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Block 9 > Week 2 > Flashcards

Week 2 Flashcards

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1
Q

On valves what allows for bacterial attachment

A

Platelets and fibrin accumulation

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2
Q

What are vegetations

Risk factor for?

A

Inflammed masses of fibrin and plateltes containing microorganisms (protection)

Emboli (loose attachement)

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3
Q

Temperature difference in Subacute and actue endocarditis?

A

38 subacute

40 actue

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4
Q

Main clinical manifestation of endocarditis?

A

Heart murmur

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5
Q

Signs of Endocarditis

A

Fever

Roth Spots

Osler nodes (pads fo fibers)

M

Janeway Lesions (palms and soles)

A

N

E

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6
Q

Most sensitive test for valvular vegetations?

A

Transthoracic or Transesophageal echocardiography

* ECG might show changes

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7
Q

Duke Criteria for endocarditis

A

2+0 or 1+3 or 0+5

Major: two positive blood cultures, echocardiogram, mumur

Minor: predisposition(valve), fever, embolic/hemorrage, immunologic phenomena, echocardiogram(not fully +)

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8
Q

Confirmation of duke criteria

A

Blood culture

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9
Q

Treatment for infective endocarditis

A

Penicillin, Gentamicin, Vancomycin

Surgical removal

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10
Q

Most common casue of myocarditis

A

Coxsackievirus B

Parovirus, HIV, CMV

Als bacteria Trypanosoma cruzi

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11
Q

Pathogenesis of myccarditis

A

Viruses invade and kill myocytes

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12
Q

What myocarditis can present as?

A

CHF

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13
Q

Diagnostic markers for myocarditis

A

Tachycardia

Troponin I

Leukocytosis, ESR, CRP

ST-segment elevation

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14
Q

Myocarditis treatment

A

Supportive, NSAIDS, cardiac monitoring, immunosuppresive drugs (controversial)

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15
Q

Types of pericarditis

sources

A

Viral - oral

Purulent - spread

Chronic (tuberculous) - mt

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16
Q

Conseuqences of pericardiits

purulent

viral

A

Self-limiting, fibrosis and adhesions, constrivitve pericarditis is rare

Cardiac tamponade (toxins), constrive pericarditis

serosanguinous pericardial effusions (early granulomatous stages), constrictive pericarditis (late)

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17
Q

Presentation pericarditis

Viral

Purulent

Chronic

A

Sharp substernal pain when supine

Fever, dyspnea, less chest pain

Dull chest pain, weight loss, night sweats, cough, dyspnea

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18
Q

Treatment of pericarditis

A

NSAIDs

Antibiotics

RIPE

Prednisone

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19
Q

Cause for

Early After-Depolarizations

Delayed After-Depolarizations

A

EAD:

pharmacological (long QT), genetic (long QT), hypokalemia, hypomagnesemia, hypocalcemia, female, bradycardia, sympathetic

DAD:

excess of Ca in SR -> spontaneous release -> NCX causes inward current

digoxin, catecholamines, hypercalcemia, increased heart rate, genetic defet

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20
Q

What are the requirements for reentry?

A

multiple parallel conduction pathways

area of unidirectional block

slowed conduction

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21
Q

Disturbances in conduction for electrical activity

A

Ischemia reduces ATP

Less Na/K pump and activation of ATP sensitive K+ channels

extracellular K+ levels increase to 10-20mM within minues of coronary occlusion

Increase in K+ extracellular

Depolarization

Slow Na+ reconvery from inactivation (increased refractory period) - unidirectional block

Slow conduction due to partially inactivated Na+ channels - slow conduction velocity

