Path Spring Ds2

Front 1

What diseases cause more morbidity and mortality than any other category of human disease?

Back 1

Diseases of arteries

Front 2

What are the two mechanisms by which vascular damage is sustained?

Back 2

Via obstruction from ATH or thrombosis (embolism) or via weakening of vascular walls that can lead to dilation and rupture

Front 3

What type of cell contains the storage organelle for vWf?

Back 3

Endothelial cells

Front 4

What are vasa vasorum and where are they located?

Back 4

They are small arterioles arising from the adventitia and coursing into the media to provide oxygen to the cells there.

Front 5

What are large arteries?

Back 5

Elastic arteries such as the aorta and its large branches (ie innominate, subclavian, common carotid and iliac) and the pulmonary arteries

Front 6

What are medium-sized arteries?

Back 6

Muscular arteries that are branches of the aorta (ie coronary and renal arteries)

Front 7

What are small arteries?

Back 7

They are <2 mm in diameter and arterioles are 20-100 micrometers in diameter. These normally lie within the substance of tissues and organs.

Front 8

Which structures regulate systemic arterial blood pressure?

Back 8

The arterioles regulate BP via contraction or relaxation of medial smooth muscle cells. This is also how blood flow distribution to various capillary beds is controlled.

Front 9

Which pathologic lesions affect elastic and muscular arteries?

Back 9

Atherosclerosis (ATH)

Front 10

Which pathologic lesions affect small muscular arteries and arterioles?

Back 10

Hypertension

Front 11

Where is the preferential site for vascular leakage and exudation?

Back 11

In the postcapillary venules

Front 12

How much of the systemic blood is in veins at a given time?

Back 12

~66%

Front 13

What is the most important pathway for disease dissemination to distant sites in the body?

Back 13

Lymphatics

Front 14

What are the most common inducers of endothelial cell dysfunction?

Back 14

Cytokines and bacterial products

Front 15

What are the main functions of vascular smooth muscle cells?

Back 15

Vasoconstriction or dilation, synthesis of collagen, elastin, and proteoglycans, elaboration of growth factors and cytokines, migration to intima, and proliferation after vascular injury.

Front 16

What are the endothelium growth promoting factors?

Back 16

PDGF, FGF, and IL-1

Front 17

What are the endothelium growth inhibiting factors?

Back 17

Heparan sulfates, NO, IFN-g, and TGF-b

Front 18

What is the main mechanism of intimal thickening?

Back 18

Migration of smooth muscle cells into the intima with subsequent proliferation and elaboration of ECM.

Front 19

What changes do vascular smooth muscle cells undergo following migration to the intima?

Back 19

They basically dedifferentiate and lose their capacity to contract and gain the capacity to divide.

Front 20

What are some consequences of exaggerated vascular healing response?

Back 20

Excessive intimal thickening that can lead to stenosis and occlusion of small and medium sized blood vessels.

Front 21

What are the two most important congenital vascular anomalies?

Back 21

Developmental or berry aneurysms involving cerebral vessels and arteriovenous fistulas

Front 22

Under what circumstances would you create an arteriovenous fistula?

Back 22

To provide vascular access for chronic hemodialysis pts

Front 23

What is the most frequent and important pattern of arteriosclerosis?

Back 23

Atherosclerosis (ATH)

Front 24

What diseases are associated with arteriolosclerosis?

Back 24

Hypertension and diabetes mellitus

Front 25

What is an atheroma?

Back 25

It is an intimal lesion that characterizes ATH. Also called atheromatous or fibro fatty plaques. They protrude into and obstruct the lumina and weaken the underlying media

Front 26

Which vessels are primarily affected by ATH?

Back 26

Elastic arteries such as aorta, carotid, and iliac arteries. Also large and medium-sized muscular arteries (ie coronary and popliteal arteries)

Front 27

Which structures (organs) are primarily affected by ATH?

Back 27

Heart, brain, kidneys, and lower extremities

Front 28

What are the major consequences of ATH?

Back 28

MI, CVA, aortic aneurysms, and peripheral vascular disease

Front 29

How does ATH affect small vs. large arteries?

Back 29

Small arteries will become occluded causing ischemic injury to downstream tissues. Large arteries become weakened and an aneurysm may result

Front 30

What 3 factors have contributed most to the reduction in mortality from ATH?

Back 30

Changes in lifestyle (ie reduced cigarette smoking, altered dietary habits, and control of hypertension), improved tx methods for MI, and prevention of recurrences.

Front 31

What is the presumed precursor lesion for atheromas?

Back 31

Fatty streak

Front 32

What is the morphology of an atheroma?

