Pathophysiology exam II

What age is more likely to experience ADR?

Older than 75

What sex is more likely to experience ADR?


What ethnicity is more likely to experience ADR?


Risk factors of ADR

� Concomitant alcohol abuse
� New drugs
� Number of drugs
� Dosages
� Concomitant herbal compounds
� Duration of treatment
� Noncompliance
� Small stature
Presence of underlying conditions (Renal insufficiency)

Common signs of Drug Toxicity

o Rashes
o Fever
o Jaundice

Adverse Skin Reactions that occur with ADR

o Erythema
o Discoloration
o Itching
o Burning
o Urticaria (hives)
o Eczema
o Acne
o Alopecia
o Bulla
o Purpura

Non skin related S&S for ADR

� Altered Taste
� Anxiety
� Dizziness
� HA
� Nasal Congestion
� Shakiness
� Vomiting
� Cramps
� Dyspnea
� Hypo/hypertension
� Palpitations
� Tachycardia
� Persistent Vomiting
� Seizures
� Pulmonary Edema
� Arrhythmia

S&S for large vasculitis

limb claudication, aortic dilation, & bruits (vascular murmur)

S&S for medium vasculitis

cutaneous nodules, gangrene of the digits, mononeuritis multiplex, & Microaneurysms

S&S for small vasculitis

purpura, glomerulonephritis, & alveolar hemorrhage

Common S&S for all sizes of vasculitis

� Fever
� Arthralgias
� Arthritis
� Weight loss
� Malaise

discoid lupus erythematosus

chronic disorder, primarily of the skin, characterized by lesions that are covered with scales

Acute Inflammation S&S

o Fever ( > 100 deg)
o Tachycardia ( > 100 BPM at rest)
o Increased Hypermetabolic State
o Elevated serum protein levels, Elevated WBCs

Chronic Inflammation S&S

� Lymphocytes
� Plasma Cells
� Macrophages
� Fibrosis

Systemic effects of chronic inflammation

� Anemia
� Fatigue
� Leukocytosis
� Lymphocytosis

Increased intravascular fluid does what to pulse rate/respiratory rate/blood pressure?

Increased Pulse and Respiration

Decreased intravascular fluid does what to pulse rate/respiratory rate/blood pressure?

Decreased BP and Increased PR and Respirations

NSAID side effects

GI discomforts, GI ulceration, renal impairment, photosensitivity

s/s of rheumatoid arthritis

� Morning stiffness
� Anorexia
� Weight loss
� Fatigue/Malaise
� Joint involvement
� Immobility & inflammation
� Muscle atrophy
� Subcutaneous nodules

Systemic Lupus Erythematosus causes

*Unknown etiology
*Environmental Triggers
*Viruses, UV light, certain medications, estrogen

Systemic Lupus Erythematosus most serious complications

affect the heart, kidneys, & CNS

What sex is affected by SLE more often?

Female, 8 times more likely, increases to 15 times during child-bearing years

Signs of SLE

Butterfly Rash, and Rheumatoid Nodules

Systemic factors that influence healing

� General nutritional status
� Vitamin C & Proteins
� Psychological well-being
� Presence of CV disease
� Cancer
� Hematologic Disorders
� Systemic Infections
� Diabetes Mellitus
� Corticosteroid or immunosuppressive therapy


Pitting edema scale 1+

Barely Perceptible Depression [2mm]

Pitting edema scale 2+

Skin rebounds to its original contour in <10 secs, [4mm]

Pitting edema scale 3+

Skin rebounds within 10-15 seconds [6mm]

Pitting edema scale 4+

Takes >20 seconds to rebound [8mm]

Increased extravascular fluid results

Edema, Ascites, or Pleural Effusion

Decreased extravascular fluid results

Decreased Skin Turgor and Fatigue (will remain elevated and look like a "tent")

How much of body fluid is intracellular?


How much of body fluid is extracellular?


Ligament/tendon healing: Acute/Max Protection phase

o Hemorrhagic (Day 1)
� Blood clot between ruptured tissues
o Inflammatory (Day 1-10)
� Chemical, cellular, vascular responses

Ligament/tendon healing: Sub-Acute/Mod Protection phase

� Fibroblasts > Collagen & Matrix Proteins
� Capillary Buds (Neovascularization)
� Wound Closure in 3-6 weeks

Ligament/tendon healing: Chronic/Min Protection phase

o Remodeling & Maturation (6 weeks - 3 years)
� Connective tissue characteristics change
� Decrease in number and types of cells
� Matrix density increases
� Matrix fiber orientation more longitudinal
� Maturation Cont.'s for many months

% of tensile strength regained 6 months after injury


% of tensile strength regained 1 year after injury


% of tensile strength regained 1-3 year after injury


Disuse atrophy

when prolonged inactivity results in the muscles getting smaller in size

Articular cartilage healing prognosis

� Generally, lacks the blood supply to repair
� Chance of repair if injured involves the sub-chondral bone (50%)
� Most commonly leads to degeneration


Dude c'mon you should know this by now

Key element of bone healing

o Blood supply
o Micromovement may FACILITATE clinical union
o Macromovement may INHIBIT and prevent clinical union

How do you treat an overuse injury with chronic inflammation at first?

