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CRRAB FINAL REVIEW > PBL Medicine- Purnuske > Flashcards

PBL Medicine- Purnuske Flashcards

1
Q

Describe physical exam findings associated with septic emboli

A

Petechial rash Septic emboli (PE, stroke) Roth’s spots Splinter Hemorrhages under the fingernails

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2
Q

What is the mechanism of action ceftriaxone?

A

Binds penicillin binding proteins (transpeptidase) and inhibits peptidoglycan synthesis Gram + and - organisms Bactericidal Less susceptible to penicillinases

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3
Q

MOA of penicillin G?

A

IV/IM form Binds to pbp (transpeptidase) preventing it from cross-linking peptidoglycan Gram + sensitive to B-lactamases

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4
Q

Define penetrance

A

the percentage of individuals with given genotype who exhibit the phenotype associated

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5
Q

What are symptoms of endocarditis?

A

FROM JANE Fever Roth Spots Osler’s Nodes Murmur Janeway Lesions Anemia Nailbed hemmorhages Emboli (septic)

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6
Q

Chest Pain Heart failure Abnormal heart rhythms “flu-like” illness

A

Myocarditis

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7
Q

What bugs causes Myocarditis?

A

Coxsachievirus B Adenovirus

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8
Q

Chest Pain Tachycardia 3-COMPONENT FRICTION RUB EKG Changes

A

Pericarditis

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9
Q

What bugs cause pericarditis?

A

COX A and B Echovirus Influenza

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10
Q

Rank the most common organisms that cause endocarditis?

A

Staph aureus Strep Viridans Enterococus Species Strep pyogenes

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11
Q

Which pathogen is associated with IV drug use?

A

Staph

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12
Q

What do pathogenicity islands usually contain?

A

Methicillin resistance

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13
Q

Where does strep viridans normally reside? Is it normal flora?

A

Yes, in the oral cavity

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14
Q

What bug is a common cause of endocarditis after GI or OB procedure?

A

Enterococcus Species

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15
Q

Describe the pathophysiology and relationship between bacterial endocarditis and heart murmurs?

A

Colonization of mitral valve –> mitral valve regurgitation –> turbulent flow –> murmur

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16
Q

What are the disadvantages of using TEE to visualize heart valves?

A

Swallowed probe More expensive Higher risk

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17
Q

Describe the relationship between endocarditis and stroke

A
  • Vegetation (clumps of bacteria + mesh of fibrin) can break off the valve and travel to other parts of the body, blocking flow
  • Risk of embolization is the highest during the first week of therapy, and in patients with mobile vegetations or >10 mm in diameter occurin on the mitral valve
  • Endocarditis can also lead to hemorrhaging in the brain and other parts of the body via septic erosion of arterial walls
  • Overalll, stroke risk in patients with endocarditis is 9.1% in the 12 months after diagnosis
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18
Q

What is the mechanism for tPA? Risks? Benefits? Contraindications?

A

Converts plasminogen to plasmin which degrades fibrin clots

Benefits = increase functional independence without affecting mortality at 3-6 months if given with in 3 hours

Risks= intracranial hemorrhage within the first 7 days after administration

Contraindications = suspected/confirmed endocarditis, intracranial hemmorhage, neuro surgery, head trauma, stroke in past 3 months, uncontrolled hypertension

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19
Q

What is the difference between stable and unstable angina?

A

Stable angina = chest pain that arises with exertion or emotional stress

Unstable = chest pain that occurs at rest

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20
Q

What is prinzmetal angina?

A

episodic chest pain unrelated to exerction

Due to coronary artery vasospasm

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21
Q

What are the clinical features of an MI

A

Severe, crushing chest pain, lasting >20mins that radiates to the left arm or jaw

Diaphoresis

Dyspnea

Symptoms are NOT relieved by nitro

22
Q

What causes a myocardial infarction?

A

Usually due to rupture of an atherosclerotic plaque with thrombosis and COMPLETE OCCLUSION of a coronary artery –> result in necrosis of myocardium and cell death

23
Q

What is the most common artery involved in MI?