Back 32

A raised focal lesion initiating in the intima with a soft, yellow, grumous core of lipid (mainly cholesterol). This is covered by a firm, white, fibrous cap.

Front 33

(T/F) Abdominal aorta is not involved in ATH lesions as often as the thoracic aorta.

Back 33

False

Front 34

What is the order of most extensively involved vessels in ATH?

Back 34

Lower abdominal aorta, coronary arteries, popliteal arteries, internal carotid arteries, and vessels of the circle of Willis

Front 35

Where do ATH lesions tend to be more prominent?

Back 35

Around the origins (ostia) of major branches

Front 36

Which vessels are usually spared in ATH?

Back 36

Vessels of the upper extremities, mesenteric and renal arteries (except at their ostia)

Front 37

(T/F) Severity of ATH in one artery doesn’t predict its severity in another artery.

Back 37

True

Front 38

What are the three principle components of ATH plaques?

Back 38

Cells (SMC’s macrophages, and other leukocytes), ECM (collagen, elastic fibers, and proteoglycans), and intracellular and extracellular lipid

Front 39

What are the three areas of an ATH lesion?

Back 39

Superficial fibrous cap, shoulder, and necrotic core

Front 40

What is the superficial fibrous cap of an atheroma composed of?

Back 40

SMC’s and relatively dense collagen

Front 41

What is the shoulder of an atheroma composed of?

Back 41

Cellular areas consisting of macrophages, SMC’s, and T lymphocytes

Front 42

What is the necrotic core of an atheroma composed of?

Back 42

Disorganized mass of lipid, dead cell debris, fibrin, thrombus, and plasma proteins. Also contains foam cells

Front 43

What are foam cells?

Back 43

Large, lipid-laden cells derived from blood monocytes mostly (but can also be SMC’s)

Front 44

What clinically significant events can happen in advanced ATH lesions?

Back 44

Rupture, ulceration, or erosion of luminal surface, hemorrhage into a plaque, superimposed thrombosis, and aneurismal dilation

Front 45

What is the most feared complication of ATH?

Back 45

Superimposed thrombosis. This happens most frequently on lesions that are ruptured, ulcerated, or hemorrhaging because pro-thrombotic factors are exposed.

Front 46

What are fatty streaks composed of?

Back 46

Lipid-filled foam cells that begin as multiple yellow, flat spots and then coalesce into elongated streaks

Front 47

(T/F) Fatty streaks cause disturbance of blood flow.

Back 47

False, they are relatively flat

Front 48

When do fatty streaks begin to appear?

Back 48

As soon as 1 yr of age. By age 10 all children will have them

Front 49

(T/F) Fatty streaks always evolve into precursors of ATH plaques.

Back 49

False, the relationship is uncertain

Front 50

What is the trend in incidence of ATH in the 40-60 yr age demographic?

Back 50

Fivefold increase compared to younger age groups

Front 51

Why is MI due to ATH not common in pre-menopausal women?

Back 51

Because estrogen exerts a protective effect against MI

Front 52

At what age does incidence of MI become equal in both sexes?

Back 52

By the 7th to 8th decade of life

Front 53

What are the 4 main risk factors for ATH that can be modified?

Back 53

Hyperlipidemia, cigarette smoking, hypertension, diabetes

Front 54

What is the major component of total serum cholesterol that is associated with increased risk of ATH?

Back 54

LDL

Front 55

How does homocystinuria affect the vasculature?

Back 55

High levels of homocysteine are present in the serum and this predisposes these pts to coronary artery disease, peripheral vascular disease, stroke, and venous thrombosis

Front 56

What is hyperhomocystinemia?

Back 56

It is high levels of homocysteine due to low dietary intake of folate and vitamin B intake, which predisposes to CVD. Supplementing these can help reduce risk of CVD

Front 57

Which markers of hemostatic/thrombotic function are potent predictors of risk for atherosclerotic events (such as MI and CVA)?

Back 57

Elevated plasminogen activator inhibitor 1, and c-reactive protein

Front 58

What protein is elevated in pts with periodontal disease that predisposes them to atherosclerotic events?

Back 58

C-reactive protein

Front 59

What factors have a less pronounced effect relating to risk of ATH events?

Back 59

Lack of exercise, obesity, stressful life style

Front 60

(T/F) ATH and its consequences may develop in absence of any apparent risk factors.

Back 60

True

Front 61

What is the effect of multiple risk factors on risk of ATH?

Back 61

It’s a multiplicative effect, in other words, if you have two risk factors then there is a fourfold risk.

Front 62

What is the “response to injury” hypothesis for ATH?

