately following end of seizure
Differentiate between Broca vs. Wernicke
• Broca aphasia – can understand, but can’t communicate. Expressive dysphagia.
• Wernicke – can’t understand (verbal/reading)
Describe each and differentiate between Delirium and dementia –

Delirium Dementia
Acute Progressive
Onset abrupt Onset gradual
ANS is overactive Progressive → nerve cell degeneration & brain
atrophy
Common in ICU’s, post-surgeries, w/ drawl Age is greatest risk factor
(ETOH, narcs)

• A major difference between delirium and dementia is that dementia is related to degeneration of
nerve cells.
Discuss Alzheimer disease patho and manifestations
• Patho: exact cause unknown, but thought to be mutation for encoding amyloid precursor protein,
alteration in apolipoprotein E, or loss of NT stimulation of choline acetyltransferase. Early onset is
autosomal dominant.
• S/s: neurofibrillary tangles, senile plaques, amyloid deposits (limit blood flow), forgetfulness, emotional
upset, disoriented, confused, lack of concentration, decline in abstraction, prob. Solving, judgement
• Dx when you rule out other causes. Definitive on postmortem exam.
• Alzheimer’s disease is caused in part by Deposition of amyloid proteins.
Discuss Basics of herniation syndromes
• Herniation – brain tissue is pushed from one compartment to another. From infection, hemorrhage,
tumor, ischemia, infarct, hypoxia.
Describe Types of cerebral edema
• Vasogenic → disruption of BBB. Caused by inc. permeability of capillary endothelium of brain after
injury to vasculature
• Cytotoxic – metabolic. BBB is not disrupted. Toxic factors impact brain → failure of active transport
system. Cells swell d/t loss of K+ & gain of Na+ (then H2O follows Na+)
• Interstitial – caused by trans-ependymal movement of CSF from ventricles into extracellular spaces of
brain tissues
 • A patient is diagnosed with cerebral edema and there is disruption of the blood brain barrier. The
student knows that this is indicative of Vasogenic edema.

Understand Basics of hydrocephalus, communicating and non-communicating

• Caused by interference in CSF flow → too much fluid w/ in cranial vault, subarachnoid space, or both
o Dec. reabsorption – Ex blockage of arachnoid vili from SAH or infection
o Inc. fluid production – Ex choroid plexus tumor
o Obstruction w/ in ventricular system (tumor or congenital malformation)
• Communicating (extra-ventricular) – from impaired absorption. Norm. pressure hydrocephalus
• Non-communicating – blockage occurs along narrow pathways that connect ventricular system. Most
common narrowing of aqueduct of Sylvius “aqueductal stenosis” btwn 3 rd & 4th
• Acute hydrocephalus – develops in several hours. Rapidly inc. ICP & deterioration
• Obstructive sources of hydrocephalus are classified as non-communicating hydrocephalus.

Differentiate Paresis vs paralysis

• Paresis = weakness
• Paralysis = loss of motor function
Differentiate Upper vs lower motor neuron syndromes
• Upper (spastic paresis or paralysis)
o Associated w/ hyperreflexia
o Spinal shock – complete paralysis, loss of reflexes, below lesion
• Lower
o Dysfunction impairs voluntary & involuntary movement
o Flaccid paresis or flaccid paralysis – muscle has reduced or absent tone
o Associated w/ hyporeflexia or areflexia
• A patient presents with a lower motor neuron disease. what is a possible finding on clinical exam?
Drop foot
Describe Huntington disease patho and manifestations
• Autosomal dominant hereditary degenerative disorder. Short arm chromosome 4.
• S/s: abnormal movement (chorea) & progressive dementia.
Describe Parkinson disease patho and manifestations
• Severe breakdown of basal ganglia involving the dopaminergic nigrostriatal pathway (dopamine
secreting)
• Loss of dopaminergic pigmented neurons in substantia nigra pars compacta w/ dopaminergic
deficiency in putamen portion of striatum → dec. activity of direct motor pathway (norm. facilitates
movement) & inc. activity of indirect motor loop (norm. inhibits movement)
• S/s: Parkinsonian tremor, rigidity, bradykinesia (slowed movement), abnormal posture, cognitive-
affective s/s, tremor at rest, cogwheel rigidity, hypoakinesia, stooped posture, not sleeping, fatigue,
pain, autonomic dysfunction, depression, dementia w/ or w/ out psychosis
• A patient presents with a resting tremor, bradykinesia, and a stooped posture. The NP knows that the
basic pathophysiology of this patient’s disorder is due to which of the following? Loss of dopaminergic
neurons in the substantia nigra
Differentiate Decorticate vs. decerebrate posturing
• Decorticate – flexed upper extremities & close to body. Brainstem is not inhibited by motor function of
cerebral cortex. (“Pointing to the CORe”)
• Decerebrate – angel wings. Severe brain & brainstem injury

