Aneurysms & Cardiac Tumors Flashcards

1
Q

Aneurism Definition

A

Ireversible dilatation of a segment from vascular system when there is weakness in wall

Arterial or Left Ventricle

Left ventricle

After MI, region heals with fibrous patch

fibrous patch will buldge out

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2
Q

Types of Aneurism

3

A

True aneurysm

The aneurism is delimited by vessel walls

BLOOD IS IN CV SYSTEM

False aneurysm

There is acumulation of blood between the wall of the artery and the surrounding tissues

Ex: ventricle after MI

BLOOD IS OUTSIDE CV SYSTEM

Dissection

If media is weak and there is a intimal tear, blood will enter in the wall of artery and it will move proximaly or distaly dissecting the blood vessel

It was called disecting aneurism, now is caled disecting hematoma

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3
Q

General complications of Aneurysm

A

Thrombus formation

Embolism

  • The blood that is traped in dilatation is not normal, blood will be stagnant
  • =>hypercoagulability
  • => Thrombogenous
  • => Thrombembolism
  • =>Clog smaller artery

Infection

Bacteria can enter the aneurysm and weaken aneurism wall, can lead to rupture

Impingment on surrounding organs

Esophagus (dysphagia)

Recurent laryngeal nerve

Ureterus

Rupture

Berry rupture

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4
Q

Laplace Law / Wall weakness (causes)

A

Laplace law

Tension in wall (T) is direct proportional with presure(P) in sphere and the radius (R)

T=PxR

Weakness in wall causes R to increase, where from it is a positive feedback

Causes of wall weakness

Atherosclerosis

Disease of intima (response to chronic injury with formation of fattyfibrous plaques)

The fibrofatty plaques from intima presses against muscularis ade produces ischemia, and the wall of the artery will be weakened

Turn-Over

  • Colagen and elastic tissue has a Turn-Over
  • There are cases where this Turn-Over is alterd
  • Ex:(Cystic medial degeneration) -There are cyst formed in the vessel wall that contain amorphous substance

Trauma

  • When the trauma is biger that the elastic tissue can withhold
  • Near ligament arteriosum trauma due to severe decelerating
  • Due to injury at brachial artery and brachial vein fistula may form

Vasculitis

  • Antigen-antibody complex present in arterial wall
  • Antibody will actiuvqte complement and celular imunity that will damage media
  • Ex: Polyarteritis nodosa

Congenital causes

  • Marfan Syndrome
  • Berry Aneurysm (Circle of Willis)- Sacular aneurysm

Mycotic aneurysm

  • Infection
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5
Q
A

Sacullar aneurysm

If small (berry)

Fusiform aneurism

Cylindroid aneurysm

Circoid Aneurysm

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6
Q

Differnt types of Aortic Aneurysm

Syphilitic aortic aneurysm

OBLITERATIVE ENDARTERITIS

AAA

Causes

Classification

Complications

A

90% abdominal

10% aortic

Syphilitic aortic aneurysm

Likes the root of aorta (may see atheroma plaques in the aorta (only with syphilis)

=> In tertiary stage (1o chancre 2o treponemia 3o after 10-40 years Neurologic, CV complications)

ALSO CALLED LUATIC ANEURYSM - caled like this because patiaent may develop psychosis (lunatic)

Diameter of

  • Aorta at root is 3-3,5 cm
  • Abdominal Aorta 2 cm

O2 suply to intima is from lumen

Adventitia and media have own blood suply (VASA VASORUM)

=> In 3o syphilis there is immune mediated damage of VASA VASORUM => Lymphocytes and plasma cells around blood vessel, and

  1. compress against the blood vessel
  2. GF are sythetised and endothelium will ploriferate, and scars will form and intima will wrinckle ( tree barking )

