Pain- Abdominal and chest and past quizlet q's Flashcards

1
Q

Describe the degeneration of the aorta over time

A

With age, the elastic component degenerates and collage becomes more prominent, which stiffens arteries and increases systolic BP

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2
Q

What is an aneurysm

A

Diameter of the artery is 1.5x or greater of its normal size (increase of 50%).

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3
Q

True vs pseudoaneurysm

A

True: Involves all 3 layers
Pseudoaneurysm: Contained rupture of the vessle wall that develosp when blood leeks out of vessel wall to the intimal and medial layers, contained by adventitia

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4
Q

Fusiform vs saccular aneuysm

A

Fusiform- Symmetrical, both sides are dalated
Saccular: Unilateral outpoutch

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5
Q

Causes of aneurysms

A
  1. Genetic- inherited connective tissue disorders affecting ascending thoracic aorta
    Medial degeneration/necrosis with loss of elastic fibers/collagen/smooth muscle that are replaced by mucoid material
  2. Artherosclersosis- descending thoracic and abdominal aortae- plaque buildup that causes hypoxia and muscle atrophy
  3. Infection- Tertiary syphilis
  4. Vasculitis
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6
Q

Which 2 genetically inherited disorders predispose you to an abdominal aneurysm

A

Marfan’s syndrome
Ehlers-Danlos syndrome

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7
Q

Which infection is tied to abdominal aneurysms

A

Tertiary syphilis (inflames vaso vasorum and causes fibrosis)
Mycotic aneurysm from bacteria that embolizes and weakens wall

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8
Q

What are the holosystolic murmurs

A

Mitral regurgitation
Tricuspid regurgitation
VSD
Murmur that occurs during the entire systolic phase of the cardiac cycle

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9
Q

Know the characteristics of mitral regurgitation
- Location
- Radiation
- Pitch
- Causes

A

HOLOSYSTOLIC MURMUR

Location: Apex
Radiation: to axilla
Pitch: High pitched, blowing murmur

Causes:
- Ischemic heart disease
- Mitral valve prolapse
- Rheumatic Fever

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10
Q

Describe the murmur of Mitral prolapse. In what patient position is it best heard? What is its location?

What is the reason for this murmur occurring?

A

Often associated with regurgitaion of blood (SYSTOLIC MURMUR)

*Associated with a systolic click and a late systolic murmur

Best heard in the L lateral decubitus position

Location: Cardiac Apex (with the diaphragm)

Reason: caused by the mitral valve leaflets bulging into the LA (click) when the ventricles contract

Myxomatous degeneration of the mitral valve leaflets

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11
Q

What are the sxs of mitral valve prolapse? What are the complications?

A

Usually asx

can have palpitation or chest pain

Also dyspnea or dizziness

Complications:
- arrythmias
- heart fialure
- endocarditis

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12
Q

Besides tricuspid and mitral regurgitation, what conditions would you hear a holosystolic murmur with?

A

Ventricular Septal Defects (VSD) = congenital abnormality causing blood to flow b/w L and R ventricles through a hole in the ventricular septum
Location: Heard b/w the 3rd/4th intercostal space along sternal border

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13
Q

Know the characteristics of tricuspid regurgitation
- Location
- Radiation
- Pitch
- Causes

A

HOLOSYSTOLIC MURMUR

Location: Lower LEFT sternal border

Radiation: to RIGHT sternal border

Pitch: High pitched, blowing murmur

Causes:

  • Infective endocarditis
  • Rheumatic Fever
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14
Q

What is rib notching?

A

increased circulation seen between intercostals on xray due to increased collateral flow (coarctation of the aorta)

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15
Q

What is the most common type of aortic aneurysm

A

AAA is more common than TAA (70% to 30%)
Risk of rupture is porportional to size, mortality is very high with rupture

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16
Q

Clinical presentation of AAA? How are most found, sx, and PE findings

A

Majority are discovered incidentally on PE or on radiographic imaging.

Most patients are asx, can have back or flank pain. If ruptured, have hypotension and shock.

Physical findings:
Pulsitile, palpable mass on abdominal exam
Occasionally an abdominal or femoral bruit

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17
Q

Diagnostics of AAA

A
  • Abdominal Ultrasound measures size and growth. Does not visualize branched vessels well
    -CT aortography and MRI gives size and visualizes vessels.
    -Aortography does not accurately measure size and is invasive
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18
Q

What population is recommended to have an AAA screening done?

