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39 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Which organisms commonly cause acute and subacute endocarditis?
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Acute - staph. aureus and strep. pneumonia
Subacute - S. viridans and S. epidermidis |
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What treatment is best for Gram negative septicemia?
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Tx with anti-TNF and anti-LPS antibodies
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In Gram neg. septicemia, macrophages and leukocytes respond to gram negative LPS.
There is a Cytokine release, TNF and IL-1 → immune overstimulation o Tx with anti-TNF and anti-LPS antibodies. • Worst thing here is to treat this with antibiotics. |
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What is the pathogenesis of gram negative sepsis?
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macrophages activated -> cytokines released = fever, inc adhesiveness of PMN, inc leakage of plasma from vessels.
complement activated => lung tissue damage clotting activated=> hemmorrage |
-Increased adhesiveness of PMNs – can prevent circulation
-Increased leakage of plasma from blood – circulatory collapse (no liquid left in vessels to carry oxygen and nutrients to tissues) -Activation of complement – leukocytes are attracted to different tissues -Severe hemorrhages in areas of the body where there are no clotting factors because they were depleted |
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what is the life cycle of malaria?
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bit by mosquito, infected by protozoa which grows in the nucleus of liver cells, protozoa split to form merozoits which affect RBCs.
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What organisms causes the plague?
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Yersinia Pestis, a gram - bacillus
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transmitted by fleas
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What are the three routes of infection of Y. Pestis?
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1.Flea bite, subcutaneous
-Colonizes lymphatic system - Harbors 2 plasmids to aid flea transmission 2.Inhalation 3.Wound infection, septicemic |
wound infectiono is most lethal
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What are Yops? What do they do?
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Yops are Yersinia outer protein. They inhibit macrophages therefore inhibiting phagocytosis and cytokine release.
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Other virulence factors – complement resistance factor, PsaA – adhesion to host cells
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How is malaria treated?
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Weekly doses of chlorozuine while in malarial areas
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Prevention,Mosquito netting impregnated with insecticide.
Some Africans lack RBC receptor for P. Vivax |
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What are the stages of malaria pathogenesis?
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Three stages:
– Cold phase: abrupt onset of shaking chills, for 1 hour – Hot phase: temperature rises to 104°F (40 °C), several hours – Wet phase: temperature falls and get a drenching sweat • Fatigue for 24-48 hours, cycle repeats |
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3 ways to inactivate a monoamine family transmitter
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1. Uptake
2. Metabolism- by synaptic cleft enzyme 3. mitochondrial enzyme MOA |
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How are adrenergic agonist classified?
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directly acting and indirectly acting
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Directly-acting adrenergic agonists act at adrenergic receptors located on effector cells
Indirectly-acting adrenergic agonists act by displacing NE from noradrenergic neurons- effect on neurons |
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What are the two families of adrenergic receptors?
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Alpha adrenergic family and
beta adrenergic family. |
Alpha-adrenergic family – family of receptors where Epi is equal or more potent than NE and both are much more potent than isoproterenol (Epi > NE >>>>> isoproterenol)
Beta-adrenergic family – Isoproterenol > Epi >>>> NE |
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What effect does epinephrine and norepinephrine have on the heart?
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epinephrine inc the heart rate and norepinephrine dec. the heart rate
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CO does not increase with NE because HR goes down and SV goes up – depends on how much those change
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How does epinephrine effect TPR?
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low conc bind to beta 2 receptors and decrease resistance.
high conentration bind to both beta 2 and alpha receptors and increase TPR |
Epi increases oxygen consumption – don’t want to give it compromised heart because it starts working harder – makes it worse
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What causes reflex bradycardia?
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caused by NE. The heart rate goes down because Ach is released
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How does isoproterenol increase HR?
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it is a beta agonist that decreases peripheral resistance. MAP falls and HR goes up.
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Name the three blood filtering organs.
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Kidneys
Spleen Lymph nodes |
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What are the tissues responses to alpha 1 adrenergic receptor activation?
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vessels contract, intestinal muscles relax (hyperpolarize), heart arrhythmia and increased contractile force
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What are the tissues responses to alpha 2 adrenergic receptor activation?
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Vascular smooth muscle – contraction
Platelets – aggregation Nerve terminals – decreased neurotransmitted release Pancreatic islets – decreased insulin secretion |
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What is raynaud's disease?
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Spasm of the blood vessels in fingers and other extremities- extremely painful.
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alpha adrenergic antagonist can be used therapeutically for this syndrome.
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What type of patients should avoid activation of beta adrenergic receptors?
