Blood-brain barrier

"star"

Decreases cell size

Disuse, poor nutrition and hormones

Abnormal changes in cells

Size, shape, etc

Bleeding into skin, underlying tissue

(bruise)

collection of blood in enclosed space

(blood clot)

Penetrating

Perforating

Bullet still in body

Bullet exited body

Protein denaturing

Hear, kidney, adrenal glands w/ hypoxia

In CNS

Digestive enzyes cause autodigestion

Pus forms

combo of coagulative and liquefactive

cottage cheese

Blunt fforce to breast/abdomen

Causes lipases

Soapy residue

widespread dead tissue

bacteria releases enzymes and toxins

Hypernatremia

Hyponatremia

High levels Na

>146 mEq/L

Low levels of Na

<135 mEq/L

Hyperkalemia

Hypokalemia

High K  (acidosis)

> 5 mEq/L

Low K (Alkalosis)

<3.5 mEq/L

Hypercalcemia

Hypocalcemia

High Ca

>12 mg/dl

Low Ca

<8.5 mg/dl

pH equation

pH of blood

-log [H+]

7.35-7.45

Uncompensated

Partially compensated

Compensated

pH abnormal-- one parameter abnormal

pH abnormal-- two parameters abnormal

pH normal-- both parameters abnormal

Polyploid

Triploidy

Tetraploidy

cell has more than diploid number

3 copies of each chromosome

4 copies of each

Aneuploidy

Monosomy

Trisomy

Does not contain multiple of 23 chromosomes

Only one copy of any chromosome

3 copies of one chromosome

Incidence Rate

Prevalence Rate

How many new cases in a year

How many people have it

1. Brief constriction of arterioles

2.Dilation--causes edema and dilutes toxins

3.Retract endothelial cells for blood migration

4. Migration of neutrophils

5.Migration of monoccytes and macrophages

6. Eosinophils and basophils--control inflammation response

7.Platelets stop bleeding if needed

1. Complement System--destruction of cells

2. Coagulation System--trap pathogens, prevents hemorrhage

3. Kinin System--Bradykinin, controls vascular permeability

> 2 wks

Body fails to remove the cause

Granulome--body walls off infection site

1. Watch your temper

2. Lighten your dark moods

3. Flatten your belly

4. Limit your bad habits

5. Rev up your metabolism

Foreign substance introduced to body to form an immunity

(Vaccines)

Tempory Immunity

(mother's milk)

10%

pentamer

first on scene

75%

Longest living

monomer

Body secretions

dimer

J chain and secretory piece

Low plasma concentration

basophils/mast cells

release histamines

allergies/parasites

monomer

Unknown 

maybe controls suppression

monomer

Cemical messengers secred by cells

lymphokines, interleukins, interferons, etc

1. Phagocytosis occurs, macrophages presents MHC-II

2.CD4 attach and APC releases IL-I

3. T cell produce IL-II

4. T cells proliferate

5. Stimulate B cells to proliferate 

6. Plasma cells make antibodies

7. memory cells remain dormant

Allergies

IgE release histamine

Inherited tendency

Tissue specific

blood typing

Antibody reactes with soluable antigen

Autoimmune diseases

Delayed

Sensitized T cells

Takes several hours

Lack of or partial lack of thymus

Decreased T cell function

Retrovirus

Reverse Transcriptase

Decreased T4 cells

HIV cocktail

Reverse Transcriptase Inhibitor

Lack of control

• Signal transduction
• Cell cycle control lost
• No DNA repair
• Abnormal cell growth
• Decreased differentiation
• No apoptosis
• Growth factors don't work
• Loss of growth factor receptors

Potentially cancer causing

Altered/mutated

Initiation

vs

Promotion

vs

Progression

Developmental stage of cancer precursor 

Expose precursor cell to promoting agent

Sturctural changes in the chromo.

