Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

48 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
Know what the MHC/HLA complex refers to.
Major histocompatibility complex genes located on chromosome 6. The antigens they encode for are called human leukocyte antigens.
Which cells have MHC II proteins and how do they work?
Antigen presenting cells like monocytes, macrophages, Bcells, langerhans, dentritic cells and Helper TCs are coded for both MHC1 and 2. MHC2 cells can present foreign or self antigens to CD4+/HTCs.
Know the origin and major functions of T-cells and their progeny.
Tcells are made in the bone marrow and migrate to the thymus. 90% of these cells are deleted because they autoreact to our own antigens. CD4+ HTCs are one kind of t-lymphocyte. They are subdivided into Th1 which help Bcells with plasma cell differentiation, Th2 which secrete interleukins, and Th3 which suppress certain immune functions. Other Cells are CD8+, the cytotoxic Tcells. Which recognize MHC1 and carryout direct attacks on antigen bearing cells, kills viruses.
Th1, Th2, Th3
Know why the CD4+ cell is specifically targeted in HIV
If this cell is knocked out of the immune system the virus can better penetrate other immune cells. It attaches to the CD4+ cell receptor via gp 120 and through interaction with chemokine receptors gains entry to and destroys the cell.
Know the 5 major antibody classes and how one differs from the other
IgM: HTC signals Bcell to mount immune response after recognizing a foreign Ag. Bcells then secrete antibody IgM. ABO system, activates complement
IgG: When exposed a second time, memory cells are activated and IgG is secreted, present in B cells. Crosses placenta, both viruses and bacteria
IgA: secretory antibody secreted in breastmilk, tears, gut, and mucous membranes.
IgD: Found on surface of B cells, little else known
IgE: involved in allergies. IgE is secreted from basophils or mast cells
Know the difference between active and passive immunity.
Passive immunity occurs when a person is given antibodies like Rhogam or colusrum. Active immunity is slower whereby active or dead organisms are given to the host and their body must fabricate an immune response to it and have antibodies at the ready in case the person is ever exposed to it again.
Know how chronic diseases and congenital errors in Hb synthesis affect the RBC
Alpha and beta thalassemia and lead poisoning both lead to microcytic anemias classified as hgb synthesis errors. Thalassemias involve genetic mutations which cause abnormal and poorly functioning hgb molecules to be synthesized. Lead and other heavy metals can displace Fe from heme and lead to poorly functioning Hgb molecules.
Know the causes of macrocytic anemia.
These anemias are caused by B12 deficiencies because B12 halts cell expansion and without it the cells continue to expand. Aka megaloblastic anemia, neurological symptoms. Such deficiencies are caused by poor diet, malabsorption (pernicious anemia), liver disease, and parasitic disease. Folate deficiency also causes macrocytic anemia. Same causes except can also be induced by pregnancy. Myelodysplastic syndrome and thyroid disease can also cause MA.
Know the difference between polycythemia vera and erythrocyctosis.
Polycythemia vera is a neoplastic disorder causing increased viscosity of blood resulting from increased rbc production by bone marrow. Mgt = blood draws. Erythrocytosis is a physiologic response to increased O2 needs. Seen in pts at high altitudes, heavy smokers, and COPD. The body produces more RBCs becaues there is a demand for them.
Know what thrombocytopenia is, how it manifests itself, and what causes it.
Thrombocytopenia is a low platelet (<150,000) count and these pts have a decreased ability to form stable clots. These pts may present with mucosal surface bleeding, petechial rashes, large bruises, and intracranial bleeds. There are 3 causes: platelet destruction (autoimmune, HIT, splenomegaly) plt consumption (acute bleed, DIC, Thrombotic thrombocytopenic purpura), and bone marrow failure (viral illnesses and cancers).
Know what diseases that cause increase in neutrophils or lymphocytes are suggestive of.
Increased neutrophils suggests bacterial infection and increased lymphocytes suggests a viral infection
Know the final common pathway of coagulation and the 2 tests employed to assess them.
The final common pathway converges at factor X which catalyzes the conversion of prothrombin-->thrombin and fibrinogen-->fibrin. The PTT assesses the time to clot formation via the intrinsic system N=20-34sec. PT reflects the time via the extrinsic pathway N=10-13sec.
Know how heparin and warfarin work and the tests used to monitor their therapeutic effect.
Heparin up regulates the activity of antithrombin III and is monitored by PTT. Coumadin disrupts the synthesis of vitamin K dependent clotting factors (2,7,9,10) and is monitored by the Pt.
Understand what causes classic hemophilia A.
