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140 Cards in this Set
- Front
- Back
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What are the major controllable risks factors for atherosclerosis?
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- hyperlipidemia
- HTN - smoking - DM |
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What complications can atherosclerosis lead to?
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- aneurysm
- thrombosis - ischemia - infarction |
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What are the 2 ways by which LDL can be cleared?
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- by the high affinity apo B recognizing receptors which is normal
- by the low affinity apo E recognizing receptors which is abnormal and causes foam cell formation |
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What are some of the minor risk factors for atherosclerosis?
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- physical activity
- obesity - increase Lipoprotein A in blood - increase homocysteine in blood - increase CRP in blood |
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What are the major uncontrollable risk factors for atherosclerosis?
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- age
- male gender - family hx - genetic abnormalities |
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What is the pathogenesis of atherosclerosis?
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- chronic endothelial damage
- damage increases permeability to endothelium to oxidized lipids - oxidized lipids release cytokines - monocytes emigrate into the endothelium - smooth muscle emigrates from media to intima - macrophages and smooth muscle engulf oxidized lipids and foam cells are formed - smooth muscle proliferation and elaboration of ECM - plaque rupture |
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What are the guidelines for lipid levels?
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- HDL greater than 40
- want total cholesterol less than 200 - want LDL less than 100 (if one or no risk factors, just need it below 160) |
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Definition of atherosclerosis?
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formation of atheromas which protrude into and obstruct vascular lumens as well as weaken underlying media
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What are the key epidemiological factors of atherosclerosis?
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- geographic and racial variation
- deaths higher in developed countries but frequency decreasing due to education - death rates in Japan 1/6 of that in US - hypercholesterolemia is related |
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What are the clinical features of atherosclerosis?
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- slow, insidious narrowing of vascular lumen leading to tissue ischemia
- sudden occlusion of lumen by thrombosis or hemorrhage into atheroma - ischemia or infarct can result - also provide a site for thrombosis and then embolism - can weaken vessel wall and cause aneurysm |
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What are the 2 general categories of hyperlipoproteinemias?
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- increase LDL
- decrease HDL |
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What does chylomicron synthesis do?
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- initiates exogenous triglyceride pathway
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What does VLDL synthesis do?
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- initiates endogenous triglyceride pathway
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What is the role of HDL?
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- scavenges cholesterol and esterifies it to initiate reverse cholesterol transport
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What is the role of LDL?
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- cleared by two receptors- one good and one bad... the pathological one causes formation of foam cells
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What are the 3 components of an atherosclerotic plaque?
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Cells, connective tissue, and intracell and extracell lipid deposition
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What are the compensatory mechanisms for decrease cardiac output?
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1) Frank Starling- increase stretch as the heart dilates, increase contraction
2) Adrenergic nervous system- increase contractility 3) Renin-angiotensin-aldosterone system 4) Cardiac remodeling |
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What is systolic heart failure?
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Deterioration of myocardial contraction, weak, floppy venticle
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What is diastolic heart failure?
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inability of heart chamber to relax, expand, and adequately fill
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What is right sided heart failure?
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- engorgement of systemic and portal venous circulation
- most common cause is L. sided heart failure |
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What is left sided heart failure?
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- damning of blood in pulmonary circulation and diminished peripheral circulation
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What is stable angina pectoris?
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- due to chronic stenosing coronary atherosclerosis
- increase cardiac demand and workload is unmet - substernal chest pain - relieved with rest or vasodilator |
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What is unstable angina pectoris?
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- due to atherosclerotic plaque disruption
- plaque components activate platelets, coag cascade, and vasospasm which leads to partially occluding thrombus= ischemia - chest pains are frequent, occur with less effort and at rest, and last for longer - pre- MI, bad |
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Describe a vulnerable plaque?
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- occludes lumen 50-75%
- lipid rich atheromas - inflammation - thin, fibrous cap |
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What is Prinzmetal Variant Angina?
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- coronary artery spasm with abrupt reduction in vessel diameter
- unrelated to physical activity, heart rate or BP - responds to vasodilators - not necessarily related to atherosclerosis |
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What is the time cut off for reversible vs. irreversible damage with a MI?
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- after 30 mins, coagulative necrosis occurs and damage is irreversible
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What is a transmural MI?
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- necrosis of entire thickness of the myocardium
- lead to ST segment elevation |
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What are the 4 possible major consequences of ischemia?