1. Cellular multiplication

2. Mechanical invastion

3. Release lytic enzymes 

4. Decreases cell adhesion

5. Increased motility

1. Tumor cell attaches

2. Degradation of matrix--breaks down basement membrane

3. Locomotion into the matrix

Lymphatic routes occur near edges of the tumor

tumor enters lymphatic vessels and carried to lymph nodes

If celsl pass into efferent vessels, metastasis of lymphatics can occur

Tumor cells penetrate blood vessels, break loose, disseminated visa circulatory

Cells must then 1. escape host defenses

2. survive mechanical trauma of bloodstream

3. Lodge in vascualar supply of target organ and invade parenchymal cells

Cancer out grows blood supply

Growth of new vessles incolves cascade similar to coagulation

Codes for a proten that inhibits cell growth of cells w/ damaged DNA

Keeps cell growth and proliferation under control

Stage 1--in original site, well differentiated

Stage 2--Metastastic cells in original site and local lymphatices, moderately differentiated

Stage 3-- Original side and distal lymphatic, poorly differentiated

Stage 4--Found in many body areas, very poorly differentiated

Incidence: < 2%

Latencey: Short

Influences: Genetic/environment

Treatment: Long-term consequences

Treatment response: very responsive

Prognosis: > 65% cure

Sites: tissues

Prevention: few strategies

Stage at diagnosis: 80% have metastasized

Incidence > 98%

Latency: Long

Influences: mostly enviornmental

Treatment: Few long-term consequences

Treatment Response: Less responsive

Prognosis: < 60% cure

Sites: organs

Prevention: 80% preventable

Stage at diagnosis: local or regional

1. pain receptors transmit affarent impuls through sensory to dorsal root
2. Synapse in spinal cord, cross ipsilateral
3. Ascend by neospinothalamis (fast) or paleospinothalamic (slow/dull) 
4. paleospinothalamic ascends into brain stem and limbic
5. neospinothalamis ascends to thalamus and cortex

Prolonged, persistant, intermittent pain

Allows for adaptation

Nerve damage, coagulation of proteins, cellular death

Rare, inherited muscle disorder, FATAL

Extremely rapid increase in temp.

leads to cardiac arrest

Slows down chemical reactions

increses blood viscosity

blood coagulaiton

vasoconstriction

promotes shivering

Sleep apnea

(Stye)

Infected sebaceous gland

Strabismus

vs

Amblyopia

Deviation of one eye from other when looking directly at something, weak muscle in one of eyes

Vision reduction or dimness for unknown reasons, diabetes

Intraocular pressures are above normal

• Confusion--disorientation to time, then place, then to person
• Lethargy--orientation to time, place person, slow vocalizaiton, decreased motor skills and oculomotor
• Obtundation--awakening in response to stimuli, continuous stimulation needed
• Stupor--bocalization only in response to painful stimuli
• Coma--no vocal, eye movements, arousal to stimuli, reflexes intact

Partial seizures

involuntary movemtns 

Sensory seizures

Abnormalities in temporal lobe

Begin with olfactory aura

loss of consciousness

Everywhere in forebrian

Preseizure sensations

losses consciousness, falls to ground suffers tonic then clonic

No outward manifestation of seizure

present physicall but absent in higher cortical functions

loss of awarness

Severe cognitive dysfunction (cause unknown)

Aggregation of insoluable amyloid

Form plaques in brain

1. CSF desplaced from cranial vault
2. Neural oxidation affected
3. Cerbral perfusion pressure falls, perfusion slows, hypoxia and acidosis
4. Brain tissue shifts from compartment of greater pressure to compartment of lesser pressure (herniation)

Hypotonia

Hypertonia

Decreased muscle tone

Increased muscle tone

Hyperkinesia

Dyskinesia

Hypokinesia

Excessive movement

Abnormal involuntary movement

Decreased movement

Coup

Contrecoup

Impact area

Opposite impact area

I--Confusion, disorientation, forget only event

II--Momentary confusion retrograde amnesia (forget previous events)

III-- confusion w/ retrograde and anterograde amnesia

IV-- Loss of conciousness < 6 hrs, no reflexes, anterograde and retrograde amnesia

Coma lasting > 6 hrs

Mild- coma 6-24 hrs, residual cognitive psychologic and sensorimotor problems persist

Moderate- Coma >24 hrs, widespread physiologic impairment, 38% recovery in 3 mths

Severe- Disrupts axon in cerebral hemi., 15% recover in 3 mths, severe consequences

Bacterial or Aseptic

Bacterial-decreased CSF glucose

Aseptic-- (viral) normal glucose levels, presence of lymphoytes

Degeneration of basal ganglia involving dopamine receptors

especially sustantia nigra

imbalance of dopamine and AcH

Progressive, inflammatory, demelination of CNS.

