Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
110 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What is the first line of defense ?
|
Mechanical & chemical barriers
|
|
|
|
What is the second line of defense ?
|
Inflamation response & Phagocitosis
|
|
|
|
What is the third line of defense ?
|
Specific immune responses & Natural killer cells
|
|
|
|
What defines Symbiosis ?
|
Symbiosis benefits the host with no harm to the microorganism
|
|
|
|
What defines Commensalism ?
|
Commensalism benefits only the microorganism with no harm to the host
|
|
|
|
What defines Mutualism ?
|
In Mutualism both organism benefit
|
|
|
|
What defines pathogencity?
|
Pathogencity benefits the microorganism and harms the host human
|
|
|
|
Nosocomial Infections
|
Are a result of treatment in a hospital or a healthcare service unit.
The most common are: infections of urinary tract, surgical site and pneumonias |
Considered nosocomial infections if they appear hours after admission or within days after discharge
|
|
|
Modes of infection transmission
portal of exit / entry |
Contact
Droplet Airborne Common Vehicle Vectorborne |
|
|
|
Contact Transmission
|
most frequent mode of transmission of nosocomial inf.
- Direct: body - body contact - Indirect: object-host |
|
|
|
Airborne Transmission
|
- Microorg. remain suspended in the air for long periods of time
- requires special ventilation in hospital - TB, legionella |
|
|
|
Droplet Transmission
|
- Droplets do not stay suspended in the air.
- Meningitis, streptococcal pneumonia |
|
|
|
Common Vehicle Transmission
|
Transmitted by contaminated items (food, water, needles)
|
|
|
|
Vectorborne Transmission
|
- mosquitos, flies, rats
- less common in USA |
|
|
|
Clinical Manifestation of infectious disease
|
- fever
- caused by a pathogen or by its products |
|
|
|
Examples of viruses
|
measles, hep B, pneumonia
|
|
|
|
Examples of bacteria
|
Staph, cholera, streptococcal pneumonia
|
|
|
|
Examples of chlamydia / rickettsiae
|
trachoma / Rocky mountain spotted fever
|
|
|
|
Examples of mycoplasma
|
Mycoplasma pneumonia
|
|
|
|
Examples of mycobacterium
|
tuberculosis
|
|
|
|
Examples of fungi
|
tinea pedis (athlet's foot)
thrush (candida) histoplasmosis |
|
|
|
Examples of protozoa
|
giardiasis, malaria
|
|
|
|
Examples of helminths
|
trichinosis, filariasis
|
|
|
|
MRSA
|
- S aureus strains that do not respond to some antibiotics (all penicilins + others)
- risk factors; long hospitalization, long term antibiotic treatment - 25% people are carriers |
|
|
|
What is primary mode of transmission for MRSA?
|
Inapropiate hygiene of hands
|
|
|
|
Types of MRSA
|
- HA-MRSA: health care associated MRSA
- CA-MRSA: community associated MRSA (athlets, children) |
|
|
|
Immunodeficiency
|
Failure of immune / inflamatory response to normaly function
|
|
|
|
Types of Immunodeficiency
|
- Primary - congenital (diferencitation and maturation of B and T cells)
- Secondary - much more common than primary |
|
|
|
Evaluation of Immunity
|
- CBC (complete blood count) with subpopulation of lymphocytes
- Immunoglobulins (quantity and subpopulations) - Amount of total complement protein |
|
|
|
Tx for Immunodeficiencies
|
- gamma globulin therapy (temporary replaces mmissing antibodies)
- transplant of bone marrow, umbilical cord cell..etc |
|
|
|
Secondary Immunodeficiencies
|
- Pshychologic stress
- Dietary insuf. - Malignancies - Physical trauma - Iatrogenic (due to tx, chemo, radio) - Infections - AIDS (acquired immunodeficiency syndrome) |
|
|
|
AIDS
Acquired Immunodeficiency Syndrome |
- Human Immune deficiency virus (HIV) infects and distroys helper T cells
- HIV suppress immune response against itself & other pathogens |
|
|
|
T helper cells
|
- can not kill infected cells or pathogens
- Activate and direct other immune cells like: - B cell class switching, - cytotoxic T cells = killer cells) - have CD4 protein on the surface |
|
|
|
Transmission of HIV
|
Major payh ways:
- blood transfussion - sexual contact - maternal feeding (infant) |
|
|
|
What type of virus is HIV ?
|
Retrovirus. Virus replicates in the host via the enzyme reverse transcriptase to produce DNA from RNA.