Hemophilia A is caused by a factor VIII deficiency. It can be detected by a prolonged PTT
Know the multiple actions of platelets in the maintenance of
Platelets release ADP and when they aggregate (stimulated by collagen)they release fibrinogen and thromboxane which causes vasoconstriction
Know the roles of von Willebrands factor in hemostasis.
VWF is a circulating protein synthesized by endothelial cells and megakaryocytes. It binds to exposed collagen and plts bind to it promoting platelet adhesion. It also stabilizes factor VIIIc, which is deficient in hemophiliacs. An absence of VWF is the most common bleeding disorder.
Appreciate the significance of Vitamin K in the coagulation process
(know what it does).
Most clotting factors are made in the liver and dependent on Vit K (obtained in diet). Inhibiting Vit K (coumadin) results in faulty clotting factors. Vit K is the antidote to coumadin OD.
know the significance of the PT, PTT, bleeding time, clot retraction tests.
Bleeding time is one way to assess plts. N=3-6mins. Clot retraction measures the ability of a blood clot to retract, dependent on proper platelet fxn and numbers. The PTT assesses the time to clot formation via the intrinsic system N=20-34sec. PT reflects the time via the extrinsic pathway N=10-13sec.
Plasminogen activators-what are they and how do they work
Converts plasminogen to plasmin which can lyse clots. Also involved: urokinase, steptokinase, and TPA.
Know what CPK and CP are
Creatine phosphate donates a phosphate to ADP which allows it to convert back to ATP. This process is mediated by the enzyme creatine phosphate kinase. Since this leaks from damaged cells the CPK in plasma is used as a measure of MIs.
Know the heart valves and what happens when they don't work
Valve b/w rt atrium and ventricle is the tricuspid. Blood then goes through the semilunar pulmonic valve to the lungs. It comes back via the pulmonary veins into the left atrium and through the mitral valve and out through aorta. When they fail to close properly S3 and S4 are heard, blood leaking around the valve.
What is autoregulation and who does it?
Coronary arteries are regulated by autonomic NS, autoregulation. They vasodilate/constrict autonomously. Cerebral and renal vessels do it too.
What are preload, afterload and ejection fractions?
Preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction.
Afterload is the pressure the muscle of the ventricles must overcome to push blood out of the cavity. afterload is the tension produced by a chamber of the heart in order to contract.
Ejection fraction is the percentage of volume in the ventricles that is expelled each beat, 50-55%
Know the important anatomical and function differences that exist
between fetal and adult CV systems.
The fetal circulation system differs in 2 main aspects. 1. oxygenated blood is received from the placenta therefore there is no need for blood to go to the lungs. Blood entering the fetal heart moves from the right atrium to the left atrium via foramen ovale. 2. The Ductus Ateriousus connects the pulmonary artery and aorta to shunt blood away from the lungs. This duct is kept open by prostaglandins produced by local hypoxia and closes after birth.
Starlings forces? Yes, what are they and how do they affect fluid
exchange across capillaries?
SF are those forces which influence bulk movement across capillary membranes. Proteins in the plasma exert a colloidal osmotic pressure which keeps fluids and lytes in the capillaries, a tissue turgor pressure also does this. These are opposed by interstitial oncotic pressure from proteins in the interstitium and hydrostatic pressure or blood pressure in the capillary. The hydrostatic pressure is high at the arteriolar end and falls at the venous end so that at the first half of a capillary bed fluids tend to leave and are reabsorbed along the other half. The forces favoring filtration exceed those favoring reabsorption.
How about those baroreceptors?
The most important factor which affects peripheral resistance is the state of the arterioles. Baroreceptors in the arch of aorta and carotid sinus signal to the vasomotor center in the medulla (under SNS control). P increases -> receptors fire and information is relayed and vessel tone is decreased as well as blood pressure. Atrial natriuretic factor is released from the stretch receptors which inhibits aldosterone secretion (promotes Na excretion ->fall in bp).
Know the significance and components of the portal vein.
Portal vein is comprised of the sup. Mesenteric vein and the splenic vein. It delivers about a liter of blood/min to the liver. Blood mixes with blood from the hepatic artery and is filtered and emptied into IVC .
Know what HMG CoA reductase is and its significance
Cholestrol biosynthesis is controlled in the liver by enzyme HMG CoA reductase. Statin drugs target this enzyme. Cholesterol can also be converted into bile acids and secreted into the bile. These salts help digest fats and absorb fat soluble vitamins. Bile also contains bilirubin and IgA and can be stimulated by CCK.
What's the enterohepatic circulation all about and how bile salts figure into the picture?
Bile salts are secreted by liver, stored in gallbladder and released into the gut and reabsorbed at the terminal ileum. These are removed from the portal vein by the liver and go back into the bile to be stored in gallbladder or secreted into small intestine. If the salts get into circulation they cause itching. (Bile salts+lecthin+cholesterol=micelles) If cholesterol secreted>capacity of micelle to hold it in solution-> gall stones.