T Calls autoreactive

Plaque predominantly in white matter 

Affects motor neurons of cerebral cortex, brain stem, ventral roots 

Weakness in single muscle group, muscle atrophy, death

Bulbar palsy (paralysis of motor centers of medulla and cranial nerves)

Autoimmune Disease

Antibody against AcH

Static encephalopathy

motor disabilites, mental retardation, seizures

Metabolic disorder

can't metabolize amino acid phenylalanine

Encephalopaty from interaction of salicyate (aspirin), viruses, and liver dysfunction

brain edema

Don't take aspirin w/ a virus

Insufficient HGH release during groth phase

no effect on intelligance

Excess HGH during growth phase

Excess HGh during adulthood

enlargement elongatin of bones of face, jaw, cheeks, hands

No affect on long bones 

Autoimmune disorder

Excess thyroxin causing eyes to bulge

Enlarged thyroid from increased demand of TH

Iodine deficiency

Follicle increase in # due to TSH stimulation

Insufficient thyroxin during adulthood

body edema

dry brittle hair, skin 

insufficient thyroxin during growth phase

absent or defective thyroid tissue

mental retardation, short stature

Low blood Ca++

Skeletal muscle twitch, spasm, contract involuntarily

Type 1--lack of insulin, beta cells destroyed by islet cell anitbodies

Type 2--enviornmental factors, some functional beta cells

Clucose level >300 mg/dl

need insulin, electrolyte and fluid replacement

Excess cortisol 

Fat redistribution

Hyposecreation of glucocorticoids and aldosterone

Serum 

vs

Plasma

Plasma-liquid portion of blood

Serum is same but without clotting factors

pinkish cytoplasm

segmented nucleus

phagocytic

60-70%

Large red granules

allergies/parasites

1-4%

Large dark blue granules

Inflammatory resonses

release hitamine and heparin

0-1%

Immature neutrophils

acute bacterial infection

# of band cells = severity of infectino and speed of new neutrophil production

20-30%

Most common WBC in body

Found in lymph nodes, connective tissue, lymphatice organs

Phagocytes

T cell recognition

3-8%

Leukocytosis

Leukopenia

High WBC

> 10,000 mm^3

Low WBC

< 5,000 mm^3

Thrombocytopenia

Thrombocytosis

low platelets

increased # of platelets

Blood cell production

in bone marrow

Specific growth factors are used for specific blast cells to create blood cells

Erythropoietin from Kupferr cells to create erythrocytes

Immature RBC. 

No nucleus, some ribosomes

used to evaluate how fast RBC produced and put into circulation

Process by which bleeding is stopped

1. Vascular spasm--reduces blood loss

2. Platelet plug formation

3. Coagulation (clotting)--activating clotting pathway

Activated by injur to, or activation of factors within the blood itself

All things needed are already in blood, they just need to be activated

1. Formation of the prothrombin acivator (prothrombinase)

2. Formation of thrombin from prothrombin

3. Formation of fibrin from fibrinogen

Stages must occur in order

Protime (PT)--measures extrinsic

Activated Partial Thromboplastin Time (APPT)--instrinsic

Bleeding Time-- Platelet 

Fibrinolysis System

Lysis of clots

Plasminogen turns to plasmin

Plasmin splits fibrin and fibrinogen and dissovles clot

Excess RBC formation

Normocytic Anemia

Microcytic "

Macrocytic "

