Path I Final Material Flashcards
Hemostasis
the process of stopping blood loss
Coagulation
principle mechanism of hemostasis
fibrin forms a net and traps the formed elements in blood forming a blood clot
blood clot
mesh of protein filaments that trap bloods formed elements to forma a red, gelatinous mass
fibrin threads
threads that hold the blood cells together and they seal the wound to prevent losing blood
Clotting factors
present in the blood at all times in their inactive form
become activated upon injury through the intrinsic and extrinsic pathways
Where are clotting factors produced
in the liver
Which vitamin is required to produce clotting factors
vitamin k
CF I
fibrinogen
CF II
prothrombin
CF V
preaccelerin
CF VII
proconvertin
CF VIII
antihemophilic factor
CF IX
christmas factor
CF X
stuart-prower factor
CF XII
Hageman Factor
CF XIII
fibrin-stabilizing factor
What activates the extrinsic pathway for blood clotting?
damage to cells within blood vessels and outside the vessels
what is released from injured cells to activate the extrinsic pathway for blood clotting?
Tissue factor aka tissue thromboplastin
What does tissue factor activate?
proconvertin, which then activates stuart-prower factor
What is required to cause coagulation?
Fibrin which is the active form of fibrinogen
What activates the intrinsic pathway for blood clotting?
exposure of collagen fibers of subendothelial cells of blood vessels to blood flow
What is the only place the intrinsic pathway can be activated?
inside an injured blood vessel
What clotting factor do exposed collagen fibers activate?
Hageman factor which activates plasma thromboplastin antecedent (CF XI) which activates christmas factor which activates stuart-prower factor
Both the extrinsic and intrinsic factors result in activation of which clotting factor?
CF X aka stuart prower factor
What does CF X activate?
the clotting cascade
prothrombin is activated to thrombin
thrombin activates fibrinogen to fibrin
What ion is a necessary component of coagulation?
Ca++
patients with severe blood loss are given calcium chloride injections to help with blood clotting
Platelet plug
the result of platelet activation
mechanically blocks the damaged blood vessel
Where does platelet activation occur?
inside a damaged blood vessel
What causes platelet activation?
exposure of collagen fibers of subendothelial cells of blood vessels to blood flow
von Willebrand factor
circulating in the blood in its inactive form
becomes activated when it exposed to collagen fibers
attaches to platelets and forms a single layer of platelets over site of exposed collagen
What does von Willebrand factor do to platelets?
causes activation, allowing a second layer of platelets to attach
causes degranulation
What do platelets release when they undergo degranulation?
ADP- promotes platelet activation
Thromboxane A2 (TxA2)- vasoconstriction
Growth factors- promote wound healing, fibroblast chemotaxis
Anticoagulation System
competes with coagulation
prevents excess or uncontrolled blood clotting
Three components of the anticoagulation system
hemodynamics
endothelial mediation
fibrinolytic system
hemodynamics
slow blood flow is important for coagulation otherwise activated CF’s will get washed out and a clot cannot be formed
Endothelial mediation
when a platelet plug is formed, surrounding uninjured endothelial cells release prostacyclin (PGI2) which prevents excess platelet aggregation
Fibrinolytic system
CF12 also activates tissue plasminogen activator which converts plasminogen to plasmin, resulting in degradation of activated CF’s
Tissue Plasminogen activator
converts plasminogen to plasmin, resulting in degradation of acvtivated CF’s
Petechiae
pinpoint sized hemorrhages
can be caused by scurvy
What nutritional deficiency causes petechiae?
Scurvy
vitamin C deficiency
purpura
“bruising” smaller than 2cm but larger than petechiae
Ecchymoses
bruises >2cm
can be caused by cushings or prolonged steroid use
Prolonged use of what drug can mimic the symptoms of Cushing’s disease?
steroids
What disease causes widespread ecchymoses
Cushing’s
Cushing’s Syndrome
overproduction of corticosteroids from the adrenal cortex leads to brittle blood vessels, severe osteoporosis, obesity, diabetes, and high BP
Thrombocytopenia
<140,000 platelets in the blood leads to an increased risk of hemorrhage
petechiae and purpura are typical
What is the normal amount of platelets found in blood?