DNA is incorporated into host's genome by integrase enzyme |
|
|
|
HIV clinical manifestation
|
- Accute ilness (3-6 weeks post exposure, lasting 2-3 weeks)
- Latent period: no symptoms, pxs carry virus - Early stage: mild symp. generalized lymphadenopathy (may last 10 y) - AIDS |
|
|
|
AIDS clinical manifestations
|
- CD4 lympocytes count bellow 200cells/mm3
- presence of opportunistic infections/disease like: diff infections, GI disorders, CN involvement, neoplasia - wasting syndrome: extreme weight loss and muscle mass loss |
|
|
|
HIV drug therapy -
Protease Inhibitor |
- inhibit the viral enzime protease
- involved in the last step before the virus is able to reproduce - atanavir, darunavir, ritonavir - navir (generic protease inhib. drugs) |
|
|
|
HIV drug therapy -
Nucleoside reverse transcriptase inhibitor drugs |
- inhibit reverse transcriptase
- abacavir, retrovir - vir (antiviral drugs) |
|
|
|
HIV drug therapy - HAAT
|
Highly Active antiretroviral therapy HAAT is a combo of 2 drugs to prevent development of resistant strains
|
|
|
|
What is the composition of blood?
|
55% plasma
45% formed elements |
|
|
|
What is the composition of plasma?
|
92% water
6% proteins 2% other |
|
|
|
Where are produced the plasma proteins?
|
Most of them are produced in the liver, except of antibodies which are produced in the lymph nodes and other lymph tissues.
|
|
|
|
Plasma properties
|
60% Albumin
38% Globullins 4% Fibrinogen |
|
|
|
cellular components of blood
|
Erythrocytes (RBC)
- 4-7 mil/mm3, - life span:80 - 120 days Leukocytes (WBC) - 5 -10 thous/mm3, - life span: days to years Platelets (throbocytes)) - 150- 400 thous/mm3 - life span: 8-11days |
|
|
|
RBC properties
|
- 48-42% of blood volume
- erythropoiesis production in bone marrow in the presence of erythropoietin (hormone in kidney), iron, B12, B9, protein -hundreds mol of hemoglobin carry O2 |
|
|
|
Leukocytes properties
|
- Produced in bone marrow,
- Differenciated into granulocites (Neutrophils-55%, eosinophils and basophils) and nongranulocytes (lymphocytes and monocytes) |
|
|
|
Platelets properties
|
- 1/3 in splenic reservoir
- most circulate |
|
|
|
Stages of hemostasis
|
1. Vasoconstriction - vasospasm
2. Platelet plug formation 3. Activation of clotting cascade 4. Formation of a blood clot 5. Clot retraction and disolution |
|
|
|
Production of clotting factors
|
- family of proteins that circulate in blood in inactive form
- mainly synthesis by liver - vitamin K required |
|
|
|
Vasoconstriction
|
- response to direct injury of tunica media
- thromboaxane and serotonin enhance vasospasm |
|
|
|
development of platelets
|
platelets develop from megakaryocytes by endomitosis (they undergo DNA replication but not cell division; the cell do not divide into 2 daughter cells)
|
|
|
|
Coagulation
|
Convert soluble factors into insoluble network of fiber strands.
3 phases: 1. formation of PTA (prothrombin activator) 2. PTA + prothrombin = thrombin 3. formation of fibrin mesh |
|
|
|
Intrinsic Pathway
|
Occurs more frecquent, is initiated by surface contact when platelets reach damaged vessel
|
|
|
|
Extrinsic Pathway
|
Occurs more rapidly, is initiated by tissue factor TF, as a result of trauma to vessel tissue or external tissues
|
|
|
|
Which path occurs more frecquently ?
|
Intrisic
|
|
|
|
Which path occurs more quickly?
|
Extrinsic
|
|
|
|
Phase 1 of coagulation: PTA
|
- two ways to PTA: intinsic and extrinsic
- Tissue factor 3 TF3 pivotal role in both pathways |
|
|
|
Phase 2 of coagulation
|
PTA catalyzes a plasma protein (prothrombin) into an enzime called thrombin
|
|
|
|
Phase 3 of coagulation
|
Thrombin catalyse the conversion of soluble fibrinogen into insoluble fibrin
|
|
|
|
Clot retraction
|
Fibrin contracts, clot is compacted, rupture edges are drawn closer to each other.
