Morph Responses Of Cv System

Front 1

Part of heart most vulnerable to ischemia

Back 1

Subendocardium: inner 1/3 of the heart. It's the last portion to receive coronary blood flow.

Front 2

Coronary circulation consists of ____ major arteries and their branches

Back 2

Three

Front 3

Normally there is ____ capillary(ies) for ____ myocyte(s)

Back 3

1:1

Front 4

systemic hypertension, aortic valve stenosis would cause what changes in the heart?

Back 4

Caused elevated pressure --> concentric hypertrophy

Front 5

regurgitant valve, congenital shunt would cause what changes in the heart?

Back 5

Cause increased volumes in the chambers --> eccentric hypertrophy

Front 6

T/F in a normal heart slice there is very little interstitial connective tissue

Back 6

T

Front 7

Characteristic changes in nuclei in hypertrophied myocytes

Back 7

See enlarged, hyperchromatic nuclei with a boxcar shape.

Front 8

What are the cellular changes underlying cardiac hypertrophy?

Back 8

Synthesis of new contractile proteins and mitochondria, induction of fetal genes/enzymes.

Front 9

Causes concentric hypertrtophy

Back 9

pressure overload

Front 10

Concentric hypertrophy: defn

Back 10

heart chamber itself is same size but muscle wall has thickened.

Front 11

ECG changes in Concentric hypertrophy

Back 11

See increase in voltage due to thickening (more muscle)

Front 12

Eccentric hypertrophy: defn

Back 12

heart chambers are dilated, but the walls aren't much thicker.

Capillaries don't keep up with myocyte growth.

Front 13

Causes eccentric hypertrophy

Back 13

Too much volume

Front 14

T/F Most of the time, either the R or L ventricles fails, but not both.

Back 14

F.

Failure of right and left ventricles may occur separately but in most cases both ventricles fail.

Front 15

Physiologic consequences relate to failed right ventricle

Back 15

increased systemic venous pressure

Front 16

Physiologic consequences relate to failed left ventricle

Back 16

increased pulmonary venous pressure; decreased systemic perfusion

Front 17

Histologically, what's seen in the lungs in CHF?

Back 17

See thickening of alveolar septa. See macrophages with hemosiderin pigment (this is due to them phagocytosing extravasated RBCs that are present in lungs due to backup pressure). THese are the heart failure cells.

Front 18

What are heart failure cells?

Back 18

macrophages with hemosiderin pigment inside the alveolar septa. They've phagocytosed the RBCs that get into the lungs due to heart failing to pump good enough.

Front 19

What is nutmeg liver?

Back 19

Aka congestive hepatopathy.

It's changes in liver due to right sided heart failure. Chronic passive congestion of liver.

Front 20

In right ventricular failure, what happens to the kidneys?

Back 20

Get severe venous congestion of the kidneys which results in impaired perfusion, and salt and water retention.

Get azotemia (abnormally high levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood).

Will get peripheral edema.

Front 21

anasarca
: defn

Back 21

massive generalized edema

Front 22

Jugular venous distension reflects elevated (left, right) heart filling pressures

Back 22

Right

Front 23

Age related changes in mass and weight of heart

Back 23

Increased weight and mass. Due to myocyte hypertyrophy, possibly systemic htn.

Front 24

What age-related change can happen to the aorta and be functionally significant?

Back 24

Can see dilation of the aortic root, which can lead to valve insufficiency.

Front 25

Brown atrophy - defn

Back 25

1) Small heart size with
2) Lipofuscin deposition in myocardium

(Age-related change)

Front 26

Basophilic degeneration: defn

Back 26

Accumulation of glycogen metabolite in myocytes

Front 27

Transthyretin: what is it? significance in relation to cardio?

Back 27

serum and cerebrospinal fluid carrier of the thyroid hormone thyroxine (T4).

Can see depositions of it in the heart in amyloid disease.

Front 28

What are age-related changes to the cardiac valves?

Back 28

See calcification of the mitral annulus that may predispose to infection.

See aortic valve calcification that may result in aortic stenosis.