Condition called OBLITERATIVE ENDARTERITIS -

  • adventitia and media turn over will be afected
  • => less extracelular matrix
  • => aorta recoil will be afected and aorta is going to baloon out
  • => syphilitic aneurysm formed.
  • =>Compression
  • => Esophagus (dysphagia)
  • =>Recurent laryngear nerve (brassy cough / hoarsnes of voice)
  • => Bony pains due to erosion of bones
  • => Respiratory chanell (Dyspnea / Stridor)
  • =>Scarring (due GF)
  • Tree barking
  • Scars around the coronary osteal stenosis
  • =>If Aneurysm extends towards aortic valve
  • =>it will stretch the anulus, and valve leaflets will close insufficient
  • Heart will be dilated and hypertrophy
  • Condition was called COR BOVINUM because it looks like a cow heart
  • Systolic up / dyastolic down (because blood can not be held back
  • Heart will be hyperdinamic
  • Blood wil go to head and then fall back in heart this will cause the head to blob with every cardiac systole and carotid will be dancing (Corrigan’s sign) and Quinke sign will be present

If Luetic Aortic Aneurysm ruptures then death will come from other cause

AAA

  • More common in Males smokers 50+
  • Most are Infrarenal
  • May extend in the common iliac area
  • Diameter of aorta >3cm
  • Pathology found accidentaly at xray calcification (but not present always) or ultrasound
  • Presents as PULSATILE MASS THAT IS EXPENSILE (extend with each systole)

CAUSES

Atherosclerosis

Posterior wall is hammered with every pulse to vertebral column => intima stressed out => atherosclerosis => 2o changes in media and adventitia.

Hypertension

Abnormal Turn-Over of conectivce tissue in aorta

Overactive MMP - MatrixMetaloProteinase enzyme (they digest connective tissue in aorta: colagen, elastin, Fibronectin, Proteoglycan

Tissue Inactivator of MP (TIMP) - underactive (this enzyme inactivates MMP

CLASSIFICATION

1. Inflamatory AAA

Wall heavily infiltrated with immune cells : macrophages / plasma cells / giant cells => produce GF => lead to periaortic fibrosis

2. Mycotic AAA

Infection starts in the wall

Most common Organism in

  • Salmonela
  • Streptococus
  • Staphylococus aureus

COMPLICATIONS

1.Compress Ureter

-hydronephrosis

2.Compress Vertebral Body

-bony erosions

3.Compress surounding artery

  • Mesenteric
  • Renal
  • Iliac
  • Vertebral Artery (spinal cord damage)

4. Embolism

  • Mural thrombus may form and embolise
  • If poplipteal aneurysm is found thatn AAA is a great posibility
  • If they have AAA atherosclerosis it is most likley that the patient has carotid and coronary

5. Rupture

  • Posterior
  • Retroperitoneal
  • Anterior
  • Peritoneus
  • pain
  • Rapid progresing shock
  • Important to operate unruptured AAA >6mm High risk of rupture, if less monitor the patient
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7
Q

Aortic dissection ( dissecting hematoma )

what is it?

how does it form?

how can it progress?

What causes?

What are the Complications?

  1. Origin of disection
  2. Progresion of dissection
    • Proximal (becks triade)
    • Distal

Clinical Presentation

Investigation

Rx

A
  • Intimal tear in aorta
  • jet of blod protrudes to media and progreses
  • creates pseudochannel and cavity in the wall of aorta

If Lucky

the wall will rerupture within the lumen

If not Lucky

Causes

The wall rupture outside

1. Man 50years / hystory of hypertension - (strongest association)

2. Young patient with Systemic or Localised abnormality of conective tissue

Ex:

Marfan Syndrome

  • mutant protein (fibrilin - scafold for elastin) in conective tissue : Elastin is fragmented => Cystic (no true cyst - cyst= fluid cavity delined by epithelium) changes in Media
  • skeletal abnormalities
  • CV abnormalities
  • ocular

Esller Danlos

3. Pregnancy: extend in coronary area, don’t know why

4. Iatrogenic: cathether induced trauma

5. Coarctation of Aorta

  • abnormal dynamics

Complications

1. Origin of disection are near the ostium of aorta (ascending part) or after subclavian branch, because there is where the blod hits and aorta is less mobile