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22
Q

Comparison between Class I antiarythmic drugs

A
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23
Q

Class I antiarythmic drugs action

A

Na+ channel blockers

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24
Q

Quinidine

Use

Side effects

A

Arrythmias w/o IHD

Cichonism, TdP, a-cholinergic

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25
Procainamide Use Side effects Active metabolite
A&V Arrythmias w/o IHD TdP, lupus like NAPA (K+ blocker)
26
Lidocaine Use Side Effects
2nd choice for VTac after DC cardioversion (ineffective against atrial arrhythmias) Pulmonary depression, seizures, fatigue, parasthesia
27
Flecainide Use Side-Effects
Atrial arrythmias K+ channel blocker, exacerbation of ventricular arrythmias
28
β-blockers mechanism use Side effects
Block pacemaker automaticity, reduce DADs, slowls conduction in AV node (slower ventricular rate in a fib) arrhythmias w/ history of CHF or MI, control ventricular rate in patients with AF Bradycardia, hypotension, left ventricualr failure, AV node block, bronchospasms
29
Class III antiarythmic drugs action Use Side effects
AF conversion to NSR, and NSR control amiodarone drug of choice of post-MI Prolong QT blocks Na+ channels, Ca2+ channels, α-adrenergic receptors, β-adrenergic receptors PULMONARY FIBROSIS
30
Class IV antiarrythmic drugs mechanism
Ca2+ blocker : slows AV node condcution, increases refractory period prevents calcium overload Rate control (a fib/flutter), PSVT to NSR, alternative to b-blocker to v-tac
31
Digoxin Mechanism Indication Side effects
Direct cardiac and central (low coses increase vagal tone) Ionotropic for CHF, vagal inhibition of AV node in A-fib 1st (2nd class 2/4) Prolonges PR, alter ST segment, low therapeutic index
32
Adenosine Receptor Drug of choice for Side effects
Gi-protein same effects as M2 (slow SA node fire, AV conduction) ; inhibits AV node reentry paroxysmal supraventricular tachycardia (PSVT) Can trigger AF
33
Anti-HT Diuretic Examples Mechanism Side effects Use
Thiazides (chlorothiazide) Loop (furosemia) K sparing (spironolactone) Short them CO depletion, long term TPR reduction Hypokalemia (muscle pain/fatigue), Hyperglycemia (inhibition of insulin release due to K+ depletion), K+/Mg2+ depletion - arrhythmias, cortiocsteroids can make it worse, decrease in Li+ removal Severe hypertension w/ retention of body fluids
34
Treatment of blood pressure with beta blockers Agents
Beta-adrenergic blocking agents (propranolol and metoprolol) Selective alpha-1 adrenergic receptor blockers (prazosin, terazosin, doxazosin) Agents that act on the CNS (methyldopa, clonidine) Agents that prevent adrenergic transmission (reserpine)
35
What is other effects b1 blocker has?
Lower renin, lower PVR (renal b1 receptor)
36
Drug interaction of beta blockers
Ca++ blockers Digitalis
37
ACE inhibitors Sexual Contraindication African-Americans
No adverse on lipids, glucose, sexual function Pregnancy African-Americans
38
Mechanism of Losartan lack of common symptom
Ang II type 1 receptor (AT1R) à decrease PVR à decrease BP Cough
39
. Direct Renin Inhibitors (Aliskiren) Side effects
Fetal Toxicity
40
Hydralazine Mechanism Vesseles Use
increases cGMP within arteriolar smooth muscle beds -\> fall in intracellular Ca++ -\> decrease in vascular resistance Arteries Severe HT
41
Minoxidil Mechanism Use Side Effects Add what? Vessels
ATP-dependent potassium channels, causing hyperpolarization and subsequent relaxation of arteriolar smooth muscle. The net effect is arteriolar vasodilation. Severe HT Hypertrichosis (Minoxidil), Hyperglycemia (decrease insulin release from Diazoxide), Reflex tachycardia, Edema Beta antagonist (reflex) and diuretic Arteries
42
Nitroprusside Mechanism Vessels Use
Release NO leading to cGMP increasen and vasodilatation Equal A/V Severe HT, HT emergencies