250,000-300,000
Von Willebrand’s Disease
genetic, autosomal
Patients with this disease do not produce von Willebrand factor
What are some signs of von Willebrand’s disease
hemorrhagic gastroduodenitis- periodic leakage of blood from mucosa of the GI tract
menorrhagia-increased amount of blood lost during menstruation
hemorrhagic gastroduodenitis
periodic leakage of blood from mucosa of the GI tract
leads to black stool
menorrhagia
increased amount of blood lost during menstruation
metrorrhagia
serious disorder, usually manifested by uterine cancer
bleeding between periods
hemophilia
nonproduction of certain clotting factors
genetic disorder, x chromosome linked
small trauma can lead to severe blood loss
Hemophilia A
nonproduction of CF VIII
Hemophilia B
aka Christmas disease
nonproduction of CF IX
Hemoarthritis
common complication of hemophilia
trauma leads to blood in the joint spaces
iron from the heme destroys the joint cartilage
blood must be removed from the joint space to prevent degeration
Hemodynamic Disorders
disorders that arise from interruptions in normal blood flow
Thrombosis
thrombus formation
platelet activation and aggregation without the threat of blood loss or vascular damage
Thrombus
always originates from the vascular wall and always maintains point of contact with the vascular wall through von Wilebrand factor, only forms WITHIN the blood vessel
Characteristics of a thrombus in an artery
dense and strong
firm and small
Characteristics of a thrombus in a vein
loose and weak
loose and large
Lines of Zahn
a special type of thrombus characterized by visible and microscopic laminations produced by alternating layers of pale and dark
what comprises the pale layer seen with lines of zahn?
platelets and fibrin
what comprises the dark layer seen with lines of zahn?
red blood cells
Where would you expect to find a thrombus with lines of zahn
the heart or aorta (arch region)
Endothelial Damage
predisposing factor to thrombosis
stretching of endothelial cells from the inner surface of blood vessel exposes collagen fibers and thrombus is formed
Hypertension
increase resistance of the vascular wall to the fluid
seriousl factor that promotes endothelial damage
Hemodynamic stress
in the arteries
normal wear and tear results in arteriosclerosis
what accelerates arteriosclerosis
hypertension
Artherosclerosis
specific changes, such as plaque formation, in the arterial walls that leads to enothelial damage in the arteries
iatrogenic thrombosis
rare, caused by medical care
i.e. iv lines or injections into veins damages the endothelia and results in thrombus formation
Causes of reduced blood flow
cardiac damage
increased blood viscosity
physical inactivity
varicose veins
Reduction of rate of blood flow leads to
disruption in axial blood flow, where platelets flow closer to the vessel wall leading to platelets being more easily activated due to their proximity to the vessel wall
Cardiac Damage
reduces the heart’s pumping ability leading to a reduction in blood flow
Myocardial Infarction
most common infarction
coagulative necrosis followed by replacement with connective tissue
dead heart tissue scars over with fibrotic tissue which is not contractile, leading to a decreased cardiac output near the fibrotic tissue
mural thrombus
thrombi formed in the chambers of the heart
Rheumatic Heart disease
mitral stenosis slows flood flow in the left atrium increasing the chance of thrombus formation which can kill the patient
What are two conditions that can lead to hyperviscosity of the blood
psoriatic arthritis
polycytemia
Polycytemia
increased red blood cell count leads to increased friction against the vascular wall
What can cause polycytemia
living at high altitudes, emphysema
erythemia
a type of leukemia
blood flows very slowly due to increased RBC count
patients could die due to thromboses
Normal red blood cell count
3-5 million/ cubic mm
What does physical inactivity predispose a patient to?
thrombus in the venous system, especially the lower legs
What is required to return blood to the heart from the lower extremities?
muscle contraction
Varicose veins
tortuosity of the veins prevents closure of the valves as the walls of the veins separate
Turbulence
disruption of laminar blood flow
what causes turbulence in blood vessels?
narrowed portion of the lumen
expanded lumen, aneurysm
twists and turns (varicose veins)
hypercoagulation
increased ability of the blood to coagulate
what causes hypercoagulation?