A. Starts in ascendent aorta, goes proximal or distal just a bit

A. Starts in ascendent aorta, and goes through the wall of arch or goes far

B. Starts after subclavian branch and goes distal

90 % of patients who have type A, die at 1 month

2.Progresion of Dissection

Proximal

  • Can rupture and get in pericardial sac => Becks Triad
    1. JVP increased
    2. Distant hard sound
    3. Low blood presure
  • Can go through the media of a coronary, and can compress the origin of coronary
    • Major clinical complication
    • Prefer the origin of Right corronary => inferior MI
  • Can get through the sprue of aortic valve => Severe Acute Regurgitation

Distal

  • Can extend Common branch
    • Unequal pulses (right fall) or pressure
    • IF SOMEONE COMES WITH TIPICAL DISSECTION PAIN TAKE PULSES
  • Can extend to comon carotid
    • Hemiplegia
  • Extend towards Anterior spinal artery
  • Extend abdomen Renal .A
  • Extend to Mesenteric A. (central abdominal pain
  • Rupture in Pericardium / Pleura / Peritoneum (rapidly progress to shock)

Clinical

Sudden severe excruciating cutting chest pain that radiates backward rapid progressing !!! SHARP PAIN (MI dull, radiate left arm maxila etc)

Investigation

  1. Transesophageal Ecocardiography
  2. Dynamic CT Scan
  3. MRI

What is the most available and done fast

!!!CXR!!! - widen of mediastinum (only 10 %)

ECG

  • Normal
  • LVH (hypertension)
  • INF MI

Rx

110 systole keep tension (KEEP TENSION DOWN!!!)

IV Nitropruside / Nitropruside / Esmolol /Labetolol

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8
Q

Cardiac Tumors

Primary cardiac tumors

  • describe them
  • what tisues are they from
  • when they apear
  • what clinical manifestetion they produce
  • Carney’s syndrome:
  • Define Hamaltoma
  • Define Constitution symptoms

Secondary cardiac tumors

  • what are they
  • what they will cause

INVESTIGATIONS

A

Primary cardiac tumors

Atrial myxoma (most comon primary cardiac tumor)

  • In left atrium from fosa ovala
  • Pedunculated
  • Gets stuck in Mitral Valve
  • Jelly like, globular, pedunculated material
  • Primitive multipotential mesenchimal cells (conective tissue)

Produce IL6 => Acute fase reaction proteins from liver (Il1, Il6, TNF alpha) => increase ESR => hypothalamus (interfere with weight regulation mechanism)

Clinical

1. Position dependent, intermitent obstruction to mitral valve (may resemble mitral valve stenosis) => syncopal atack “syncope = transient loss of consciuosnes due to transient global ischemia to cerebral cortex”

2.Constitution symptoms (low grade fever / malaise / weight loss / chills / night sweats / and decreased appetite. !!!!!!!! MANY TUMORS PRODUCE CYTOKINES THAT ACT ON LIVER THAT ACT ON HYPOTHALAMUS

3.Embolisation - rupture and embolise and causes stroke

Carney’s syndrome:

  • Myxoma autosomal Dominant,
  • Famiial
  • Exxtracardiac: SKIN

Rhabdomyoma

  • Most common primary tumor in children
  • Tumor of myocardial tumor
  • APOPTOSIS deficient during developement of myocardial chambers,
  • They are hamaltoma’s Are congenital malformations (abnormal arhitecture of tissues due to abnormal development)
  • Associated with TUBEROUS SCLEROSIS

Secondary cardiac tumors

More common

  • Metastasis
  • Direct Extension
  • Pleura
  • Lung carcinoma
  • Breast carcinoma

Will cause

  • Hemoragic Pericarditis
  • Pericardial Effusion

Investigation

Left atrium best seen with Transesophageal Ecocardiography (LEFT ATRIUM IN FRONT OF THE ESOPHAGUS)

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