43
Chylomicrons Composition Lipoproteins What actives LPL? Purpose? Where is the remainder put to ApoC? What does Apoc E allow?
TG \>90% Apo A, B-48 initially; Apo E and Apo C’s acquired in circulation Apo C-II; release FFA+glucerol to adipose/muscle tisuse HDL Reuptake of remnants by liver CE \> TG
44
Cause of death due to endocarditis?
Hemodynamic collapse after rupture of the aortic or mitral valves or by septic emboli to the CNS
45
One is chest X-ray of pericarditis?
Flash shape enlarge cardiac silhouette
46
VLDL Where are they made? Contents/markers? What releases fatty acids? What does it become Remnants?
Liver TGs + apoB-100, ;; apocC, apoE (bloodstream) LPL IDL Converted into LDL by hepatic lipase and/or lipoprotein lipase, or IDL can be taken up by the liver
47
Which lipid particle has highest cholesterol content?
LDL
48
HDL Where is it made Proteins Important enzymes
Liver and small intestine apoA-I, apoC-II and apoE **LCAT** = Lecithin Cholesterol Acyl Transferase Esterifies cholesterol, which moves into interior of particle to enlarge HDL **CETP** = Cholesteryl Ester Transfer Protein Transfers CE from HDL to other lipoproteins
49
Primary chylomicronemia What is it? Result
Mutation in the gene which codes lipoprotein lipase (LPL deficiency) Higher Chylomicrons and VLDL
50
Familial hypercholesterolemia What is it? Result?
•Mutations in gene encoding LDLR 2x cholesterol serum up if heterozygous, CVD and MI by 20 if homozygous
51
Familial combined hyperlipidemia (IIb) What is it? Result
The most common genetic disorder that increases blood cholesterol and TG High TG in teens, MI, CAD, obesity, increase in VLDL, chylomicron remnants
52
Loop diuretics adverse effects
Hyperkalemia
53
Amlodipine Action Adverse Effect Use
Selective Ca++ blocker, Vasodilation, lowers BP Flushing, ankle edema, reflex tachy African Americans and angina
54
Verapamil & Diltiazem and Amlodipine difference
Verapamil & Diltiazem do not casue reflex tacy
55
Angiotensin-Converting Enzyme (ACE) example
Captopril
56
Angiotensin II type 1 receptor blockers example
Losartan
57
Captopril Mechanism Averse effects Use
Inhibit ACE Cough and hyperkalemia CHF, 1&2 HF
58
Losartan Mechanism Adverse effects
Selective Ang II type 1 receptor No cough, but fetal toxicity
59
Direct Renin Inhibitors
Aliskiren
60
Familial dysbetalipoproteinemia Cause Result Presentations
mutation in apolipoprotein E (ApoE) Total cholesterol up, TG up, HDL down Xanthoma, atherosclerosis, CAD
61
Familial hypertriglyceridemia Cause Result Presentation
AD mutation, leading to excess VLDL production Increase in TG but not cholesterol Premature CAD
62
Maintenance of blood pressure systems
63
HMG-CoA Reductase Inhibitors “The Statins” mechanism effects use when to take additive effects what can interfere
inhibits HMG-CoA reductase decrease LDL, TG, increase HDL\ hypercholesterolemia (familial, 2/2 diabetes, LDL reduction) before the bed (most is synthesized during night) resins or ezetimibe grapefruit (potentiation by P450 inhibition)
64
Bile-Acid Binding Resins Examples Mechanism Effect Side effects
Cholestyramine, Colestipol, Colesevelam Increase fecal excretion Decrease LDL Constipation, GI issues, impared ADEK absortption
65
Niacin Mechanism Side Effects
Inhibits VLDL secretion less TG and LDL Flushing and itching
66
Fibrates Mechanism Side effects
•Activates peroxisome proliferator-activated receptors (PPAR) alpha (increase lipolysis) -- upregulation of protein lipase Gallstones
67
Ezetimibe Mechanism Side effects
Cholesterol absorption Diarhea and liver disease
68
Orlistat Mechanism Use for
Inhibits activity of intestinal lipases Obesity
69
Ursodiol Mechanism
Dissolution of radiolucent gallstones. Increases concentration at which saturation of cholesterol occurs, so slowly dissolve gallstones

Block 9 (6 decks)

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