Back 62

It considers ATH to be a chronic inflammatory response of the arterial wall initiated by injury to the endothelium. The injury initially results in increased permeability, leukocyte adhesion, and thrombotic potential. Then LDL get incorporated into the lesion and modified by oxidation. Monocytes adhere to endothelium and migrate into the intima and eventually become foam cells. Platelets then begin to adhere and SMC’s migrate from the media into the intima and proliferate and produce ECM. Lipids continue to build up both inside and outside of the cells.

Front 63

What agents can potentially cause endothelial injury or dysfunction that would lead to ATH?

Back 63

Circulating derivatives of cigarette smoke, homocysteine, and viruses or bacteria

Front 64

What are the two most important determinants of endothelial alterations?

Back 64

Hemodynamic disturbances and hypercholesterolemia

Front 65

(T/F) Plaques often form in areas where there are disturbed blood flow patterns.

Back 65

True

Front 66

What disorders can lead to dyslipoproteinemias?

Back 66

Mutations that yield defective apolipoproteins, nephritic syndrome, alcoholism, hypothyroidism, and diabetes mellitus

Front 67

What effect does lowering serum cholesterol have on ATH?

Back 67

Slows rate of progression, causes regression of some plaques, and reduced risk of cardiovascular events

Front 68

What class of drug is used to reduce serum cholesterol?

Back 68

Statins

Front 69

How does Hyperlipidemia contribute to atherogenesis?

Back 69

Directly impairs EC function through increased production of oxygen free radicals which deactivate nitric oxide. Lipooroteins accumulate within the intima at sites of increased permeability. LDL gets oxidized and is ingested by macrophages which then become foam cells.

Front 70

(T/F) Coronary arterial ATH may be decreased by antioxidant vitamins in the diet.

Back 70

True

Front 71

(T/F) Macrophages have no role in depositing lipids into the intima.

Back 71

False, they release lipids as well

Front 72

What injurious effect do macrophages play in progression of ATH?

Back 72

Release of lipids into the intima, release of IL-1, TNF, and other chemokines that recruit other leukocytes. They also produce toxic reactive oxygen species that lead to the oxidation of LDL. They produce growth factors that contribute to SMC proliferation as well.

Front 73

How is a fatty streak converted into a fibrofatty atheroma?

Back 73

SMC’s migrate into the intima and proliferate and produce ECM proteins that get deposited in the intima

Front 74

Which growth factors have been implicated in the proliferation of SMC’s in an atheroma?

Back 74

PDGF, FGF, and TGF-a

Front 75

Which infectious agents are thought to contribute to ATH?

Back 75

Herpesvirus, cytomegalovirus, and Chlamydia pneumonia (strongest evidence for this last one)

Front 76

What is the biggest concern with respect to the fibrous cap of an atheroma?

Back 76

Disruption of the cap leading to a superimposed thrombus that can cause total blockage of an artery

Front 77

What is the most important risk factor modification to reduce risk of ATH?

Back 77

Lowering total cholesterol and LDL while increasing HDL

Front 78

What secondary prevention methods are used to prevent recurrence of ATH events?

Back 78

Lipid-lowering drugs (statins) and anti-platelet drugs

Front 79

What are the threshold levels of blood pressure to be generally considered hypertension?

Back 79

Sustained diastolic >90 mmHg or sustained systolic >140 mmHg

Front 80

What conditions contribute to prevalence and vulnerability to complications?

Back 80

Increasing age and black race

Front 81

What is the most common form of hypertension, composing 90-95% of cases?

Back 81

Idiopathic (essential hypertension). The remainder of benign hypertension is usually secondary to renal disease

Front 82

What conditions of the adrenal glands can cause hypertension?

Back 82

Primary aldosteronsim, Cushing syndrome, and pheochromocytoma. However, these are much less common

Front 83

What are the clinical symptoms of malignant hypertension?

Back 83

Severe hypertension, renal failure, retinal hemorrhages, papilledema. These only represent about 5% of hypertension cases and usually result in death in 1-2 years if untreated

Front 84

Review slides 11-12 of lecture 1C

Front 85

What factors interplay to determine blood pressure level?

Back 85

Multiple genetic factors, environmental, and demographic factors. These affect cardiac output and total peripheral resistance

Front 86

What are the humoral vasoconstrictors?

Back 86

Angiotensin 2 and catecholamines

Front 87

What are the humoral vasodilators?

Back 87

Kinins, prostaglandins, and nitric oxide

Front 88

What is the process by which kidneys regulate blood pressure?

Back 88

The juxtaglomerular cells of the kidneys produce rennin which converts aniotensinogen to Angiotensin 1, which is then converted by ACE to Angiotensin 2. Angiotensin 2 increases peripheral resistance and blood volume (by stimulating aldosterone secretion and thus increasing tubular sodium reabsorption).

