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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
Q

What is lab marker is good for looking at re-infarction?

A

Creatine Kinase MB

Goes up and down quickly

26
Q

WWhat is the acronym for motivational interviewing?

A

O-open ended questions

A- affirmation

R- reflective listening
S- summarize

27
Q

What are two complications of therapies for MIs?

A

Reperfusion injury- free radical further damages myocytes

Calcium inlux that leads to hypercontraction of myofibrils = contraction band necrosis

28
Q

What are the microscopic changes seen in MI?

A

1 Day- coagulative necrosis

1 week- Inflammation (neutrophils and MACs)

1 month- healing (granulation tissue, fibrosis)

29
Q

LDL receptor genetics? for hypercholesteremia

A

Autosomal Dominant

CHanges in LDL receptor gene

30
Q

Treatment for an MI?

A

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
Q

Describe Heart sounds

A

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
Q

Define locus heterogeneity

A

Is a single disorder, trait, or pattern of traits causes by mutations in multiple genes at different chromosomal loci

33
Q

Describe the pathogenesis of atherosclerosis

A
  • 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
Q

Modifiable risk factors for atherosclerosis

A

Hypertension

Hyperlipidemia

Diabetes

Smoking

35
Q

Non-modifiable risk factors for atherosclerosis

A

Age

Genetics

Gender

36
Q

What is a thoracic aneurysm and what is it usually caused by?

A

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
Q

What are common compliations of a thoracic aneurysm?

A

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
Q

Abdominal Aortic Aneurysm is usually caused by…

A

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
Q

Describe the pathophysiology of acute aortic dissection

A

= 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
Q

Results of acute aortic dissection? Symptoms?

A

Descending- will compress the renal arteries

Ascending- cardiac tamponde - sudden death

Symptoms:

Sharp, tearing chest pain, that radiates to the lower back

41
Q

Raynauds phenomenon? And what are the color changes due to?

A

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
Q

Candidate Gene approach

A

Case control approach

Looking for statistcal association between specific gene variant and disease of interest

43
Q

Linkage Analysis

A

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
Q

Genome Wide Association Studies

A

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
Q

Define Syncope

A

Transient loss of consciousness secondary to cerebral hypoperfusion characterized by rapid onset, short duration, and complete spontaneous recovery

46
Q

What are the three classifications of syncope?

A

Neurally mediated

Cardiogenic

Autonomic dysfunction

47
Q

Describe neurally mediated (reflex) syncope

A

Vasovagal- need precipitating event

Situational- happens after coughing, sneezing, peeing, pooping, exercising, etc.

Carotid sinus syncope- shaving, massage, others

48
Q

Describe cardiogenic syncope

A

hypoperfusion to the brain due to an arrhythmia, structural disease,

49
Q

Describe syncope due to autonomic dysfunction

A

Can be primary autonomic failure: lewy body disease, parkinson

OR

Secondary: Diabetic or amyloid neuropathy, spinal cord injury

(Includes orthostatic hypotension)

50
Q

How long do you have to be arrhythmia-free before driving according to the american heart association?

A

6 months

51
Q
A

CRRAB FINAL REVIEW (12 decks)

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