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- Angina
- Acute MI - Ischemic cardiomyopathy - Sudden cardiac death |
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What is left sided HTN?
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- HTN leads to hypertrophy of left side of the heart
- remodeling occurs, interstitial fibrosis due to inadequate vasculature - asymptomatic, CHF, arrhythmias - BP control is key!! |
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What is pulmonary HTN?
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- caused by lung or lung vasculature pathology which increases pulmonary vascular resistance
- leads to cor pulmonale= dilated R. ventricle - increase RVH, dilatation and R. sided heart failure - hepatosplenomegaly, renal congestion, cerebral hypoxia, pleural and pericardial effusions, ascites, and peripheral edema |
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What is cor pulmonale?
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- dilated R. ventricle
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What are the defining features of Staph?
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- gram positive cocci
- form grape like clusters - catalase positive - prefers aerobic environment - ferment glucose - abscess formation |
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Where does Staph adhere to?
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- nasal epithelium
- skin or traumatized endothelium |
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What are the cytolytic toxins of Staph?
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- alpha
- beta - gamma - delta - leukocidins |
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What are enterotoxins of Staph?
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- superantigens, not inactivated by heating, cause massive cytokine release
- A, B, C1, C2, D, E, AND - Enterotoxin F=pyrogenic toxin C- toxic shock syndrome toxin 1 - antigen presents to Vbeta region (different than normal toxins) - massive activation of T cells (20-30%) - sudden onset of symptoms |
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What are ETB adn ETA of Staph?
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- ETA: exofoliatin toxin
- ETB: epidermolytic toxin - cause Staph scalded skin syndrome - serine proteases |
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What are two major types of Staph?
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- Staph aureus (coagulase, ferments mannitol, contains Protein A and ribitol teichoic acid in cell wall, produce alpha toxin and DNAase)
- Staph coagulase neg (no coagulase, |
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What are three of the most common types of Staph?
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- Staph aureus (coagulase)
- Staph epidermidis - Staph saprophyticus |
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What are the main clinical manifestations of a staph infection?
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- Cutaneous infection
- Deep infections (osteomyelitis, CNS, GI, endocarditis, LRTI, bacteremia, etc...) - Dz by exotoxin (gastroenteritis, toxic shock, scalded skin) |
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What are the main drugs used to treat infection?
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- Nafcillin, Oxacillin, Dicloxacillin (penicillin)
- therapy length depends on site of infection |
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How do you treat methicillin resistant S. aureus?
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- Vancomycin
- Trimethoprim - Cephalosporins |
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What is the genetic basis of methicillin resistance?
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- on mec A gene complex which is on SCC mec
- penicillin resistance conferred by B-lactamase coded by blaz gene - methicillin resistance results from altered penicillin binding protein (PBP) |
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What is Panton- Valentin Leukocidin?
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- causes hemorrhagic pneumonia and damages host defense and erythrocye membranes
- LukS-PV and LukF-PV - produced by less than 5% of S. aureus - mainly involved in infections with necrotic lesions involving skin or mucosa - USA 300 is main strain - treat with vancomycin |
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What are the physical signs of acute coronary artery dz?
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- pallor, sweating, anxiety, tachycardia, increase BP
- S4 gallop - mitral regurg - paradoxically split S2 - Pulsus alternans |
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What are the killer chest pains?
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- acute coronary syndromes
- pulmonary embolism - aortic dissection - pneumothorax |
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What is the prognosis of pt with aortic stenosis?
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- onset of sxs is poor prognosis regardless of age
- CHF- 2 year survival - Syncope- 3 year survival - Angina- 5 year survival - dz progresses variably |
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What are the main characteristics of a strep infection?
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- gram positive diplococci in pairs and chains
- catalase negative - prefers anaerobic/CO2 atmosphere |
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What are the common Strep infections?
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- Pharyngitis
- Impetigo - Erysipelas - Scarlet Fever - Necrotizing fasciitis - Toxic shock-like syndrome |
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What are the post strep sequelae which antibiotics work to prevent?
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1) Rheumatic Fever: fever, subcut nodules, chorea, polyarthritis, rash, and myocarditis, Aschoff bodies, valve damage and endocarditis later in life
2) Acute glomerulonephritis: Ag-Ab complex deposited in the kidney, edema, HTN, hematuria and proteinuria |
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What are the virulence factors of Strep pyogenes?