Know the impact of GH on hepatic function
Growth hormone stimulates synthesis and secretion of growth factors by the liver.
Describe the process of MHC coding.
In a virally infected cell, some of the synthesized protein goes to the proteosome where they are broken up and sent to the ER. Class I molecules bind to them there and the complex is taken to the membrane where they interact with CD8+ Tcells.
What do NK cells kill and what increases their population?
NK cells kill tumors or virally infected cells. They normally comprise 10% of WBC population but expand during treatmetn with cytokine IL-2.
What is the role of the B cell in launching an immune reponse?
B cells have surface IgM or IgD. If a BC sees an antigen it has been programmed to recognize, usually after processing with a Tcell, and an immune response is activated, colonal expansion occurs and memory cells are saved. Bcells may also differntiate into Plasma cells to secrete antibody (IgM).
What happens during the DHT (PPD) skin reaction?
Upon contact with the tuberculin antigen, sensitized Tcells that have already seen the Ag before release cytokines that attract and hold macrophages to the infected site. This causes swelling and irritation.
List the 3 kinds and subtypes of anemia.
Microcytic: Iron deficiency, anemia of chronic disease, and Hgb synthesis error.
Normocytic: Acute bleeding, red cell hemolysis, bone marrow failure.
Macrocytic: B12 deficiency, Folate deficiency, and thyroid disease
What is polycythemia? List the 3 types of polycythemia and their causes.
Polycythemia is an increase in RBCs
Polycythemia vera, a neoplastic condition where RBCs are over produced by the bone marrow.
Erythrocytosis, a physiological response to increased O2 needs.
Hemoconcentration where blood becomes more concentrated due to water loss.
What is thrombocytopenia? What causes it?
Thrombocytopenia: decreased platelets plt<150. Caused by plt destruction (autoimmune, splenomegaly, HIT), plt consumption (DIC, Bleeding, TTP), and bone marrow failure (viral illneses, malignancies).
What is thrombocytosis? and what causes it
Increased platelets caused by reactive thrombocytosis (physiologic rxn to stress - fever), essential thrombocytosis (neoplastic condition like polycythemia vera)
List 3 natural anticoagulants
Antithrombin III
Protein C/S
Tissue plasminogen activator
Explain the extrinsic clotting system
Vessel wall injury causes release of thromboplastin. This combines with factor VIIa which causes the converstion of factor X->Xa and the final common pathway produces a fibrin clot.
List some effects of chronic ETOH consumption on the liver.
Decreased clotting factor synthesis-->prolonged bleeding time.
Decreased albumin synthesis+portal hypertension--> ascites/peripheral edema
Decreased NH3 clearance --> hepatic encephalopathy
portal hypertension --> varicies--> rupture
Increase in lactate --> gout
Hypoglycemia resultin gfrom decreased GNG
How is blood supplied to the heart? What kind of MI will happen with occusion of each of these?
Via the coronary arteries which branch off of aorta: Rt coronary --> posterior wall of heart (inferior MI), Left main coronary which branches into L Ant Dec artery (Anterior MI), Left circumflex (posterior or lateral MI)
What is atherosclerosis and what cell plays a role in its etiology?
It is the progresive buildup of plaque in the artery which causes a narrowing of the artery.
monocytes/macrophages/foam cells
Know what CRP (c-reactive protein) is and what it signifies
CRP is a member of the class of acute phase reactants as its levels rise dramatically during inflammatory processes occurring in the body. It is thought to assist in complement binding to foreign and damaged cells and affect the humoral response to disease. It is also believed to play an important role in innate immunity, as an early defense system against infections. Increased levels have been linked to an increased risk for heart disease.
Describe the P QRS T aspects of an EKG and what 3 abnormalities may exist and what they indicate.
P: depolarization over the atria
QRS: Ventricualr depolarization
T: Ventricular repolarization
Increased P-R=dig toxicity
Peaked/depressed Twave: hyper/hypokalemia
ST elevation: MI
What are the blood tests for an MI?
Troponin, CPK/CK-Mb
What drugs are used for long term treatment of an MI?
What are statins and what is their MOA?
HMG-CoA reductase inhibitors form a class of hypolipidemic agents, used as pharmaceuticals to lower cholesterol levels in people with or at risk for cardiovascular disease. They cause cholesterol lowering by inhibiting the enzyme HMG-CoA reductase, an enzyme involved in the rate of cholesterol synthesis. Inhibition of this enzyme in the liver stimulates the LDL-receptors, which results in an increased clearance of LDL from the bloodstream and a decrease in blood cholesterol levels.