extensive burns certain kidney diseases heart failure widespread metastatic tumor growth birth control pills
sequela
the pathological consequences of an eent
Sequelae of thrombosis (6)
resolution organization recanalization propagation infarction Embolism
Resolution
thrombus disappears due to high fibrinolytic function in the blood, therefore the least dangerous but also a high chance of developing another thrombus (transient ischemic attack)
Organization
phagocytic digestion of the thrombus 2-3 days after it forms, replaces by connective tissue
recanalization
reorganization leads to formations of canals within the thrombus
endothelial cells line the canals
Propagation
enlargement of the thromus in areas open to clotting factors and their activation
usually occurs in veins where flow is slow and there are bifurcations
Infarction
the process in which an infarct is formed
infarct
region of necrosis caused by oxygen deficiency
White infarct
develops in tissues that have 1 blood vessel supply ie the heart
red infarct
when a tissue is supplies by more than one blood vessel ie lungs
Ischemic stroke
most common area for stroke
liquefactive necrosis with cavity formation
gliosis
the process of repairing the CNS via neuroglia in the brain
does not shrink which is a huge advantage for the brain
what is the mechanism of infarction
thrombosis
What is the most common factor that results in infarction
arthrosclerosis
vasculitis
a factor leading to infarction
inflammation of the vessel wall due to autoimmune disease
all five components of inflammation are involved and leads to decreased lumen size and ischemia
giant cell arteritis
in the superficial temporal artery
aka hortons disease
symptoms include headache, visibile tender arteries, fever, weakness, temporary loss of vision
what often accompanies temporal arteritis
polymyalgia rheumatic- pain in the proximal regions of hip and shoulder muscles
opthalmic arteritis
temporary loss of vision
permanent if left untreated
paraesophageal hernia
stomach protrudes through diaphragm into thorax
diaphragmatic contractions occlude veins leading to infarction and gangrene
Sheehan’s syndrome
aka postpartum syndrome
anterior pituitary hypertrophies during pregnancy and if hemorrhage occurs within the uterus, the body responds by vasoconstriction in the whole body leading to necrosis of the anterior pituitary which only has a venous blood supply
Factors affecting infarction
tissue vulnerability
pattern of vascular supple
oxygen delivering capacity of the blood
rate of occlusion development
anastomosis
union of two or more artery branches
Embolism
sudden occlusion of blood vessels by an embolus
embolus
an abnormal mass moving through the bloodstream
thromboembolism
most common type of embolism
piece of thrombus breaks off
Fat embolism
from long bone fractures
can cross capillaries and travel in reverse direction to the brain causing purpuric brain hemorrhage
Air embolism
at least 300 mL
gas within the vessels would increase pressure and block fluid flow
air lock
pathology in which air embolism blocks blood flow
bends
aka caisson disease or divers disease
elevation changes and canges in concentration of nitrogen in blood due to pressure change
pt right side up so they can breathe out the gas
Who named vitamins?
Kazimerz Funk- polish biochemist
december 1913
Who discovered the first vitamin?
Elmer McCollum
discovered vitamin A
june 1913, Kansas city university
Water soluble vitamins
B, C
Fat soluble vitamins
ADEK
Vitamin B1 is also known as
Thiamine
Function of B1
maintains neural membranes and nerve conductions, especially in peripheral nerves
prevents development of cancer
What is the most important source of B1?
the husks of grains
refined grains lose B1
What demographic is more likely to be deficient in B1
Alcoholics
women in their first trimester
fast-growing teens
Why are alcoholics likely to be B1 deficient?
alcohol competes with b1 in neural functions and in biochemical reaction
Beriberi
vitamin B1 deficiency
severe nervous system disorder
discovered by Christiaan Eijkman
Dry Beriberi
Vitamin B1 deficiency
effects the nervous system
characterized by non-specific peripheral polyneuropathy with myelin degeneration and disruption of all three neurological arcs
which neruological arcs are disrupted with dry beriberi
sensory
motor
reflex
maifestations of dry beriberi
wrist drop, foot drop, toe drop
paresthesia, numbness, loss of reflexes
Wet beriberi
Vitamin B1 deficiency
heart
characterized by damage to the cardiovascular system
manifestation of wet beriberi
enlargement of the heart with thinning of the muscle wall (flabby myocardium)
peripheral vasodilation
peripheral pitting edema
cardiac failure
Wernicke encephalopathy
Vitamin B1 deficiency
Affects mamillary bodies in the brain leading to atrophy
characterized by psychological problems
Psychological problems seen with Wernicke’s encephalopathy