• When a nonpainful stimuli creates a pain response this is known as Central sensitization.
Describe Focal brain injuries
• Contusion – brain bruise. Coup-contrecoup
• Laceration – brain tissue tear
• Extradural (epidural) hematoma – blood above dura mater
 • Subdural hematoma – blood btwn dura & arachnoid
• Intracerebral hematoma – bleeding in the brain
• Open – head trauma (skull Fx w/ exposed cranial vault)

Describe Diffuse brain injuries

• d/t head rotation (primary) or shaking
• brain undergoes shearing stress → axonal damage (concussion → severe DAI)
• O2 free radicals r/t secondary injury
• Categories are mild concussion, classical concussion, mild/mod/severe DAI
Define Mild concussion: I, II, III
I. Confusion, disorientation, momentary amnesia
II. Momentary confusion & retrograde amnesia
III. Confusion w/ retrograde & anterograde amnesia w/ loss of consciousness
**no loss of consciousness w/ Grade I-II**
Define Grade IV concussion
• Cerebral systems are disconnected from brain stem & RAS
• Physiologic & neuro dysfunction w/ out bad anatomic disruption. Loss of consciousness < 6 hrs.
• Post-concussive syndrome – HA, cognitive impairments, psych & somatic complaints, cranial nerve s/s
Describe Diffuse Axonal Injury (DAI) – form of TBI
• Mild – coma 6-24 hrs.
o Residual impairments. Decerebrate/decorticate posturing.
• Moderate – coma > 24 hrs.
o Widespread impairment through cerebral cortex & diencephalon. Actual tearing of some axons in
both hemispheres. Recovery is incomplete. Decerebrate & decorticate posturing.
• Severe
o Many axons are messed up extending to diencephalon & brainstem. High mortality.