As an acute

Types of Hypertension

1. Borderline
2. Sustained
a. occurs over 3 testing periods
3. Labile
a. comes & goes
4. Malignant
a. markedly elevated BP
Usually not responsive to typical medications

Stages of hypertension

Stage 1= 130-139/80-89
Stage 2= >140/>90
Hypertensive crisis= >180/>120


the thickening and hardening of the walls of the arteries, due to hypertension

S&S of atherosclerosis

� Arterial wall damage
� Permits the infiltration of macromolecules
� Platelets aggregate at the site of injury and plug up the wound
� Cholesterol-filled plaques can take years to form

orthostatic hypotension causes

o Prolonged Immobilization
o Anti HTN meds
o Peripheral neuropathy
o Volume depletion (burns, DM, Na or K depletion)
o Venous pooling
o Performing the Valsalva maneuver
o Autonomic system dysregulation

orthostatic hypotension signs

Drop in systolic pressure of >20 mm Hg and/or pulse increase of 20 bpm

orthostatic hypotension symptoms

Light-headedness, dizziness, nausea, loss of consciousness and sudden weakness.

S&S of Buerger's disease

� Episodic & Segmental
� Intermittent claudication
o localized to arch of foot or palm of hand
� Raynaud's phenomenon
� Coldness, numbness, tingling or burning of the affected hand or foot

S&S of venous insufficiency

� Wet & weepy wounds
� Purplish color is due to hemosiderin/fibrin deposits in the "gaiter" region


Blockage of the LUMEN of the arteries


Thickening of the arterioles

Monckeberg's Medial Sclerosis

Tunica media of vessels becomes CALCIFIED

Berry or Sacular Aneurysm

a. 35% mortality rate
b. Located in cerebral area typically
c. Due to congenital defects
d. Rupture leads to subarachnoid hemorrhage

fusiform aneurysm

a spindle-shaped bulge, Lumen has increased in size due to atherosclerosis

dissecting aneurysm

A condition in which the inner layers of an artery, such as the aorta, become separated, allowing blood (at high pressures) to flow between the layers.

false aneurysm

rupture of the arterial walls, causing pouching

What patient population is more at risk for Monckeberg's medial sclerosis?

This usually occurs in patients with diabetes mellitus due to the excess glycosylation of proteins

Pathogenesis of primary/secondary hypertension

vessels thicken > arteriolorsclerosis > leading to L ventricular enlargement

S&S of arterial insufficiency

� Intermittent claudication
� Reduced or absent pulses distal to obstruction
� Burning ischemic pain at rest
� Ischemic extremities are characterized by decreased skin temperature, dry, scaly or shiny skin, poor nail & hair growth, & ulcerations on WBing

Risk factors of peripheral vascular disease

� Age
� Smoking
� Diabetes
� Hyperlipidema
� Ethnicity: African American

Commonalities in S&S of all venous disorders

� Swelling
� Warmth & blue discoloration of extremity
� Dependent edema
� Prominence of superficial veins
� Skin ulcerations & tenderness
� Deep calf tenderness
� Fever
� Chills
� Malaise
� Cyanosis of affected extremity

Special test for DVT

Wells DVT score

S&S of thoracic outlet syndrome

� Paraesthesias of fingers
� + Adson's sign
� + result from hyperabduction
� + result from costoclavicular test
� Pain in anterior chest wall

Adson's sign

obliteration of the radial pulse when the arm is abducted to a position above the shoulder, causing compression of the proximal vessel; associated with thoracic outlet syndrome

S&S of ankylosing spondylitis: Early stages

o Low grade fever
o Fatigue
o Anorexia, wt. loss
o Anemia
o Sacroilitis
o Spasm of paravertebral muscles
o Intermittent LBP

S&S of ankylosing spondylitis: Advanced stages

o Constant LBP
o Ankylosis
o Muscle wasting in shoulder & pelvis
o Loss of lumbar lordosis
o Marked kyphosis
o Decreased chest expansion
o Arthritis
o Iritis (inflammation of the iris)
o Carditis
o Pericarditis
o Fatigue & weight loss
o Low grade fever