Global confusion apathy listlessness disorientation opthalmoplegia
Opthalmoplegia
seen in Wernicke’s encephalopathy
paralysis of one or more eye muscles as a result of deep damage of the CNS resulting in irregular eye movements, not simultaneous
patient is close to death when this is seen
Korsakoff’s psychosis
Vitamin B1 deficiency three manifestations: anterograde amnesia- loss of memory of evens occurring after the cause of amnesia inability to acquire new inflammation confabulation-excessive talking
Vitamin B2
Riboflavin
ariboflavinosis
riboflavin deficiency
does not effect nervous system
What population usually experiences B2 deficiency
those with chronic debilitating disease, renal and oncologic disease
Symptoms of ariboflavinosis
cheilosis
glossitis
superficial interstitial keratitis
dermatitis
cheilosis
symptom of ariboflavinosis
non-inflammatory
cracks in the corner of the mouth, may lead to infection and become cheilitis (which is a secondary infection)
Glossitis
symptom of ariboflavinosis
inflamed tongue, may lead to atrophy of the tissue and loss of taste
Superficial interstitial keratitis
symptom of ariboflavinosis
hardening of the cornea
cornea is usually avascular, with B2 deficiency a capillary net forms around and penetrates into the cornea resulting in inflammation and corneal ulceration
ulceration is painful due to nociceptors
fibrosis and loss of vision with healing
Dermatitis
inflammation seen in especially the nasolabial folds, behind the ears, and groin
Vitamin B3
niacin, nicotinic acid, nicotinamide
used as medicine for its vasodilation ability, can be produced from tryptophan via normal gut flora
B3 in plants
bound and cannot be absorbed when eaten
B3 leads to
decreased production of low density lipoproteins (LDL’s) which leads to prevention of arteriorsclerosis
Pellagra
vitamin B3 deficiency
The three D’s:
dermatitis- develops on skin exposed to the sun, casal’s necklace & glove-and-stocking lesions
diarrhea- atrophy of epithelial cells of interstitial mucosa with involvement of submucosal layer
dementia- degeneration of cortical neurons
Death
Vitamin B6
pyridoxine
found in all foods
thermolabile- a small amount of heat will destroy it
Which medications compete with B6 in biochemical reactions and can cause deficiency?
Ixoniazid- anti Tb, not used as frequently today
Estrogens- high production of hormone treatment
D-penicillamine- medicine used for the treatment of Wilson’s disease and systemic sclerosis
Symptoms of B6 deficiency
chelosis/chelitis glossitis peripheral polyneuropathy convulsions (especially in infants and children) increased sloughing of epithelial cells
Nidus
organic core of urinary stones
in the case of B6 deficiency- a clump of epithelial cells from the increase in epithelial sloughing.
Seborrheic dermatitis
seen with B6 deficiency
dandruff
scalp is scaly and greasy
Vitamin B12
cyanocobalamin
aka extrinsic factor of castle
not found in plants, animal are the only food source
cannot be absorbed directly, requires assistance via proteins
R-binder
secreted by the salivary glands
binds to B12 and carries it from the stomach to the duodenum
dissociates from B12 in the duodenum
Intrinsic factor of castle
aka intrinsic factor
produced and secreted by the parietal cells of the stomach
binds to B12(aka extrinsic factor of castle) when it reaches the duodenum and then moves to the ileum
ileum has receptors which bring the intrinsic/extrinsic factor complex into the blood where they dissociate from each other
Causes of B12 deficiency
diet autoimmune disorder (idiopathic)
Autoimmune chronic gastritis
cause of B12 deficiency
immune system produces parietal canalicular antibodies which destroy parietal calls in the stomach resulting in a lack of intrinsic factor
Blocking antibodies with B12 deficiency
autoimmune
bind to intrinsic factor, blocking the receptor for B12, and B12 cannot bind the intrinsic factor
Binding antibodies with B12 deficiency
autoimmune
bind to receptors for intrinsic factor in the ileum
B12 deficiency leads to:
pernicious anemia
demyelination
Pernicious anemia
aka malignant anemia
a type of megaloblastic anemia
decreased RBC’s decreased hemoglobin in RBC’s or both
lack of B12 interferes with normal hematopoeisis
Demyelination in B12 deficiency
irreversible myelin degeneration leading to a decreased rate of conduction
seen in posterior and lateral column tracts of the spinal cord, peripheral nerves, and DRG
What are some results of demyelination in B12 deficiency
numbness/tingling in the hands/feet
ataxia(abnormal gate due to spinocerebellar tract involvement)
paraplegia- subacute combined degeneration of the spinal cord, affects PNS and sometimes CNS (megaloblastic madness)
What is the correlation between severity of pernicious anemia and demyelination in B12 Deficiency?
No correlation
What may exacerbate nervous system pathologies with B12 deficiency
folic acid supplementation
What are two types of megaloblastic anemia?