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patients with compromised hearts
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beta adrenergic agonists isoproterenol and dubutamin increase force and rate of contraction and nodal conduction velocity of the heart.
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Name 3 beta 2 adrenergic receptor agonist
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tertbutaline, albuterol, metaproterenol. all treat asthma
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Relaxation of bronchial smooth muscle
Suppression of mast cell leukotriene and histamine release Enhanced mucociliary function Decreased microvascular permeability Inhibition of phospholipase A2 Contraindications for beta blokers- Asthma and Diabetes |
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What is the muscarinic receptor, M1, agonist? antagonist? tissue? response?
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agonist: oxotremorine
antagonist: Atropin, Pirenzapine tissue: autonomic ganglia response: depolarization |
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Muscarinic agonist do what?
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Slows HR, dec. force of contraction
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2 drugs that are resistant to cholinesterases?
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carbachol
benthanechol |
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What does Acetylcholinesterase hydrolyze? Where is it located? What is it inhibited by?
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it hydrolyzes ACH and methacholine. It is located on pre and post synaptic sites of neruons. It is inhibited by low conc levels of bisquaternary ammonium bases
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Butyrocholinesterase – hydrolyzes butyrcholine more rapidly than any other choline ester
Also hydrolyzes acetylcholine and benzoylcholine but not methacholine Is more sensitive to inhibition by organophosphorus agents than is acetylcholinesterase Located in plasma, liver, flial cells, variety of organs. |
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what are two muscarinic receptor blocking agents?
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Atropine and Scopolamine
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CV Effects – small doses slow HR, large doses cause tachycardia
little effect on BP toxic doses cause vasodilation (atropine flush) Respiratory actions – bronchodilation, decreases secretions, increased rate and depth of breathing. |
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What is the action of digoxin on cardiac myocytes? what is the electrophysiology effect on the heart?
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it increases intracellular Ca levels and therefore increases contractile force (and CO).Binding and effect of it depends on extracellular K+ levels.
Increases conduction rate thru and automaticity of atria and ventricles Increased automaticity of SA node – able to depolorize by itself better Decreases conduction rate thru AV node PR interval is prolonged in patients taking digoxin – clinically important |
• However, other parts of atria and even ventricles also increase in automaticity and can be easier made to depolarize – baad, causes fibrillations
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Main use of digoxin?
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positive ionotropic effect increasing stroke volume.
sometimes as an antioarrythmic bc of its side affect of slowing of AV node |
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what are the two types of neoplastic leukocytosis?
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Leukemia and lymphoma
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Leukemia is Generalized malignant WBCs in peripheral blood + bone marrow
CML (leukemia characterized by the unregulated growth of myeloid cells in the bone marrow) is associated with Philadelphia chromosome translocation, involves genes 9 and 22 – know that Lymphoma – localized collection of malignant WBCs in lymph nodes or other solid organs or tissues • Hodgkin’s • Non-hodgkin’s |
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In non-hodgkins lymphoma, what is the percentage of nodal and extranodal lymphoma?
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60% nodal – swollen lymph nodes
40% extranodal – destructive soft tissue mass (GI tract, Waldeyer’s ring, bone) |
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What are thiazides used for? How does it work? Name a common one.
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used for HTN. Lowers BP by decrease in blood sodium concentration, which decreases sensitivity of vasculature to vasoconstrictors. a common thiazide is hydrochlorothiazide.
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Thiazide actions are to increase the volume of very concentrated urine
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Name a common K sparing diuertic.
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Amiloride – triamterene-like for all practical purposes (know that)
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Triamterene
General actions - Thiazide-like - Blocks distal tubular Na uptake in exchange for K+ secretion, in principal cells of the nephron - Overall effects is decreased potassium secretion in exchange for sodium reabsorption (causes K+ retention) |
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PT, prothrobin time is used to test what?
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the extrinsic pathway, or tissue factor pathway, for coagulation. PT would be elevated, in a VII, II, V, X and fibrinogen defincecy.
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side effect of sympathetic inhibitors?
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orthostatic hypertensioin
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angII receptor blocker is a sub for the 'prils' ace inhibitors. what does it do?
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used for htn
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niacin/ vitamin b3 does what to antidiabetic drugs?
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antagonizes it.
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Fibrates lower what?
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cholesterol. also increase risk of myopathy?
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nitroglycerin does what?
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its a vasodialator.- may reduc ischemia and its symptoms but does not lower mortality long-term
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All Sympathomimetics (like albuterol) counteract nitroglycerine’s desired actions by increasing blood pressure – neither alpha nor beta activation is good
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