Antibody production

B lymphocytes are antibody factories


o Largest immunoglobulin that predominated in initial immune response
� Mostly in intravascular compartment


Defends external body surfaces, mucus membrane


Serves mainly as an antigen receptor & may function in controlling lymphocyte activation or suppression


The major antibacterial & antiviral antibody & is the predominant antibody in the blood


o Primary for parasitic infections
� Also functions by activating mast cells & releasing histamine in allergic reactions, anaphylaxis, asthma & urticaria

Type 1 hypersensitivity

IgE mediated hypersensitivity
Allergies, Anaphylaxis, Atopy

Type 2 hypersensitivity

IgM or IgG formed against SELF, specifically on SURFACE of own body

Type 3 hypersensitivity

o Immune complex diseases
o Forms antibodies on something floating IN the body, NOT on surface

Type IV hypersensitivity delayed

� antigen processed in macrophage > antigen recognition > T cell activation
� Amplification & recruitment of macrophages & T cells
� Damage to area where antigen is present

Type IV hypersensitivity cell mediated cytotoxicity

� Target antigen after recognition of antigen by T cells > activation of T helper & killer cells
Destruction of target cells & adjacent tissues


graft from a person's own body


a graft from another species


use of identical twin's tissue


skin graft from another person or a cadaver

Mononuclear cells

monocytes and lymphocytes


neutrophils, eosinophils, basophils

Natural killer cells and immunity

� Larger granular lymphocytes
� Function is to KILL viruses, other intracellular microbe-infected cells, & tumor cells
� Kill without prior sensitization or activation

How do neutrophils kill?

- Kills via phagocytosis, digestion, and
respiratory burst
- When a bacteria is detected, neutrophils
(discharge their lysosome enzymes into the tissue fluid), which catalyze a reaction called the
respiratory burst

S&S of anaphylaxis: General

Malaise and weakness

S&S of anaphylaxis: Dermal

Hives, erythema

S&S of anaphylaxis: Mucosal

Periorbital edema, Nasal congestion, pruiritus, Flushing, pallor, or cyanosis

S&S of anaphylaxis: Respiratory

Sneezing, rhinorrhea, dyspnea

S&S of anaphylaxis: Upper airway

Hoarseness, stridor, tongue & pharyngeal edema

S&S of anaphylaxis: Lower airway

dyspnea, asthma

S&S of anaphylaxis: GI

Increased peristalsis, vomiting, dysphagia, nausea

S&S of anaphylaxis: CV

tachycardia, dysrhythmia, Hypotension, cardiac arrest

S&S of anaphylaxis: CNS

Anxiety, Seizures


Subunits of an antigen that elicit an immune response


� stem cell from bone marrow that produces blood cells.
� When a hemocytoblast divides into two daughter cells, one of the new cells becomes a blood cell. The other remains a hemocytoblast, ensuring there are always enough hemocytoblasts available.

Interleukin fxn

� Increase the temperature set point in the hypothalamus
� Increase serotonin in brainstem & duodenum
� Stimulate production of prostaglandins thus leading to decreased pain threshold
� Increase syntheses of collagenases resulting in destruction of cartil

passive acquired immunity

Antibodies or sensitized lymphocytes produced by 1 person are transferred to another person

active acquired immunity

Protection by natural or artificial (vaccine) introduction of an antigen into a responsive host

S&S of shingles

� vesicular eruption occurs unilaterally in distribution of a dermatome supplied by the dorsal root or extramedullary cutaneous nerve sensory ganglion
� Usually seen on the trunk or along 5th cranial nerve
� Starts with pain, tingling along the affected s

Causative factors for pressure ulcers

� Unrelieved pressure & results in damage to underlying tissue
o Bony Prominences
o External pressure
o Friction
o Shearing forces
o Maceration
o Decreased skin resilience
o Malnutrition
o Decreased circulation

S&S of cellulitis

� Erythema
� Edema
� Tender
� sometimes nodular
� Erysipelas


epithelial cells found in all layers of the epidermis that produces keratin, a skin protein


a. forms melanin & found in the basal layer
b. Protects against sunburn, UV carcinogenesis, & determines skin color

Langerhans cells

tissue macrophages that aid in immune response

Developing pressure ulcers

Pressure > ischemia > tissue necrosis

layers of epidermis

stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum

S&S of stasis dermatitis

� Itching
� feeling of heaviness
� hemosiderin staining
� open shallow lesions

S&S of contact dermatitis

� Pruritus, erythema, edema occurs 1-2 days after exposure
� Signs begin at site of exposure then extend distally
� May progress to vesiculation, oozing, crusting, & scaling