Vitamin B12 deficient anemia- pernicious anemia
folic acid deficient anemia
Megaloblastic Anemia
folic acid or B12 deficiency results in large blood cells
Folic Acid’s role in hematopoeisis
donates carbon for DNA in red blood cells
B12’s role in hematopoeisis
activates tetrahydrafolate
Blastic cells
immature form of blood cells
normally only found in red bone marrow
will appear in circulation with megaloblastic anemia
Normoblast
normal cells
Megaloblast
mature, large cells
Macrocytes
large cells
Red Blood Cells in pernicious anemia
become macrocytes
too large to fit in the capillaries
cannot bend due to a rigid cell membrane, leading to decreased oxygen in the tissues
Neutrophil behavior in megaloblastic anemia
become hypersegmented
nuclei have more than 5 lobes
normal is 2-5
Pancytopenia
total decrease in the number of blood cells
Anemia
decreased RBC’s
Leukopenia
decreased WBC’s
Thrombocytopenia
decreased platelets
Does folic acid supplementation help in a B12 deficiency?
Yes by giving the patient carbon to make DNA, however the tetrahydrofolate can only be used once in the absence of B12
Does B12 supplementation help in a Folic acid deficiency
No
if a patient is showing anemia due to folic acid defiency, there is no tetrahydrofolate, so adding a THF activator will not do anything
Main differences between folic acid and B12 deficiency
folic acid deficiency causes cheilosis while B12 deficiency does not
B12 deficiency affects the nervous system and Folic acid does not ( with the exception of a developing fetus)
Methotrexate
leukemia drug
inhibits reductase, thereby interfering with hematopoeisis
purpose is to inhibit cancer cell replication, leads to suppressed immune system
Vitamin C
cannot be produced in the human body
found in many food sources
Function of Vitamin C
hydroxylation of procollagen to hydroxyproline (hydroxylation increases tensile strength of connective tissue )
synthesis of collagen peptides
powerful antioxidant
Vitamin C as an antioxidant
works with vitamin E, secures cell membranes from disruption with selenium
reduces oxidation of LDL’s
Scurvy
vitamin C deficiency
Symptoms of scurvy
bleeding diathesis
skeletal changes
delayed wound healing
Bleeding diathesis
development of petchie and ecchymosis
bleeding gums, abnormal gum, development, tooth loss
subperiosteal and retrobulbar hematomas
Subperiosteal hematomas
seen with scurvy
between bone and periosteum
leads to bleeding into joint space, iron destroys articular cartilage leading to hemarthrosis (secondary osteoarthritis)
Retrobulbar hematomas
blood behind the eyeball
increased pressure pushes the eye forward leading to loss of vision
Skeletal changes with scurvy
Bowed legs (in growing children)
tooth loss due to alveoli
protrusion of ribs and sternum (pigeon chest)
Excessive Vitamin C
enhances the immune system however could result in relapse of a cold as the body eliminates vitamin c when there is an excess
Vitamin A
discovered in 1913 by McCollum
has several forms
fat soluble, so must be eaten with fat to be absorbed
Retinol
Form of Vitamin A
storage and transport form
90% is stored in the liver and is enough for a six month supply for the body
Retinal
Form of Vitamin A
maintains normal vision in dim light
Retinoic Acid
Form of Vitamin A
important in determining the life span of epithelial cells
Carotinoids
natural precursors for retinal
Retinoids
synthetic/artificial
teratogenic
Function/Deficiency of Retinal
maintains normal vision in reduced light
important in the production of visual pigments in photoreceptors
deficiency results in night blindness aka chicken disease/blindness
Visual pigment for rods
rhodopsin
visual pigment for cones
iodopsin
Retinoic acid functions
potentiation and differentiation of specialized epithelial cells, mainly mucous secreting cells
enhances immunity to infections, particularly in children
Retinoic Acid Deficiency
Xeropthalmia, xerosis, sqpaumous metaplasia, follicular and papullar dermatosis, pulmonary infection, nidues formation
Bitot’s Spots
due to retinoic acid deficiency
xerosis, sloughed epithelial cells of the conjunctiva form plaques close to the cornea
Nidus
a urinary tract obstruction with an organic core
formed as a result of increased epithelial sloughing due to Retinoic acid deficiency
Hypervitaminosis A
More common/dangerous with synthetic vitamin A use
Acute Hypervitaminosis A
signs/symptoms similar to that of a brain tumor/intracranial pressure
headache, nausea/vomiting, papilledema (swelling of the optic disc)
must rule out high BP
Chronic Hypervitaminosis A
Weight loss, nausea/vomiting, dry mucosa, bone/joint pain, hepatomegaly leading to liver fibrosis, DISH
Vitamin E
alpha tocopherol
a collective name
4 tocopherols and 4 tocotrienols
antioxidants that neutralize free radicals
functions in cell membrane maintenance in concert with vitamin c and selenium
Which types of cell membrane are most vulnerable to vitamin A deficiency
RBC’s
Neurons
Vitamin A deficiency
nervous system pathology- axon degeneration in the posterior column of the spinal cord, loss of nerve cells in the DRG
myelin degeneration of sensory axons, degenerative changes in the spinocerebellar tract
symptoms of spinocerebellar tract degeneration
absent tendon reflexes ataxia dysarthria loss of position and vibration sense loss of pain sensation
When does RBC pathology with vitamin E deficiency cause anemia?