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- hemolysins (Streptolysin S and O)
- Streptokinase - Hyaluronidase - Nucleases - C5a peptidase - M proteins - Streptococcal pyrogenic exotoxins (super antigens) |
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What is the treatment for a strep pyogenes infection?
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- Penicillin/ampicillin/amoxicillin
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What are the main infections of Group B Strep (strep agalactiae)?
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- neonatal pneumonia, sepsis and meningitis
- skin wound infections - endocarditis - early and late onset neonatal dz - UTIs - pregnant women can carry GBS and give to neonate- need to give prophylaxis meds to positive moms |
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What is the treat for GBS?
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- penicillin/ampicillin
- add gentamicin to enhance killing |
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What are the main features of a Viridans Strep infection?
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- E. faecalis and E. faecium
- turn agar green- alpha hemolysis - causes dental carries, endocarditis, and abscesses - lack hemolysins and toxins of beta strep - S. bovus, S. mitis, and Milleri group |
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What are the characteristics of enterococcus?
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- gram positive cocci in pairs and short chains
- alpha, beta, or gamma hemolytic - Group D antigen in cell membrane - PYR positive - hydrolyzes bile esculin |
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What are the main infections caused by enterococcus?
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- UTI
- bacterial wound infections - sepsis - endocarditis - meningitis (rarely) |
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What is the treatment for E. faecalis?
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- pen/amp
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What is the treatment for E. faecium?
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- vancomycin and gentamicin
- if vanco resistant, use LINEZOLID |
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What are some of the characteristic signs of infective endocarditis?
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- Osler nodules
- splinter hemorrhages - conjunctival petechiae - Janeway lesions - Roth spots |
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What are the three mechanisms of dysrhythmias?
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1) automaticity
2) triggered activity 3) re-entry of excitation |
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What are the 3 determinants of pacemaker rate?
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1) max diastolic potential
2) slope of diastolic depolarization 3) level of threshold potential |
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What are 4 mechanisms which cause arrhythmias due to altered automaticity?
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1) sinus node block
2) ectopic rate increases sinus rate 3) sinus rate drops below ectopic rate 4) increase ectopic rate and decrease in sinus rate ALSO sinus tachy and sinus bradycardia |
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What are some factors which enhance automaticity?
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- hypokalemia
- stretching tissue - ischemia |
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What is the mechanism of a DAD?
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- transient subthreshold depolarization that follows a preceding AP
- abnormally elevated intracell Ca possibly from ischemia - spontaneous release of Ca from internal stores stimulates inward Na/Ca exchange current to depolarize membrane potential, resulting in a DAD |
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What are possible causes of DADs?
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- cardiac glycoside toxicity
- high concentrations of catecholamines - ischemia - rapid heart rates - all in combo NOTE: all increase [Ca] |
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What is the mechanism of a EAD?
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- transient depolarization that occurs during the later part of the AP plateau
- may lengthen AP duration, can cause prolonged QT syndrome - may be precipitated by interventions that prolong AP - underlie torsades de pointes |
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What are possible causes of EADs?
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- acidosis
- quinidine - slow heart rate - low plasma K - prolonged QT syndrome |
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What are the 3 requirements for re-entry of excitation?
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- Geometry for a conduction loop
- Slow conduction - Unidirectional block |
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What are possible mechanisms of therapy for re-entry of excitation?
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- increase refractory period of normal tissue (anti-arrhythmic drugs)
- produce complete block through damaged region (ablation) - enhance conduction through damaged region (no mechanism to do this yet) |
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What is 1st degree heart block?
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- P-R interval > 0.2 s with consistent P-R interval
- usually not symptomatic and not a problem |
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What is 2nd degree heart block?
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- P-R interval > .2 s with intermittent conduction failure to the ventricles so dropped R waves
- Type I Wenckebach periodicity: gradually increasing PR interval leading to conduction failure to ventricles, increasing by decreasing increments - Type II- constantly lengthens P-R interval leading to conduction failure to ventricles |
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What is 3rd degree heart block?
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- no consistent P-R intervals
- complete failure of conduction between atria and ventricles |
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What are bundle branch blocks?
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- intraventricular conduction disturbances based on QRS complex- usually see notching of QRS
- duration of QRS increases with increasing mass of ventricular myocardium - QRS> 120 ms considered abnormal |
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What are possible causes of tachycardia?