RBC's are normal size

" are abnormally small

" are abnormally large

Normochromic

Hyperchromic

Hypchromic

RBC's normal amounts hemoglobin

" abnormally high amount of Hgb

"abnormally low amount of Hgb

Red cell lysis

fragile cells, infections, drugs, autoimmunity

enlarged spleen, jaundice

Blood loss

surger or trauma

shock and acidosis

Bone marrow hypoplasia or aplasia

Chemo, viruses, genetics

 petechiae, ecchymosis, bleeding

Macrocytic-Normochromic

Low B12

peripheral nueropathy

Macrocytic-Normochromic 

Inhibits DNA sytheses

alcohol, malnourishment

no neurological symptoms

Microcytic-Hypochromic

Excessive bleeding, poor diet

Microcytic-Hypochromic

Dysfunctional iron uptake by erythoblasts

lead poisoning

Excessively large number of RBC's in blood

Relative--increase RBC w/ loss of plasma

Absolute--high altitue, smoking, etc

two or more diastolic BP of >90 with systolic BP > 140

Primary- unknown cause

Secondary- known cause

Complicated- prolonged primary with secondary effects

Malignant- rapid rise/acute onset

Thromboangitis obliterans (TAO)

Buerger's Disease

Inflammatory disease of peripheral arteries

cyanosis

episodic vasospasm in arteries and arterioles beginning in the fingers and toes

Secondary to other systemic diseases

Enviornmental factors

Remove stimulus

Myocardial Ischemia

Atherosclerosis

Anginia pectoris

Myocardial Infarction (MI's)

Cells ischemic within 10 seconds of coronary blockage

Arteries can't compensate for lack of oxygen

After infection with Group A beta hemolytic streptocci

Carditis of all 3 layers, vavular stenosis, aschoff bodies

Failur of ductos arteriosus (connection between pulmonary arter and aorta) to close

Overwork ventricles

left-to-right shunt

Foramen ovale doesn't close

movement across interatrial septum

Ventricular septal defect (VSD)

overriding aorta straddles the VSD

Pulmonary vlave stenosis

Right ventricle hypertrophy

Tricuspid doesn't form

blood flows from atrial septal defect or foramen ovale to left heart through ventricular dect to the right ventricle to get to the lung

Mixes oxy and unoxy

Self-limiting vasulitis that can result in cardiac complications

leading cause of pediatric acquired heart disorders

uncomfortable breathing

air hunger

Hyperpnea

(Kussmaul respiration)

Reflex breathing

alternating periods of deep and shallow breathing

apnea followed by increased ventilation, again followed by apnea

Black Lung Disease

Fibrous tissue in lungs from inhaled dust particles

Acute lung injury in adults

Deposits of protein and fibrin precipitates

Collagen deposits

Causes right-sided cardiac hypertrophy

Cor Pulmonale

Right ventricular disease due to pulmonary hypertension

enlarged right ventricle

Acute lyringotracheobronchitis

Caused by RSV

Barking cough

Life-threatening emergency

caused by Haemophilus influenza type B

emergency airway and REDUCE INFLAMMATION

Hyaline Membrane disease

lack of surfactant

Pre-term infants

give surfactant

lung damage from neonatal chronic lung disease

premature birth, immature lungs

give oxygen and surfactant

Autosomal recessive

abnormally thick mucus

obstuct bronchioloes 

pound on back on downward incline

Respiratory syncytial virus (RSV)

causes necrosis

calcium, oxalates, phosphates

underlying disorders

flank pain radiating to groin area

can cause renal failure

interruption of nerve supply to bladder

Loss upper motor function (between cortex and sacrum)--loss of voluntary voiding 

Loss lower moter function (below sacrum)--lose voluntary and unvoluntary voiding

Group of symptoms from primary disease

secondary to glomerulonephritis

increased glomerular permeability

edema, hyperlipidemia, hypoalbuminemia

Elevated BUN and creatinine livels

pre-renal--shock, ischemia, etc.