A

+ use of tobacco in men over 65 or older, risk factor modification with aggressive control of lipids and blood pressure, smoking cessation

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19
Q

Chest x-ray: know the reasons for a widened mediastinum and water bottle heart

A

Widened Mediastinum = AORTIC DISSECTION

Water bottle heart = big cardiac silhouette from fluid = pericardial effusion

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20
Q

What drugs decrease rate of enlargement and risk of rupture in AAAs

A

Beta Blockers

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21
Q

Know the difference between a left and right heart catheterization

A

RIGHT: Venous access

  • Intercardiac pressure (check fluid, good CO measurement)

LEFT: Arterial access

  • Inject dye
  • Look at vessels
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22
Q

TEE Indications?

A

Transesophageal echocardiogram to look at valves better

  • Gives better image of LA appendage - blood clot?
  • Vegetations (endocarditis) or abscess
  • Aortic dissection
  • ASD or PFO
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23
Q

Describe EVAR

A

Endovascular Aortic Repair (EVAR): Invasively place a stent-graft under fluoroscopy over the aneurysm.

Surgery:

Requires resection of the aneurysmal segment and replacement with a Dacron tube graft inserted in place of the diseased aorta. The major branches are then reimplanted to the graft.

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24
Q

How do you repair a TAA?

A

Thoracic endovascular aortic repair (TEVAR):
- reserved for TAA patients at too high a risk of open repair
- Complications: occlusion of branch arteries + endovascular leak

Surgery:

  • Dacron tube graft
  • If there is extension to the aortic valve, then a prosthetic valve will need to be performed
  • As with all open heart surgeries, a coronary angiogram should be performed prior in case they need bypass
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25
How fast do aneurysms usually grow? What is the risk of rupture? Mortality rate?
Rate of enlargement is typically ~0.2 - 0.3 cm per year Risk of rupture is proportional to size. Aneurysms > 6 cm have a > 20% chance per year of rupture whereas those between 5-6 cm have a 6% chance Mortality is very high with rupture: 25% die in the field and 50% die prior to surgery once in the hospital. The remaining survivors have a 50% operative mortality
26
Be familiar with statins - high, mod, low intensity regimens - dosing for each - LDL Reduction % for each
HIGH INTENSITY statins are those that can lower LDL by 50% or greater - Atorvastatin 40-80 mg OR Rosuvastatin 20-40 mg MODERATE INTENSITY statins can lower LDL by 30% to 49% - Atorvastatin 10-20 mg OR Rosuvastatin 5-10 mg - Simvastatin 20-40 mg OR Pravastatin 40-80 mg LOW INTENSITY statins lower LDL < 30% - Simvastatin 10 mg OR Pravastatin 10-20 mg
27
How do statins lower cholesterol? - MOA - LDL Reduction % (generally)
Statins inhibit the rate limiting enzyme responsible for cholesterol biosynthesis. The resulting reduction in intracellular cholesterol concentration promotes increased LDL receptor expression which results in augmented clearance of LDL from the blood Reduction averages 20-60%
28
What are the Pleiotropic Effects of statins?
- Improvement in endothelial dysfunction - Antioxidant and anti-inflammatory properties - Plaque stabilization by reducing lipid content
29
Know how to diagnose TAA symptoms, medications used, and when to perform surgery
Presentation: - Mostly asx - Cough or dyspnea if compress trachea - Dysphagia if compress esophagus - Hoarseness if presses against the recurrent laryngeal nerve PE: - Possible aortic valve regurgitation murmur - signs of heart failure if aortic root is dilated Diagnosis: - Occur between the root and diaphragm - Chest X-ray can show a widened mediastinum (aortic dissection or aneurysm) - CTA and MRA provide excellent visualization - Aortography - Transesophageal echocardiogram (see aorta and posterior heart) Treatment: - Repair again is at 5.5 cm or greater → TEVAR or surgical repair - Patients with sxs or underlying medial necrosis disorders can be considered for earlier repair given the faster rate of expansion and risk of rupture - Risk factor modification - Tight BLOOD PRESSURE CONTROL + beta blocker
30
How do you repair a TAA?
Thoracic endovascular aortic repair (TEVAR): - reserved for TAA patients at too high a risk of open repair - Complications: occlusion of branch arteries + endovascular leak Surgery: - Dacron tube graft - If there is extension to the aortic valve, then a prosthetic valve will need to be performed - As with all open heart surgeries, a coronary angiogram should be performed prior in case they need bypass
31
Know the difference between hypertensive emergency and urgency
Severe blood pressure is generally defined as > 180 mmHg systolic or > 120 mmHG diastolic EMERGENCY: severe blood pressure WITH evidence of end organ damage URGENCY: severe hypertension WITHOUT end organ damage
32
What are signs of End Organ Damage?
Brain - Encephalopathy or signs of stroke/intracerebral hemorrhage (CT scan) Eye - Retinopathy (fundoscopic exam) Heart - Evidence of damage to the heart including ischemia (troponin leak, EKG changes) and heart failure (echo to assess LV, chest x-ray and BNP for pulmonary edema, elevated JVP) Kidney - Renal damage as evidenced by elevated creatinine or proteinuria/hematuria Aortic dissection
33
How do you treat hypertensive emergency?
- Admit them to the ICU - Give them drugs via IV line (CCB, BB, nitrates, direct vasodilators) Goals: - Reduce MAP by NO MORE THAN 25% in the first few hours - If stable, lower to a goal of 160/100 within the next 2-6 hours - Add oral agents and wean off IV meds **If lowered too quickly, hypoperfusion can occur and lead to irreversible ischemia and neurologic damage
34
What is an aortic dissection?
Occurs when there is a tear in the intima resulting in separation of the intima from the media. This creates two passages for blood; the TRUE LUMEN and a second, “FALSE LUMEN” in the media Patients describe their pain as "tearing" If there is too much blood in the false lumen, it can block off the true lumen
35
What are the 2 biggest risk factors for Aortic dissection
Age and Hypertension
36
Where is aortic dissection most commonly
ascending (65%), then descending (20%), aortic arch (10%), abdominal aorta (5%)
37
What are the types of classifications of dissection and risk factors
LOCATION: 1) DeBakey 1) Type I extends from the aortic arch and beyond b) Type II is confined to the ascending aorta c) Type III is in the descending aorta 2) Stanford - Type A involves the ascending aorta - Type B does not involve the ascending aorta (descending only) CHRONICITY: - Acute (< 2 weeks from onset) - Chronic (> 2 weeks from onset)
38
What is the presentation of both types of Aortic Dissection?
MUST NOT MISS DX Proximal dissections have chest pain (80%) that is severe and TEARING in description. It may radiate to the BACK interscapular area (47%) or abdomen (21%) Descending aortic dissections have BACK pain (64%), abdominal pain (43%), and chest pain (63%)