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- sympathetics
- drugs - ischemia - hypokalemia - fever - hyperthyroidism |
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What are possible causes of bradycardia?
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- sick sinus syndrome
- sino-atrial block - depressants - infarction - fibrosis |
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What is the mechanism of hypokalemia?
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- increases potassium grad but decreases membrane permeability b/c shuts down potassium channels so don't waste potassium
- more difficult for K to leave cell during repolarization, slope of repolarization slow, amplitude of T wave smaller |
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What is the mechanism of hyperkalemia?
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- with increase K, increase membrane permeability to K b/c depolarize the resting membrane potential
- passively, less K leaves the cell but actively, more K leaves the cell, repolarize faster, slope of repolarization is much greater, higher T wave amplitude |
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What is ST segment elevation?
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- Q-T depression
- S-T elevation |
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What are the spatial factors which influence ST segment changes during ischemia?
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1) size of ischemia or infarcted area- larger the ischemic area the greater the changes in ST segment
2) location of ischemia or infarcted area- if in subepicardial area, have segment elevation during systole, if in subendocardial area, have segment depression during systole 3) location of recording electrode 4) wall thickness- larger the ventricular wall at site of ischemia, the larger the ST segment change |
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What are the non-spatial factors which influence ST segment changes during ischemia?
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1) differences in transmembrane voltage between ischemic and normal tissues during diastole and systole
- diastole: b/c decrease blood flow, K accumulates in ischemic area and shifts membrane potential more positive - systole: alterations in ionic channel function alter plateau of AP |
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What is healing over?
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- Disappearance of ST segment changes
- this is due to an increase in internal resistance between damaged and normal cells - in damaged area have hypercalcemia - nexal connections close down - doesn't heal, heart is still damaged, but is protective |
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What EKG changes do you see with ischemia?
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- ST segment changes- usually ST segment depression
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What EKG changes do you see with infarction?
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- ST segment changes- usually ST segment elevation
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What does a normal Q wave look like?
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- left to right activation of interventricular septum
- low amplitude - short duration |
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What Q wave abnormalities are seen in ischemia or infarct?
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- infarcted region produces no electrical activity so transparent to EKG
- unopposed left to right vector produces large negative deflection - high amplitude - long duration |
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What are other conditions which may cause Q wave abnormalities but in reality there is NO infarct?
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- Familial hypertrophic cardiomyopathy: septal hypertrophy causes pseudo infart pattern
- Left bundle branch block: large right to left activation pattern which obscures Q wave diagnosis |
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What factors modify the QRS complex?
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- Position of heart in thorax: pregnancy, pneumothorax, hypertrophy, and congestive heart failure
- conduction velocity: drugs, electrolytes, or metabolic induced changes - activation sequence: bundle branch block, accessory pathways, re-entry, or dz |
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What does a normal T wave result from?
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- repolarization of heart from epicardium to endocardium so normally upright T wave in most leads
- vector of repolarization in SAME direction as vector of depolarization |
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When do you see peaked (tall) T waves?
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- hyperkalemia: increases the slope of repolarization causing taller and narrower T wave
- myocardial ischemia: increase K in tissue b/c no blood flow so similar mechanism |
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When do you see an inverted T wave?
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- ischemia and infarction
- cerebral dz- subarachnoid hemorrhage - may be present normally in children and infants |
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What are the main features of Strep pneumoniae?
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- major cause of community acquired bacterial multilobar pneumonia and meningitis in adults and otitis media in children
- gram positive football shape diplococci - polysaccharide capsule is main virulence factor - alpha hemolytic - autolysis - vaccines available |
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How do you diagnosis Strep pneumonia?
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- gram stain
- Quellung rxn - Optochoin sensitivity - bile liquefies colony |
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What is the treatment for Strep pneumonia?
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- penicillin if susceptible
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What are the main characteristics of Neisseria?
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- gram negative "kidney bean diplococci
- growth enhanced in CO2, require chocolate media - oxidase positive |
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What are the main features of Neisseria meningitidis?
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- All 13 serogroups are immunogenic except Group B
- transmitted by respiratory droplets - developed world has sporadic cases of Group B, undeveloped world has many cases of A and C |
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What are the clinical manifestations of N. meningitidis?