Primary skin lesion

initial reaction to pathologically altered tissue and may be flat or elevated
ex: macule, papule, plaque, nodule, tumor, wheal, vesicle, pustule

secondary skin lesions

changes that take place in the primary lesion due to infection, scratching, trauma, or various stages of a disease
Ex: scale, crust, thickening, erosion, ulcer, scar, excoriation, fissure, atrophy

In situ

Describing a tumor that has not yet broken through the basement membrane

Stage 0 cancer

carcinoma in situ

Stage 1 cancer

confined to organ of origin

Stage 2 cancer

increased risk of spread because of tumor size

Stage 3 cancer

local CA has spread but may not be disseminated to distant regions

Stage 4 cancer

CA has spread & disseminated to distant sites

Encapsulated neoplasms

� Encapsulation is when a neoplasm grows within a connective tissue or capsule
� Most encapsulated neoplasms are benign

benign neoplasia characteristics

o No Metastasis
o Encapsulated
o Non-invasive
o Slow Growing
o Well Differentiated
o Little or no anaplasa

Malignant neoplasia characteristics

o Metastasis
o Non-encapsulated
o Invasive
o Rapid Growth
o Poorly differentiated
o Anaplasia to varying degrees

When benign & malignant tumors are classified by cell types, they are named by the_____________

tissue of origin

5 major classifications of tumors by cell type?

o epithelial
o connective & muscle
o nerve
o lymphoid
o hematopoietic

Axonotmesis (Class 2)

o Complete interruption of axon with loss of all function subserved by the cell
� Recovery of function may occur if Wallerian degeneration and regeneration occur

Neurometsis (class 3)

o Complete interruption of entire nerve fiber including cell membrane and myelin sheath
� Requires surgical re-attachment if recovery of function is to occur

S&S of carpal tunnel syndrome

� Nocturnal Pain, Tingling, Numbness, Paresthesia
� Muscular Weakness occurs later
� Loss of grip strength, inability to pinch & sensory loss causes clumsiness of the hands

Transient neuropraxia

Due to ischemic block of neuronal conductivity and presents as a rapidly reversible loss of function (arm falling asleep)

Delayed reversible neuropraxia

� due to demyelination and presents as loss of function that recovers after a few weeks following re-myelinization (Bell's palsy, Guillian-Barre)

Myelin production in PNS

Schwann cells

Myelin production in CNS


In a myopathy, weakness tends to be_________


In a neuropathy, motor symptoms tend to first occur_________



single peripheral nerve is affected


several peripheral nerves affected


involves nerve root as it emerges from spinal cord


involvement of several nerve roots > may be from infection causing inflammation


involvement of muscle. Usually involves proximal muscle weakness, wasting, and hypotonia without sensory impairments

Compressive positions of the wrist in CTS

� Sleep
� Computer desk position
� Flexion or Extension = produces ischemia and impingement on the nerve

Guillain-barre syndrome S&S

� 1st symptom is often paraesthesia in the toes, within hours or days distal weakness in the LEs
� Weakness spreads to UEs, trunk, & facial muscles.
� Absence of DTRs
� Palatal & facial muscles involved in � of cases
� If ANS involvement: tachycardia, abn

Myesthenia gravis S&S

� Ptosis (ocular) & diploplia
� Repetition of muscle activity = fatigue
� Proximal muscle weakness variability
� Chewing meat produces fatigue
� Speech is nasal
� Difficulty swallowing (aspiration possible)

collateral sprouting

New axon and dendrite extensions allow existing neurons to form new connections


New connections are made between active neurons to create alternate neural pathways

What nerves are effected by bell's palsy?

Facial Nerve VII

S/S of Bell's Palsy

� Can come on rapidly, often overnight
o Mouth Droops
o Nasolabial Fold flattens
o Palpebral fissure is widened because eyelid doesn't close
� Taste, Lacrimation & Salivation affected

Wallerian degeneration

degeneration of a nerve distal to an injury

Ulnar palsy presentation

� Claw-hand deformity with MCP extension & IP flexion of ulnar distribution
� Flattened hypothenar eminence along with abduction of little finger coincides with weakness of palmaris brevis & abductor minimi
� Atrophy of interossei on dorsal hand
� Paralys

Radial palsy presentation

o If axilla, then weakness in Triceps, Brachioradialis, Supinator
o If damage at upper arm, then triceps is spared
o In both instances, there is paralysis of the wrist extensors, extensors of the thumb, fingers and diminished grip strength
o Sensory loss