Platelet growth factor stimulates the wall rebuild |
|
|
|
Clot removal
Fibrinolysis |
Endothelial cells secrete tPA (plasminogen activator)
Plasminogen +tPA = plasmin |
|
|
|
PTA
|
- prothrombin activator
- starts the clotting process - converts protrombin into trombin |
|
|
|
tPA
|
- tissue plasminogen activator
- gets ready of the clot - converts plasminogen into plasmin |
|
|
|
Thrombin
|
Converts fibrinogen into fibrin
|
|
|
|
What factors can limit the clot formation?
|
1. by blood flow
2. circulating anticoagulant factors -Antithrombin III (enhanced by heparin): - Protein C and protein S |
|
|
|
What does heparin do ?
|
- do not disolve clots
- prevents further clotting - activates antithrombin III |
|
|
|
What is the reusult of a Protein C and protein S deficiency ?
|
More blood clottes are formed
|
|
|
|
Types of hemorrhages
|
1. arterial : spurting, pulsatile
2. venous: steady flow 3. capillary |
|
|
|
Capillary hemorhages
|
petechia - minute
purpura - slightly larger ecchymoses - large 1-2cm |
|
|
|
What are the platelet disorders?
|
- Thrombocytopenia
- Thrombocythemia - Alterations of platelet functions |
|
|
|
Thrombocytopenia
|
Platelet deficiency due to:
- decreased production (drug rx, autoimune disease B12 deficiency & folate, cancer, cho, radiation) - increased consumption (heparin induced, spleen issues) - bleeding from mucous membranes - blood do not clot - can be fatal |
|
|
|
Thrombocythemia
|
- aka thrombocytosis
- high no of platelets in blood - splenectomy (secondary condition but expected) |
|
|
|
Alterations of platelet functions
|
- normal pl. count but increased bleeding time
- drugs: ASA (aspirin) - systemic -liver disease - hemat diseases, leukimya, mieloma |
|
|
|
Name the clases of anticoagulants
|
1. Antiplatelets: aspirin, thienopyridines, combo platelet aggregation inhibitor
2. Heparin & LMWH 3. Coumadin |
|
|
|
Aspirin
|
- inhibits thromboaxane 2 production
- weak antiplatelet agent dosage: baby 81mg, regular 325 mg - usualy by itself, not associated with other anticoagulants - side effects involve GI system |
|
|
|
thienopyridines
|
- most common Plavix
- 75 mg/day for 1 year or lifetime |
|
|
|
combo platelet aggregation inhibitor
|
- given oraly, combination of 2 drugs (ADP and thromboxyn)
|
|
|
|
LMWH
|
- smaller molecule, more of the dose is absorbed and therapeutic
- given subq - Lovenox the most common |
|
|
|
Heparin
|
- inhibits clotting factor X
- activates antithrombin III - large molecule not easily absorbed - given subQ, IV, not orally, in hospital - routinely platelet count because of induced thrombocytopenia |
|
|
|
Heparin & LMWH (lovenox)
|
- anticoagulants of choice because of rapid effect, onset is immediate when IV
- on long term they are followed by ASA and Coumadin |
|
|
|
Coumadin (Warfarin)
|
- rat poisoning
- inhibits vitamin K synthesis - orraly, dosage changed almost weekly - not for pregnant px - dietary consumption of vit K can countereffect of Coumadin - Advantages: oral form, long term therapy - Disadv: may take days to onset, must be discontinued before a surgery, px must follow directions strict - dosage depending on the protime(how quick the blood coagul) |
|
|
|
PT
|
- normal values are 11-13sec
- for a px with valve replacem, can be adjusted to 18 sec |
|
|
|
INR
|
1.o = no anticoagulant effct
2.0 - 3.0 normal values 5.0 = clinically dangerous |
|
|
|
Factors affecting INR
|
- alcohool and ASA increase PT (both are anticoagulants)
- increase in vitamin K intake = decrease of INR |
|
|
|
Px in the doctor's office with INR=6.0 (too high). What can the doctor do ?