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- petechial rashes
- meningiococcemia: fever, chills, hemorrhage, shock, purpura, and adrenal hemorrhage - meningitis: HA, mental status change, neurological signs - Fulminant meningococcemia: septic shock and adrenal hemorrhage, DIC, coma and death |
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How do you treat N. meningitidis?
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- Penicillin or cephalosporin
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Who is the vaccination for N. meningitidis given to?
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- army recruits
- children at age 11 - travelers to Africa/Saudi Arabia - college freshmen in dorms - microbiologists - outbreak populations - pts with asplenia or complement deficiency |
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What are the main features of Neisseria gonorrhea?
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- antigenic variation in pili and opa proteins
- require chocolate media, enhanced in CO2 - high rates among adolescents and young adults |
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What are the clinical manifestations of N. gonorrhea?
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- Localized infection such as urethritis, cervicitis, prostatitis, pharyngitis, conjunctivitis
- Pelvic inflammatory dz - Disseminated gonococcal infection: arthritis, dermatits, endocarditis, meningitis |
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How do you treat N. gonorrhea?
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- ceftriaxone, cefixime, azithromycin for 1 day OR
- doxcycline for 7 days |
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What are the types of penicillin resistance seen with N. gonorrhea?
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- decrease affinity for penicillin binding protein
- B- lactamase |
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What are the defining characteristics of H. influenzae?
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- gram negative coccobacilli
- requires chocolate agar to grow - polysaccharide capsule which confers virulence- Type B= invasive and BAD - transmission by respiratory droplets - infection most often seen in children, used to be most common cause of invasive childhood infection until vaccine |
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What are the clinical manifestations of H. influenzae?
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- often seen in children:
- Meningitis - Epiglottits - Cellulitis - Septic arthritis |
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How do you treat H. influenzae?
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- severe dz: cephalosporin
- less severe dz: macrolides - many are ampicillin resistant due to beta-lactamase - vaccine highly effective |
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What are the defining characteristics of Bordetella Pertusis?
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- gram negative coccobacilli
- Pertussis toxin which has B subunit which BINDS to target cell and A subunit which initiates ACTION - Adenylate cyclase toxin which increases cAMP and results in impaired chemotaxis and impaired superoxide pdt - FHA: binds to respiratory cells and macs to promote phagocytosis without respiratory burst - Tracheal cytotoxin: destroys ciliated epithelial cells |
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Where is adenylate cyclase toxin seen and what does it do?
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- seen in Bordetella Pertussis
- increases cAMP and results in impaired chemotaxis and impaired superoxide pdt |
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Where is FHA found and what does it do?
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- found in Bordetella Pertussis
- binds to respiratory cells and macs and promotes phagocytosis without respiratory burst |
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Where is tracheal cytotoxin found and what does it do?
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- found in Bordetella Pertussis
- destroys ciliated respiratory cells so impaired clearance of bacteria |
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What is whooping cough?
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- caused by Bordetella Pertussis
- Catarrhal Stage- non specific symptoms, 1-2 weeks - Paroxysmal Stage- repetitive coughing with whoops, 2-4 weeks - Convalescent Stage- secondary complications, coughing but less than earlier, 3-4 weeks |
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What is the treatment for Bordetella Pertusis?
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- Erythromycin
- supportive care - vaccination in adults and children |
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What are the defining characteristics of Legionella?
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- slender gram neg rods but don't stain with gram stain b/c too small
- live in water - clinical manifestations are Pontiac Fever and Legionellosis |
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What is Pontiac Fever?
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- caused by legionella
- febrile influenza like illness w/o respiratory component |
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What is Legionellosis?
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- caused by legionella
- severe pneumonia - multisystem dz |
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What are the main characteristics of Enterobacteriaceae?
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- gram negative rods
- indigenous flora of the GI tract |
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Which enterobacteriaceae are non- lactose fermentors?
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- Shigella
- Salmonella - Proteus - Yersinia |
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What are the main diseases caused by E. coli?
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- gram negative sepsis
- UTI (80% of community acquired) - neonatal meningitis - gastroenteritis |
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What are two syndromes associated with E. Coli 0157?
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- Hemorrhagic colitis
- Hemolytic Uremic Syndrome due to Shiga- like toxin |
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What are the triad of symptoms associated with HUS?
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1) Acute renal failure
2) Thrombocytopenia 3) Hemolytic anemia - tx with oral rehydration and NO antibiotics |
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With what type of E. coli do you NOT use antibiotics or anti-motility agents?