in premature infants whose RBC’s are more susceptible to destruction
Hypervitaminosis E
Decreased coagulative ability of blood due to interference with vitamin K, decreasing CF production
Vitamin E inhibits
atheroma formation in atherosclerosis through reducing oxidation of LDL’s
Vitamin K
coagulation of blood
produced by the gut flora
usually in any animal food products
Vitamin K is important in producing which clotting factors
Prothrombin (CF 2)
Proconvertin (CF 7)
Christmas Factor (CF 9)
Stuart-Prower Factor (CF 10)
Aside from clotting factors, vitamin K is also used to produce
Proteins
specifically osteocalcin
Osteocalcin
produced with vitamin K
a hormone that promotes calcification of bones
Vitamin K indirectly prevents
osteoporosis
Vitamin K deficiency leads to
bleeding diathesis
Hemorrhagic disease of newborns
could result in intracerebral hemorrhage (stroke)
Why are newborns particularly susceptible to vitamin k deficiency
their gut flora is not yet established
Symptoms of vitamin K deficiency
intracranial hemorrhage echimoses melena hematoma hematurea bleeding gums
iron deficiency
hypochromic microcytic anemia
iodone deficiency
hypothyroidism
goiter
selenium
Kashan’s disease
myopathy, congestive cordiomyopathy
copper
muscle weakness
hypopigmentation
zinc
acrodermatitis enteropathica anoerxia, diarrhea growth retardation hypogonadism, infertility impaired wound healing impaired night vision impaired immune function depressed mental function
PEM
protein energy malnutrition
range of clinical syndromes characterized by an inadequate dietary intake of proteins and calories to meet the body’s needs
somatic protein compartment
skeletal muscle
reserve, only taken when needed
Visceral protein compartment
predominantly in the liver
can determine of this compartment is used by checking the levels of albumin in the blood
80% of normal weight is
malnourished
60-80% of normal weight is
kwashiorkor
<60% of normal weight is
marasmus
Marasmus
lack of calories and protein
somatic compartment is used resulting in emaciated extremities
visceral protein compartment untouched (normal albumin levels)
Symptoms of Marasmus
emaciated extremities head disproportionately larger anemia multivitamin dificiency immunosuppressed
Type I Hypersensitivity
anaphylactic type, allergy
In Type I Hypersensitivity, there is a release of
vasoactive amines and other mediators from the mast cells or basophils and affecting vascular permeability and smooth muscles in various organs
Which immoglobulin is released with a type I Hypersensitivity
IgE
which cytokines are released with a type I Hypersensitivity
IL-4 and IL-5
Type II Hypersensitivity
antibody dependent
mediated by antibodies directed against target antigens on the surface of cells or other tissue components
Three subtypes of Type II Hypersensitivity
complement-dependent
Antibody-dependent cell mediated cytotoxicity
Antibody mediated cellular dysfunction
Type III Hypersensitivity
immune complex mediated
hypersensitivity is mediated by deposition of antigen-antibody complexes, followed by complement activation and accumulation pf PMN’s
Type IV Hypersensitivity
Cell-Mediated
Hypersensitivity reation, cell mediated response (no Ab/complements involved) with sensitized lymphocytes ultimately leads to cellular and tissue injury
Delayed Type Hypersensitivity
Type IV
antigen activates CD4 T cells resulting in the release of cytokines and recruitment of macrophages
T Cell Mediated cytotoxicity
Type IV
T8 cytotoxic cells
account for antiviral, antitumor and graft rejection