|
Give px a vit K injection
|
|
|
|
Thrombolytic therapy
|
- bind to fibrin strands in the clot and convert plasminogen into plasmin
- can be only effective if they are used hours after the onset of thrombosis |
|
|
|
What drugs are used in Thrombolytic therapy?
|
- streptokinase (cheep but tx can not be used within 6 months, allergic rx)
- urokinase (not in USA, from fetal renal tissue) - tPA (no allergic rx, cost 10 times more than streptochinase) |
|
|
|
Coagulation Disorders
|
1. defects of clotting factors (hemophilia)
2. hemostasis impairement (vitamin K deficiency, impaired liver fx) 3. Thromboembolic disorders (clots are debveloped spontaneously) |
|
|
|
Arterial thrombus
|
Is composed of mostly platelet aggregates with fibrin strands (high blood flow conditions)
- source of cerebrovascular accidents |
|
|
|
Venous thrombus
|
Is composed mostly of RBC with fibrin strands and a few platletes (low blood flow conditions)
- majority source of pulmonary embolism |
|
|
|
What is characteristic for thromboembolic disorders ?
|
Virchow's triad
1. vascular wall injury = venous stasis 2. Circulatory stasis = endothelial or tissue damage 3. Hypercoagulability state |
|
|
|
Px is in atrial fibrilation, on cumin treatment. Is it possible to have a blood clot ?
|
Yes, he can, he can be in hypercoagulability state (pregnancy, cancer) and coumadin will be override by the px state.
|
|
|
|
Virchow's triad - phase 1
|
- long trips or bedresting
cloting factors aren't washed away with blood flow - trauma, surgery, venipuncture, chemical irritation - heart valve disease / replacement - atheriosclerosis - accute myocardial infarction - indwelling catheters |
|
|
|
Virchow's triad - phase 2
|
- endothelial roughening atherisclerosis
- endothelial damage - atrial fibrilation - left ventricular disfunction - immobility or paralisis - venous insuficiency - venous obstruction from tumor, obesity or pregnancy |
|
|
|
Virchow's triad - phase 3
|
- increased concentration of cloting factors (pregnancy, hormone therapy, chemo)
- decreased antithrombotic elements (deficiency of Antithr. III, protein C and S) - decrease synthesis of tPA (more likely to clott) |
|
|
|
Px comes in for leg circulation evaluation. On Coumadin treatment.
Can we find clottes ? |
Yes, that does not mean that he will not build clotts again
|
|
|
|
Thrombocytosis can be defined as:
- normal thrombocytes count - high thrombocytes count - low thrombocytes count - trombocytopenia |
high thrombocytes count
|
|
|
|
Hypercoagulability includes;
- protein C and S deficiency - increased antithrombin III - increased synthesis of tPA - all of above |
protein C and S deficiency
|
|
|
|
&0 old male dies in emergency room after autopsy is discovered polycythemia vera. The cause of death is probably;
- cerebral trombosis - infection sepsis - acute renal failure |
cerebral trombosis
|
|
|
|
Hepatitis and liver cirrhosis results in thrombolytic hemostasis disorders.
True / False |
False
produce less clots |
|
|
|
Goal of intrinsic and extrinsic cascade is to produce:
- prothrombin activator - plasmin - thrombin |
prothrombin activator
|
|
|
|
The most common cause of deep vein thrombosis is:
- venous stasis - hypercoagulability |
venous stasis
|
|
|
|
30 years old diagnosed with HIV. Which of the following Tx would be the most effective?
- high active retroviral tx - reverse transcriptase inhibitors - protease inhibitors |
- high active retroviral tx
|
|
|
|
Px in atrial fibrilation are more likely to develop clots from secondary hemostatic disorders?
True / False |
False
|
|
|
|
Lovenox is preferential to Coumadin because of lower risk of birth defects
True / False |
True
|
|
|
|
2 most common indications for emergency thrombolytic use is deep vein thrombosis and stroke.
True / False |
False
|
|
|
|
tPA has a high potential for antigenic response requiring careful administration
True / False |
False
|
|
|
|
The minority of pulmonary embolic events come from the lower extremities.
True / False |
False
a majority |
|
|
|
What is the most potent activator of platelets ?
- collagen exposure - platelet factors - none of the above - both of the above |
- collagen exposure
|
|