See fibrous thickening of the valve leaflets. (not usually functionally significant)

Front 29

What is the most important cause of vascular disease?

Back 29

Atheroscleroris. Hardening and plaque formation of arteries

Front 30

Difference between eccentric vs. concentric plaques

Back 30

Eccentric: involves only a portion
Concentric: involves entire intima

Front 31

What is the anatomy of the plaque?

Back 31

There's a fibrous cap, a lipid/amorphous core. This is touching the intima.

Front 32

condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol.

Back 32

atherosclerosis

Front 33

What's in the fibrous cap of the atheroma?

Back 33

The fibrous cap is a layer of fibrous connective tissue, which is thicker and less cellular than the normal intima. The fibrous cap contains macrophages and smooth muscle cells. The fibrous cap of an atheroma is composed of smooth muscle cells, macrophages, foam cells, lymphocytes, collagen and elastin.

Front 34

What's in the lipid/amorphous core of the atheroma?

Back 34

Lipid-laden macrophages (foam cells) and amorphous debris

Front 35

The fibrous cap is (under, above) the endothelium.

Back 35

Under, in the intima. The endothelium is still making contact with the lumen.

Front 36

What are the components of the cascade of events that occur which promote atheroma formation?

Back 36

Triggers like hyperlipidemia, smoking, and other stresses promote all of the events:

1) Expression of cell adhesion molecules that attract monocytes INSIDE the intima. These become activated macrophages that engulf oxidized LDL --> foam cells.

2) Smooth muscle cells migrate into the intima and proliferate in response to cytokine and GF release.

3) LDL comes into the intima and is oxidized and phagocytosed by macrophages.

4) Extra ECM is laid down.

Front 37

Fatty streaks: defn

Back 37

composed of macrophage white blood cells, not fat, is the term generally given to the earliest stages of atheroma.

irregular off white to yellow-white discoloration near the luminal surface of the artery. The streaks are not actually fat but small collections of monocyte-derived macrophages located beneath the inner, endothelial layer of arteries. The fatty streak mainly consists of foamy appearing macrophage cells, sometimes with some additional T lymphocytes, aggregated platelets, localized smooth muscle cells, etc. Fatty streaks may be precursor of atheromas and not all fatty streaks are destined to become fibrous plaques.

Can be seen even in young children!

Front 38

T/F Fatty streaks are destined to become plaques eventually.

Back 38

F. Some may resolve, and some may become plaques.

Front 39

Commonly affected vessels

Back 39

Lower abdominal (infrarenal) aorta.

Coronary arteries.

popliteal arteries.

Internal carotid (especially bifurcation).

Circle of willis

Front 40

What happens when the plaque calcifies?

Back 40

calcification of the plaque makes it very brittle and prone to breaking off

Front 41

What happens when there's a hemorrhage into the plaque?

Back 41

Expansion of the plaque

Front 42

What happens when the plaque ulcerates?

Back 42

The fibrous capsule is disrupted - can become embolized

Front 43

What are characteristics of a plaque that is VULNERABLE to rupture?

Back 43

An eccentric (partial thickness) plaque with a thin fibrous cap and a large lipid core

Front 44

What are characteristics of a plaque that is LESS VULNERABLE to rupture?

Back 44

Concentric (full thickness) plaque with a larger fibrous cap than lipid core. More stable and less likely to embolize.

Front 45

Arteriosclerosis: defn

Back 45

general term describing any hardening (and loss of elasticity) of medium or large arteries

Front 46

Arteriolosclerosis

Back 46

narrowing of small caliber vessels (arterioles)

Front 47

Arteriolosclerosis: two major forms

Back 47

1) Hyaline
2) Hyperplastic

Front 48

What is organ most affected by Arteriolosclerosis?

Back 48

kidney

Front 49

refers to thickening of the walls of arterioles by the deposition of homogeneous pink hyaline material.

Back 49

hyaline arteriolosclerosis

Front 50

What happens in hyaline arteriolosclerosis?

Back 50

There is leakage of plasma proteins and excessive ECM production.

Results in a narrowed lumen that impairs glomerular blood supply.

associated with aging, hypertension, diabetes mellitus

Front 51

What is hyaline arteriolosclerosis associated with?