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- Enterohemorrhagic E. Coli b/c increases chances of HUS
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What are the main characteristics of Shigella?
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- transmitted by fecal oral route (5 Fs: food, flies, fingers, fomites, and feces)
- ALWAYS a pathogen - clinical manifestations: fever, abdominal pain, diarrhea with pus and blood |
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What are the main characteristics of Edwardsiella tarda?
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- type of enterbacteriaceae
- found in cold blooded vertebrates, fresh water fish, and cat fish - cause gastroenteritis, self limiting with watery diarrhea |
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What are the main characteristics of Salmonella?
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- type of enterobacteriaceae
- often result of contaminated poultry or dealing with reptiles - Clinical manifestations: **febrile gastroenteritis, enteric fever (very serious, fever and severe GI symptoms including bleeding), bacteremia (in immune suppressed pts), focal infections, can by asymptomatic |
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What are the main characteristics of Citrobacter?
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- type of enterobacteriaceae
- C. freundii, C. koseri - nosocomial infections of urinary and respiratory tract - also endocarditis and bactermia |
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What are the main characteristics of Klebsiella?
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- type of enterobacteriaceae
- K. pnemoniae causes primary lobar pneumonia with necrosis and hemorrhage- currant jelly sputum - also causes bronchitis, UTI, and bacteremias |
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What are the main characteristics of Enterobacter?
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- type of enterobacteriaceae
- cause opportunistic infections - frequently resistant to multiple antibiotics |
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What are the main characteristics of Serratia?
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- type of enterobacteriaceae
- S. marcescens - nosocomial infections, pneumonia, septicemia, UTI, surgical wound - BRIGHT RED PIGMENT |
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What are the main characteristics of Proteus?
|
- type of enterobacteriaceae
- P. mirabilis and P. vulgaris - SWARMING on plate - P. mirabilis causes UTIs and wound infection - P. vulgaris causes infection in immune compromised pts |
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What are the main characteristics of Yersinia?
|
- type of enterbacteriaceae
- Y. entercolitica - urea positive - animals are main reservoir (esp pigs... think chitterlings) - fever, diarrhea, abdominal pain... can mimic appendicitis - also seen with blood transfusion |
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Explain the glutathione system and why it is dependent on G6DP?
|
- G6DP produces NADPH
- NADPH is necessary for the pdt of reduced glutathione - reduced glutathione is necessary for handling oxidative stress |
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What are Heinz bodies?
|
- precipitate Hb in RBC formed due to oxidative stress
- cause damage to RBC membrane - cause intravascular and extravascular hemolysis in G6DP enzyme deficiency |
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What causes macrocytic anemia?
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- B12 deficiency
- Folate deficiency |
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What causes normocytic anemia?
|
- blood loss
- marrow failure - hemolysis |
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What causes microcytic anemia?
|
- Iron deficiency
- Defect in Hb synthesis - anemia of chronic dz |
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What are lab markers of hemolysis?
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- falling Hb and hematocrit
- MCV may be high normal - hyperbilirubinemia - decrease or absent haptoglobin - elevated LDH - positive Coombs - peripheral blood smear findings (spherocytes, polychromasia, schistocytes) |
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What is the mechanism for HDN?
|
- fetus inherits paternal RBC antigens which are not shared by the mother
- fetal RBC pass into maternal circulation - maternal immune response produces IgG which crosses back into the fetal circulation - extravascular hemolysis and anemia, also can have heart failure, hepatosplenomegaly, liver congestion and failure, anasarca, and death |
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What are the characteristics of warm autoimmune hemolytic anemia?
|
- takes place at 37 C
- IgG, can have complement activation - extravascular clearance of RBC - seen with autoimmune dz and lymphoid malignancy |
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What are the characteristics of cold autoimmune hemolytic anemia?
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- takes place below 25 C
- IgM, complement activation - extravascular clearance - happens after infection or with lymphoid malignancies |
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When do you see a positive DAT?
|
- acute and delayed hemolytic transfusion rxns
- hemolytic dz of the newborn - autoimmune hemolytic dz - drug dependent hemolysis |
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Tetralogy of Fallot
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1) infunibular pulmonary stenosis
2) right ventricular hypertrophy 3) ventricular septal defect 4) overriding aorta |