39
How do you diagnose an Aortic Dissection?
- CTA (angiography) and MRA(angiography) having the highest sensitivity and specificity. - D-dimer - Radial pulse equality - A chest x-ray can have a widened mediastinum but lacks sensitivity. - Aortography is excellent to visualize the true and false lumen but is invasive. - EKG to r/o ACS
40
Based on the classification naming system of aortic dissections, what is the highest percent of aortic dissection types
DeBakey 1/Stanford A proximal are 60%
41
Management for type A and B dissection
Proximal (type A) aortic dissections - IMMEDIATE SURGERY (repairing intimal tear, suturing the edges of the false channel, and possibly inserting a synthetic aortic graft) Type B aortic dissections with evidence of end organ damage or progression of the dissection: - Has torn into renal or mesenteric a. for example - Surgical management Uncomplicated distal (type B) dissections without end-organ damage - Medical management Priority of therapy starts with REDUCING AORTIC WALL stress (which is affected by the velocity and rate of ventricular contraction as well as blood pressure). Medical stabilization therefore targets a REDUCTION of HEART RATE < 60 bpm and BLOOD PRESSURE < 120 mmHG systolic
42
How do we medically manage aortic dissection?
First Line Agents are IV Beta Blockers: - Labetalol - Esmolol Second Line Agents are IV nondihydropyridine Calcium Channel Blockers: - Verapamil - Diltiazem If blood pressure is not at goal can add IV ACE inhibitors or vasodilators (potentially can increase shear stress)
43
What are the Postoperative surveillance guidelines for aortic dissection?
What are the Postoperative surveillance guidelines for aortic dissection?
44
What is PAD?
Lesion that limits blood flow in non-coronary artery that provides blood supply to the limbs or an organ Peripheral artery disease
45
What are the causes of PAD
Arterial occlusion from atherosclerosis/stenosis or thromboembolism
46
Risk factors for PAD
-Smoking, diabetes, HTN, Hyperlipidemia
47
Prevelance of PAD
15-20% of the population over 70
48
Pathophysiology of PAD
Adenosine and NO vasodialate arterioles, and in PAD, artherosclerotic endothelium does not release vasodialators and obstructed arteries don't respond to vasodilating stimuli Muscle fibers undergo denervation and lead to decreased strength and atrophy
49
Classic symptom of PAD
Claudication Exertional limb fatigue and pain that is relieved with rest Amount of exercise required to precipitate the pain is related to severity of the stenosis Area of pain is a small area below stenotic artery
50
If you suspect that your patient has PAD, which artery is stenotic if they have pain in their butt/hips/thighs? Their Calves? Their Arms?
- Distal aorta and iliac artery - Femoral and popliteal arteries - Subclavian or axillary arteries
51
PE for PAD
- Peripheral pulses- check bilateral to see if there is weakness on either side - Brurits on abdomen - Wounds and ulcers - CV exam, assess carotids - BP in both arms
52
DX for PAD
Diagnostics: - ANKLE-BRACHIAL INDEX: a measurement of LE perfusion which compares the blood pressure in the pedal artery with the higher of two brachial artery blood pressures - ARTERIAL DUPLEX U/S: Blood flow velocity increases through a stenotic lesion. Using doppler, the U/S is able to measure systolic and end diastolic velocities and determine the degree of stenosis. - ANGIOGRAPHY: gold standard to diagnose arterial disease. Reserved for those who will undergo peripheral revascularization or other studies were non-diagnostic. - CTA and MRA
53
Which test determines the degree of stenosis in PAD
Arterial Duplex Ultrasound- blood flow velosity increases through a stenotic lesion
54
Treatment for PAD
-Exercise therapy- 1st line non-pharmacologic treatment. Walk until they feel claudication pain, and then rest until no more pain, and then do it again. - Pharmacology - Bypass surgery
55
Pharmacological management of PAD
- Asprin or Clopidogrel (plavix) - It's recommended that all sx pts with PAD should be on these OR - Cilostazol (Pletal)-- Suppresses platelet aggregation, vasodilator. Increases exercise capacity and sx.
56
If you have a SX PAD patient who does not have CAD, what is the first line treatment
Cilostazol (Pletal), which helps PAD sx, but does not target CAD
57
If you have a PT with SX PAD and CAD, what treatment is best?
Clopidogrel or asprin-- to target CAD, but not Pletal/Cilostazol because they do not target CAD.
58
Revascularization indication
Indicated for lifestyle limiting claudication after failed medical therapy Also when the pt has ulcerations, gangrene, and to avoid limb loss if they do not have blood flow to the area and have to get it to heal. Percutaneous innervation: Success depends on length, put in stent. Patent for 1 year. Surgical:Bypass long segments of disease with grafts.
59
Cause of Acute arterial occlusion
Embolization from heart or vascular site, or thrombus formation Embolization from venous circulation that arrives at arterial circulation through defect in atrial septal wall (PFO or ASD). Paradoxical embolism
60
Critical vs acute limb for acute arterial occlusion