A

LAD - causes infarction of the anterior wall and anterior interventricular septum

24
Q

Toponin I

A

most sensitive and specific marker for MI

Rise 2-4 hours, peak 24, return by 7-10 days

25
What is lab marker is good for looking at re-infarction?
Creatine Kinase MB Goes up and down quickly
26
WWhat is the acronym for motivational interviewing?
O-open ended questions A- affirmation R- reflective listening S- summarize
27
What are two complications of therapies for MIs?
Reperfusion injury- free radical further damages myocytes Calcium inlux that leads to hypercontraction of myofibrils = contraction band necrosis
28
What are the microscopic changes seen in MI?
1 Day- coagulative necrosis 1 week- Inflammation (neutrophils and MACs) 1 month- healing (granulation tissue, fibrosis)
29
LDL receptor genetics? for hypercholesteremia
Autosomal Dominant CHanges in LDL receptor gene
30
Treatment for an MI?
Aspirin and/or heparin/eptifibatide: limits thrombosis Morphine: pain Supplemental O2: minimize ichemia Nitrates: vasodilates B-blocker: slows heart, decreases O2 demand and risk for arrhythmia ACE inhibitor: decreases LV dilation Fibrinolysis or angioplasty- open blocked vessel
31
Describe Heart sounds
S1 (lub)- closure of the tricuspid and mitral valves S2 (dub)- closure of the pulmonary and aortic valves S3- normal in children, ventricular dilation (systolic ventricular failure) S4- low ventricular compliance
32
Define locus heterogeneity
Is a single disorder, trait, or pattern of traits causes by mutations in multiple genes at different chromosomal loci
33
Describe the pathogenesis of atherosclerosis
* Damage to the intima * Lipid deposits in the intima * Lipids become oxidized in intima * Macrophage and neutrophils become filled with fat in intima * This is called a foam cell/ fatty streaks * Then there is smooth muscle migration, proliferation, and extracellular matrix deposition * This forms a fiberous plaque NOTE\* Necrotic Lipid core, covered by a fibromusclar cap!
34
Modifiable risk factors for atherosclerosis
Hypertension Hyperlipidemia Diabetes Smoking
35
Non-modifiable risk factors for atherosclerosis
Age Genetics Gender
36
What is a thoracic aneurysm and what is it usually caused by?
balloon like dilation of the thoracic aorta Due to weakness in the aortic wall usually caused by tertiary syphilis * tertiary sphilis = endarditis = inflammation of small arteries (including vaso vasorum) * Decreased blood flow to the media and adventia * Weakening of wall
37
What are common compliations of a thoracic aneurysm?
Dilations of the aortic valve root (leads to aortic valve insufficiency) Compression of mediastinal structures as it balloons Thrombosis or emobli (disruption of laminar blood flow)
38
Abdominal Aortic Aneurysm is usually caused by...
Atherosclerosis Usually below renal artiers, and above bifurcation Thickening of wall - decreased O2 perfusion - atrophy of media and adventia - weakening of blood vessel wall
39
Describe the pathophysiology of acute aortic dissection
= intimal tear with dissection of blood through media of the aortic wall Usually occurs in proximal 10 cm of the aorta Need two things * stress (like the proximal 10 cms) * Pre-existing weakness of the media (usually caused by HTN) * HTN causes arteriolosclerosis of vaso vasorum * Decreaed perfusion to media * Media atrophy/weakening
40
Results of acute aortic dissection? Symptoms?
Descending- will compress the renal arteries Ascending- cardiac tamponde - sudden death Symptoms: Sharp, tearing chest pain, that radiates to the lower back
41
Raynauds phenomenon? And what are the color changes due to?
Type of peripheral artery disease characterized by decreased blood flow to skin due to arteriolar vasospasm in response to cold temps or emtional stress. White = vasoconstriction & ischemia Blue = tissue hypoxia and cyanosis Red= rewarming and reperfusion
42
Candidate Gene approach
Case control approach Looking for statistcal association between specific gene variant and disease of interest
43
Linkage Analysis
Family-based approach Look for pre-specified gene markers in highly variable in DNA regions. Those found more common in diseased members are said to be linked to the causative gene. Then pursued with fine mapping
44
Genome Wide Association Studies
SNPs are genotyped across the entire genome in subjects with and without the disease. SNPs that differ in frequency between cases in comparison with controls are "associated" with disease
45
Define Syncope
Transient loss of consciousness secondary to cerebral hypoperfusion characterized by rapid onset, short duration, and complete spontaneous recovery
46
What are the three classifications of syncope?
Neurally mediated Cardiogenic Autonomic dysfunction
47
Describe neurally mediated (reflex) syncope
Vasovagal- need precipitating event Situational- happens after coughing, sneezing, peeing, pooping, exercising, etc. Carotid sinus syncope- shaving, massage, others
48
Describe cardiogenic syncope
hypoperfusion to the brain due to an arrhythmia, structural disease,
49
Describe syncope due to autonomic dysfunction
Can be primary autonomic failure: lewy body disease, parkinson OR Secondary: Diabetic or amyloid neuropathy, spinal cord injury (Includes orthostatic hypotension)
50
How long do you have to be arrhythmia-free before driving according to the american heart association?
6 months
51

CRRAB FINAL REVIEW (12 decks)

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