Intrarenal--ischema, tubular necrosis, toxins

post-renal--obstruction, urethral strictures

Most common cause of acute renal failure in adults

Ischemia generates oxygen radicals and inflammatory mediators

loss of nephron mass

Uremia--decline of renal function and accumulation and retention of toxic wastes in blood

Causes acute renal failure in kids

Endothelial lining of glomerular arterioles become swollen and occluded with platelets and clots

RBC damaged and sequestered in spleen

Retrograde of urine into ureters

abnormal or ectopic insertion of ureter into bladder

Absence of menstruation for 3 or more cycles

pregnancy

Caused by disturbances in menstrual cycle not secondary diseases

failur to ovulate

estrogen proliferates endometrium, progesterone limits it

Follicles grow but never ovulate so they simply stay in ovary and grow

Anovulation caused enlarged, polycystic ovaries

leads to infertility

Infection/inflammation of vagins

STDs Candida albicans

Cervicitis

Inflammation of cervis

one or more STDs

Inflammation of skin of vulva and perianal area

Contact with irritants

Vaginal infection spreading to vulva

muscles of floor of uterus are torn and not repaired

descent of cervix or entire uterus into vaginal canal

Depressed Tc cells 

Ectopic tissues respond to hormonal stimulation

Vulvar Cancer 

Cervical Cancer

HPV infection

early sexual activity

multiple partners

Inflammation of urethra

STDs

insertion of foreign objects, trauma

Varicose veins of the penis

inflammation of vein in spermatic cord

Collection of fluid within tunica vaginalis

imbalance between secretion and reabsorption

Cyst between head of epididymis and testis

asymptomatic

Testis rotates in vascualr pedicle

interrupts blood supply

spontaneous or due to trauma

surgically repair within 6 hrs

Enlarged prostate

restricts urethra

remove hyperplasia tissue

Inflammation of the prostate

palpable lumps in breast

lumps fluctuate with mentrual cycle

painless, firm, solitary, well-circumscribed mobile mass of young adult

upper-outer quadrant

Subareolar ducts dilate and fill with debris

Inflames and may rupture

Benign

well delineated multiple cystic masses

usually involves skin

well circumscribed tumors within th educt

well differentiated cells

Fibrous, firm, glistening, gray-tan mass

70% of all breast cancer

> 3 cm

circumscribed and encapsulated

lateral half of breast

Associated with noninfiltrationg ductal carcimonma

infrequent metastasis

Hx of fibrocytic disease

upper quadrants

Paget disease

Eczema of areola

subareolar carcinoma

usually bilateral

>17 cm

localized

may rupture skin

rare metastasis

Treponema pallidum

No natural reservoir in enviornment

Sexual transmission

Primary--chancre, painless, if untreated will go to secondary

Secondary--Systemic dissemination, skin lesions up to 8 wks, rash on palms and soles, gray on mucous membranes

Latent--Silent infection, still carrier, lack symptoms

Tertiary--10-30 yrs later, gummas, neurosyphilis

Chlamydia trachomatis

most common

intracellular elementary body

give antibiotics

Genital warts

HPV

may cause cancers

1. Asymptomatic, about 1 year

2. clinical symptoms, infections reoccur

3. terminal, opportunistic diseases occur and bring death

accompanies illness, trauma, sepsis

most common ulcer to be hemorrhagic

bright red blood from rection

lower GI bleed

Dark tarry stools

large amount in upper GI

blood in minute auantities that is detected by microscopic or chemical means

chronic bleeding

Chronic inflammatory disease causes ulceratin of the colonic mucosa

Unknown cause, may be genetic

Increase risk colon cancer

Lots of firbrous tissue-decrease motility/contraction

Idiopathic

Increased T suppresser cells

Usually in ileocolon

Causes skip lesions

Prodromal--2 wks after exposure, highly contagious, fatigue, anorexia, malaise, nausea, etc.

Icteric--Yellow phase, painful swollen liver, jaundice

Recovery--jaundice resolution, 6-8 wks after exposure, symptoms diminsh, liver stays swollen/tender