Describe Spinal cord trauma; patho and manifestations

• Patho: occurs from vertebral injuries (simple Fx, compressed Fx, comminuted Fx & dislocation)
• Complete spinal cord transection – loss of motor func., muscles are flaccid, lost reflexes, los pain,
temp, touch, proprioception, resp. impairment
• S/s:
o Paraplegia – paralysis of LE
o Quadriplegia – paralysis of all extremities
Define Spinal shock
• Spinal cord trauma → spinal shock → loss of motor, sensory, reflex, & autonomic functions below cut
across area
Differentiate between different syndrome associated with Spinal cord injury
• Partial spinal cord transection – asymmetric flaccid motor paralysis/reflex loss, some senses
 Syndrome About
Brown-Sequard Ipsilateral paralysis/loss of touch. Contralateral loss of pain & temp.
Central cord Motor deficits > UE than LE
Anterior cord Loss of motor, pain, temp. Intact = touch, pressure, position, vibration
Posterior cord Impaired light touch & proprioception
Cauda equina LE motor deficits, sensorimotor dysfunction; B/B & sexual dysfunction
• Central cord syndrome results in which of the following syndromes? Motor deficits with upper and
lower extremity weakness
Describe Autonomic hyperreflexia (dysreflexia)
• Massive/uncompensated heart response to stimulation of SNS
• Sudden/dangerous inc. in BP (life threatening)
• S/s: HTN, bradycardia, pounding HA, blurred vision, piloerection
Describe CVA patho and manifestations
• Thrombotic stroke – arteries supplying brain occluded from thrombi d/t atherosclerosis &
inflammatory disease → damaged artery walls
• Embolic stroke – fragment breaks off a thrombus that’s formed outside of the brain d/t A-fib
• Hemorrhagic stroke – D/t HTN, ruptured aneurysm, AV malformations, cavernous angioma or from TBI
• Lacunar stroke – really tiny infarct in tiny vessels d/t lipohyalinosis, subintimal lipid-loading foam cells,
or fibrinoid materials that thicken the arterial walls. R/t smoking, HTN, DM
• A patient is diagnosed with Afib and then has a CVA. How would this patient’s CVA likely be classified?
Embolic stroke
Discuss TIA
• BRIEF episode of neuro dysfunction d/t focal disturbance/brain/retinal ischemia. S/s last < 1 hr.
thrombus particles → intermittent blockage
Describe SAH (subarachnoid hemorrhage) patho and manifestations
• Blood escapes from defective/injured vasculature into subarachnoid space
• S/s: vasospasm – d/t blood breakdown → free radicals disrupt blood vessel layers & release
inflammatory factors → delayed cerebral ischemia
• Other s/s: thunderclap HA, N/V, loss of LOC, neuro probs. d/t inc. ICP. Kernig/Brudzinski sign
Describe Basics of vascular manifestations
• Intracranial aneurysm – d/t defect in vascular wall. s/s is acute SAH, intracerebral hemorrhage, or a
combination
Differentiate Headaches; types and patho/clinical manifestations
Types Patho S/s
Migraine Genetic & environment. Phases Unilateral throbbing, worse w/ movement,
(premonitory, aura, HA). N/V, photophobia
Cluster Trigeminal activation Unilateral trigeminal distribution of severe
pain w/ ipsilateral autonomic s/s (tearing on
affected side, ptosis of same eye, stuffy
nose)
Tension-type Central & peripheral mechanism Feeling of a tight band/pressure around
head w/ gradual onset
• What is the basic pathophysiology behind cluster headaches? Trigeminal nerve activation
Describe CNS infections; pathogens, patho, clinical manifestations
Type
Bacterial Infection of pia mater & arachnoid Bacteria makes pus. Vessels are
meningitis of fluid of subarachnoid space hyperemic & neutrophils move to
subarachnoid space. Inflammatory
rxn → exudation
Aseptic Viral, non-purulent, lymphocytic Limited to meninges
meningitis
Fungal Chronic, less common
meningitis
• Meningitis s/s: depend on type. Can be throbbing HA, neck stiffness, rigidity, dec. responsiveness,
Kernig & Brudzinski
• Encephalitis – acute febrile illness (viral) w/ nervous system affected.
o S/s: fever, delirium, confusion, seizures, involuntary movement, inc. ICP
Describe MS patho and manifestations
• MS – acquired autoimmune. It’s a progressive, inflammatory, demyelinating disorder of CNS. Scarring,
plaque formation, & loss of axons
• Mixed – optic signs; brainstem signs (diplopia, vertigo, nystagmus, dysarthria)
• Spinal – spinal tracts & dorsal column involved. Weakness, numbness, or both. Spastic ataxia.
Bladder/bowel s/s
• Cerebellar – motor ataxia, hypotonia, asthenia
• Multiple sclerosis is characterized by which of the following? Inflammatory demyelination of the
central nervous system
Describe ALS (amyotrophic lateral sclerosis) patho and manifestations
• Patho: upper & lower motor neurons of cerebral cortex, brainstem, & spinal cord affected
(degeneration of non-motor neurons in cortices & spinal cord)
• s/s: disease → progressive weakness → resp. failure & death
Describe Myasthenia gravis; patho and manifestations
• Patho: acquired chronic autoimmune disease resulting from defect in nerve impulse transmission at
NMJ
o IgG antibody is produced against acetylcholine receptors
• S/s: weakness/fatigue of muscles of eyes & throat → diplopia & trouble chewing, talking, or
swallowing. c/o fatigue after exercise & hx of recurring URI’s.
• Myasthenia crisis – severe muscle weakness → quadriparesis/quadriplegia, resp. probs w/ SOB,
extreme probs swallowing
• Cholinergic crisis – can be d/t drug overdose. Looks like myasthenic crisis BUT it happens 30-60 min.
after taking anticholinesterase med
o S/s: diarrhea, cramping, fasciculation, dec. HR, pupil constriction, inc. salivation, inc. sweating
• Myasthenia gravis is the result of autoimmune destruction of acetylcholine receptors