Critical limb: still have SOME blood flow, not a lot, and need to revascularize-- Resting limb pain that results from severe disease and blood flow compromize. Ischemic ulcers and gangrene Acute limb: 100% occlusion due to no blood flow, emergency from abrupt occlusion of peripheral artery flow that compromizes viability of tissue, embolic event or arterial thrombosis. Severe pain, emergent revasculirazation.
61
6 P's in Acute arterial occlusion
PAIN - pain in limb PULSE - cant feel distal pulse) PALLOR - color change (Can get to be very purple after time) PARESTHESIA - numbness PARALYSIS - lose movement POIKILOTHERMIA -coolness to touch (no blood flow/occlusion)
62
Renal artery stenosis is associated with which disorders
HTN, Ischemic nephropathy Clues: Abrupt onset of HTN, previous well controlled HTN (remember, its a cause of secondary htn) Azotemia- elevated nitrogenous waste in blood Flash pulmonary edema(acutely SOB, increased hydrostatic pressure and edema)
63
What is a cause of flash pulmonary edema?
Renal Artery Stenosis causes hypertensive emergency → LV cannot squeeze → everything goes backward into lungs → flash pulm edema → hypoxia
64
TX for renal artery stenosis
Medical therapy-- Multiple drug agents, ACE-1, ARB, BB, CCB, Diuretics DO NOT use ACE-1 or ARB if bilateral RAS or solitary kidney d/t worsening kidney fx Percutaneous revascularization/surgical revascularization up next.
65
What is important to remember about the treatment of RAS with an ACE-I or ARB?
an ACE-I or ARB is SAFE to use if have unilateral RAS If have bilateral RAS or a solitary kidney, they are contraindicated
66
What is vasculitis
Restrict blood flow, cause ischemia. Vasculitis is vessel wall inflammation resulting from immune complex deposition or cell mediated immune reactions directed against the vessel wall = DAMAGE TO VESSEL WALL When it heals, it becomes fibrotic, creeps into lumen, creates flow limiting lesion
67
What are the large cell and medium cell vasculitis syndromes
Large cell: Giant cell arteritis (Temporal arteritis), and Takayasu arteritis Medium Cell: Kawaski, Thromboangiitis obliterans (Buerger disease)
68
Takayasu Arteritis - What vessel does it affect? - Demographic - Presentation - Diagnosis - Treatment
- LARGE VESSEL, Affects aorta and major branches (off arch) - Younger asian females 10-40 yo - Can cause aneurysms, ischemia, or dissection Presentation: - Claudication and “PULSELESSNESS” due to absence of carotid and limb pulses - Systemic complaints, malaise and fever. granulomatous inflammation with inflammation with lymphocytes and multinucleated giant cells Treatment: - Steroids and cytotoxic drugs may reduce inflammation - Surgical bypass of obstructed vessels is an option
69
If you have a young female with pulselessness, what disease does this instantly make you think of?
Takayasu arteritis
70
Giant Cell arteritis (Temporal arteritis) - What vessel does it affect? - Demographic - Presentation - Diagnosis - Treatment
- LARGE VESSEL - Most common vasculitis in FEMALES over age 50 - Associated with polymyalgia rheumatica - Affects medium to large sized vessels of the aortic arch or CRANIAL vessels Presentation: - Typically have diminished temporal pulses - HEADACHE - facial pain - impaired vision Diagnosis: - Confirmed by temporal artery biopsy Treatment: - high dose steroids for acute flares
71
Your 60 year old female patient presented complaining of a headache, facial pain, and claudication of the jaw, and imparied vision. What disorder are you considering
Temporal arteritis Check temporal pulses (deminished)
72
Diagnostic for Temporal arteritis
Ultrasound Temporal artery biopsy- need long specimen due to segmental patchy granulomas, could miss diagnosis Histology- shows granulomas and multinucleated giant cells
73
THROMBOANGIITIS OBLITERANS (Buerger's disease) - What vessel does it affect? - Demographic - Presentation - Diagnosis - Treatment
- SMALL TO MEDIUM VESSELS - Seen in men < 45 years of age and has a very strong association with smoking - Affects distal vessels of the upper and lower extremities - Arterial occlusion leads to claudication and ischemia of the digits Presentation = triad of sxs: 1) distal artery occlusion 2) raynaud phenomenon (vasospasm) 3) superficial vein thrombophlebitis Diagnosis: - tissue biopsy Treatment: - Stop smoking - Revascularization is not an option given the distal location of the disease
74
What is Raynaud Phenomenon? Presentation? Difference b/w primary and secondary?
Vasospastic disease of the digital arteries that occurs in susceptible people when exposed to cool temperatures or emotional stress Presentation = triphasic color response 1. WHITE → toes/fingers blanch to white as flow is interrupted 2. CYANOSIS → local accumulation of desaturated hemoglobin 3. RED COLOR → blood flow resumes White → blue → red + NUMBNESS, PARESTHESIAS, or PAIN Primary = Benign (exaggerated sympathetic discharge to stress/cold with heightened vascular sensitivity and release of vasoconstrictor stimuli) Secondary = underlying condition (sclerosis or inflammation from connective tissue disease (scleroderma or lupus) OR arterial occlusive disease), carpal tunnel syndrome or drug effect
75
Vasospasm differential commonly in arm
Thoracic outlet syndrome-- commonly causes blood clots in arms because of decreased blood flow
76
Tx for vasospasm
Avoid cold environments Dress in warm clothes Pharm agents (relax vascular tone) Calcium channel blocker Alpha adrenergic blocker Phosphodiesterase type 5 inhibitors