esophagus ends in a puch or forms a connection with the trachea

aspiration, respiratory distress problems

Kwashiorkor

vs

Marasmus

severe protein deficiency

deficiency of all nutrients

1. Myosin heads hydrolyse ATP and become energized and reoriented

2. Myosin heads bind to actin forming cross bridges

3. Myosin heads rotate toward the center of the sarcomere (power stroke)

4. As myosin heads bind to ATP the cross bridges detach from actin

1. Fracture Hematoma

2. Callus Formation

3. Remodeling

Temporary displacement of two bones

Loss of contact between articular cartilage

Inflammation of a tendon where it attaches to a bone

tennis elbow

Inflammation of muscular tissue with subsequent calcification of muscle tissue

Impact injury to muscle causes release of Ca

Unknown cause

Excessive reabsoprtion of spongy bone and accelerated formation of softened bone

Bone infection

Open wound most common cause

Could be hematogenous infection

38% of bone tumors

adolescents and young adults

Contain masses of osteoid and callus

Located in metaphyses

Middle-aged/older adults

Infiltrates trabeculae in spongy bone; metaphyses or diaphysis

Amputation

Tumor of middle-aged adults

Metaphyses of femur or tibia

fibrous mass of collagen

Originate from myelogenous tissue

Extensive bone reabsorption

Slow, relentless growth

Ankylosis--immobility of a joint

systemic

immune inflammatory disease

Ligaments, tendons, joint capsule

Scar tissue ossifies and calcifies; joint fuses

Metabolic disorder, disrupts body's control of uric acid

Uric acid crystalize and deposits in connective tissues

Triggers inflammatory response

Creates a tophi (urate crystal granuloma)

Inflammatory joint disease

Autoimmune damage to connective tissue

Muscle fiber shortening without contracting

Failure of sarcoplasmic reticulum

Chronic musculoskeletal syndrome

Increased sensitivity to touch, no inflammation

Studies unclear

Reduction in muscle and normal zsize of muscle cells due to prolonged inactivity

bed rest, trauma, casts

Malignant tumor of striated muscle 

Arises from embryonal cells that differentiate into striated muscle

"Brittle Bone Disease"

Defect in collagen production

Interrupted blood supply to the femoral head

Deformation due to ischemia 

Childrom from 3-10 yrs

Trendelenberg gait

Dilated superficial blood vessels

Fine, irregular red lines produced by capillary dilation

<0.5 cm

Circumscribed areas of blood 

>0.5 cm

Lesions <1 cm

Caused iby infiltration or hyperplasia of dermis

Lesions with large surface area

> 1 cm

Fluid-filled, thin-walled lesion

Bulla >.5 cm

transient lesion with well-defined and changing borders

Hives and insect bites

Plugged hair follicle

Acne, blackhead, whitehead

Encapsulated mass of dermis or subQ layers

solid or fluid filled

Type IV Hypersensitivity Reaction

Allergen comes in contact with skin, binds to carrier protein, formas a sensitizing antigen

Type I Hypersensitivity

Activation of mast cells, eosinophils, T lymphs

Red, weeping crusts, lichenification

Inflammaitn of the skin involving the scalp, eyebros, eyelids, and ear canals

Seborrhea--overactive sebaceous gland

Acute, recurring disorder of the skin and mucous membranes

Allergic or toxic reaction to drugs/microorganisms

"Bulls-eye" lesion

Infection from folliculitis spreading into the dermis

Boil

Superficial Group A step infection of the skin

superficial cellulites

Staph or Strep infection of the skin

Purulent vesicles rupture and crust

Type I Hypersensitivity

Histamine release causes endothelial cells of skin to contract

Sclerosis of skin, progress to internal organs

Lesions exhibit massive deposits of collagen with inflammation

Failure of heart to pump

Myocardail ishemia, MI, CHF

Insufficient intravascular fluid volume

Loss of blood, trauma, surgery

Immune alterations

Type I Hypersensitivity leads to vasodilation, peripheral pooling, relative hypovolemia

Infectious processes

If diabetic-causes increase in glucose levels

Initiates and promotes vasodilations

Progressive dysfunction of 2 or more organ systems

Shock and sepsis most common cause

9%-anterior/posterior head and neck

9%-anterior/posterior each upper arm (18% both)

36% anterior/posterior of torso, including buttocks

9% anterior/posterior lower limb

1% for perineum

Epidermis

Milde pain, erythema, delayed blistering

Sensory maintained

Epidermis and dermis

Erythema, edema, rapid blistering

Loss of some skin function

Skin function and sensory lost

epidermis, dermis, subcutaneous

White, cherry red, black skin

Severe scarring

Related to total body surface are burned

20-40% adults, 8-25% children

Systemic capillary system permeability increases

Infuse more fluid than is being lost