Back 51

associated with aging, hypertension, diabetes mellitus

Front 52

Hyperplastic arteriolosclerosis: pathogenesis

Back 52

Can be caused by malignant hypertension. There is thickened concentric smooth muscle cell layer and thickened, duplicated basement membrane in the kidney.

Front 53

Hyperplastic arteriolosclerosis may be accompanied by _____ necrosis

Back 53

fibrinoid

Front 54

Which type of arteriolsclerosis is associated with an "onion skin" appearance? Why?

Back 54

Hyperplastic arteriolosclerosis. It's because there is duplicated basement membrane in the kidney arterioles.

Front 55

(Monckeberg’s) medial calcific sclerosis: defn

Back 55

Calcific deposits in the media of small to medium muscular arteries.

Front 56

In medial calcific sclerosis, the size of the lumen is not compromised. Why?

Back 56

Because the process is deposits in the MEDIA, not the intima.

Front 57

In what type of arteries does medial calcific sclerosis occur?

Back 57

Small to medium muscular arteries

Front 58

Vascular dilatation due to a weakened vessel wall

Back 58

aneurysm

Front 59

Syphilis is associated with what type of aneurysm?

Back 59

Ascending aorta and arch.

Front 60

Abdominal aortic aneurysm : typical patient

Back 60

Male over 50 with atherosclerosis

Front 61

Lines of Zahn: defn

Back 61

visible and microscopic laminations produced by alternating pale layers of platelets mixed with fibrin and darker layer containing red blood cells. Their presence implies thrombosis at a site of rapid blood flow that happened before death

Front 62

T/F Lines of Zahn occur in sites of sluggish blood flow

Back 62

F. Rapid blood flow.

Front 63

Where do berry aneurysms occur?

Back 63

In bifurcations in the circle of willis.

Front 64

Syphilis associated aneurysm: pathophysiology

Back 64

obliterative endarteritis of vasa vasorum leads to ischemic fibrosis of aortic arch. Can cause compression/erosion of airways, esophagus, bone, or rupture.

Front 65

What happens in aortic aneurysm dissection?

Back 65

There is entry of blood into aortic wall through an intimal tear, causing the wall to split.

Front 66

Vasa vasorum : defn

Back 66

network of small blood vessels that supply large blood vessels.

Front 67

Cystic Medial Degeneration: defn

Back 67

Pre-existing abnormality that predisposes patient to aortic dissection.

A degenerative breakdown of collagen, elastin, and smooth muscle caused by aging contribute to weakening of the wall of the artery

Front 68

Separation and loss of elastic elements in aortic media; cyst-like spaces filled with mucopolysaccharide rich matrix

Back 68

Cystic Medial Degeneration

Front 69

Risk factors for aortic dissection

Back 69

Age
Hypertension
Connective tissue disorder

Front 70

What CT disorders are associated with aortic dissection?

Back 70

Marfan syndrome, coarctation, bicuspid aortic valve

Front 71

What is Giant Cell Arteritis aka?

Back 71

Temporal arteritis

Front 72

Giant Cell / Temporal Arteritis : defn

Back 72

inflammatory disease of blood vessels most commonly involving large and medium arteries of the head

Front 73

Giant Cell / Temporal Arteritis: sx

Back 73

Pain and tenderness over temporal artery.

Involvement of ophthalmic artery may cause vision loss suddenly.

Front 74

heterogeneous group of disorders that are characterized by inflammatory destruction of blood vessels

Back 74

vasculitis

Front 75

Polyarteritis nodosa: defn

Back 75

Vasculitis with involvement of small and medium arteries, like renal, coronary, hepatic, mesenteric. These become swollen and damaged from attack by rogue immune cells.

Can get gangrene in the tissue supplied.

Front 76

What other disease is Polyarteritis nodosa associated with?

Back 76

30% have Hep B antigen in serum

Front 77

Thromboangiitis obliterans/Buergers disease: what is it?

Back 77

A vasculitis of intermediate and small arteries and sometimes veins.
Associated with lower extremities and young adults and smoking.