Front 89

Where is aldosterone made?

Back 89

In the adrenal cortex

Front 90

How does renal artery stenosis contribute to secondary hypertension?

Back 90

Glomerular flow becomes decreased and there is less pressure in the afferent arteriole of the glomerulus. This induces rennin secretion leading to eventual vasoconstriction and increased sodium intake/water retention in the kidneys.

Front 91

What is a pheochromocytoma and how does it contribute to hypertension?

Back 91

It is a tumor of the adrenal that causes increased production of catecholamines that cause vasoconstriction leading to hypertension.

Front 92

What environmental factors play a role in development of hypertension?

Back 92

Stress, obesity, smoking, physical inactivity, and heavy salt consumption (big factor)

Front 93

Does sodium intake contribute to essential or secondary hypertension?

Back 93

Both

Front 94

What effect does hypertension have on the blood vessels?

Back 94

It accelerates atherogenesis, causes degenerative changes that could lead to dissection, cerebrovascular hemorrhage. In small vessels it is associated with hyaline arteriolosclerosis and hyperplastic arteriolosclerosis.

Front 95

What is hyaline arteriosclerosis?

Back 95

Vascular lesions consisting of homogenous pink hyaline thickening of the walls of arterioles with loss of structural detail and narrowing of lumen. It is most commonly found in elderly patients whether hypertensive or not (but more generalized and sever in hypertension pts)

Front 96

What disease almost always causes hyaline arteriosclerosis?

Back 96

Diabetes

Front 97

What disease is often caused by hyaline arteriosclerosis?

Back 97

Benign nephrosclerosis which includes impaired renal blood supply, loss of nephrons, and contraction of the kidneys

Front 98

What most often causes hyperplastic arteriosclerosis?

Back 98

Malignant hypertension with diastolic pressures >120 mmHg

Front 99

What are the characteristics of hyperplastic arteriosclerosis?

Back 99

Onion-skin, concentric, laminated thickening of the walls of arterioles with progressive narrowing of the lumina

Front 100

What condition is associated with necrotizing arteriolitis (especially in the kidneys)?

Back 100

Malignant hypertension causing fibrinoid deposits and acute necrosis of the vessel walls

Front 101

Which types of aneurysms are considered to be true aneurysms?

Back 101

Atherosclerotic, syphilitic, congenital vascular aneurysms and left ventricular aneurysm following MI

Front 102

What is an aneurysm?

Back 102

A localized abnormal dilation of a blood vessel of the heart that is bounded by arterial wall components or the attenuated wall of the heart.

Front 103

What is a false aneurysm?

Back 103

It is a breach in a vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space. Also called a pulsating hematoma and is most commonly a post-MI rupture

Front 104

What occurs in an arterial dissection?

Back 104

Blood enters the wall of the artery dissecting between its layers. These are often but not always aneurismal

Front 105

What are the most important causes of aortic aneurysms?

Back 105

ATH and cystic medial degeneration of the arterial media

Front 106

What are the characteristics of a saccular aneurysm?

Back 106

Essentially spherical and usually only involving a portion of the vessel wall. They are often partially or completely filled by thrombus.

Front 107

What are the characteristics of a fusiform aneurysm?

Back 107

Involves a long segment and varies in diameter and length. It may involve the entire ascending and transverse portions of aortic arch or abdominal aorta.

Front 108

Where would an abdominal aortic aneurysm most commonly be positioned?

Back 108

Below the renal arteries and above the bifurcation of the aorta

Front 109

Abdominal aortic aneurysms are frequently accompanied by smaller fusiform or saccular dilations of which arteries?

Back 109

The iliac arteries

Front 110

What are the two variants of abdominal aortic aneurysms?

Back 110

Inflammatory and mycotic AAA’s

Front 111

Describe an inflammatory AAA

Back 111

It is characterized by dense peri-aortic fibrosis accompanied by an abundant inflammatory reaction with many macrophages and often giant cells. Cause is uncertain

Front 112

Describe a mycotic AAA

Back 112

It is an atherosclerotic lesion that has become infected by circulating organisms that further destroy the media and lead to dilation and rupture.

Front 113

What are the clinical consequences of an AAA?

Back 113

Rupture, obstruction, embolism, impingement, or presentation (it all depends on the location and size)

Front 114

What vascular lesion is characteristic of tertiary syphilis?

Back 114

Obliterative endarteritis which may involve small vessels anywhere in the body but is most devastating when vasa vasorum of aorta is involved

Front 115

How would you distinguish a syphilitic aneurysm from an ATH aneurysm?

Back 115

By location, an ATH aneurysm almost never occurs in the thorax. Syphilitic aneurysms can occur on the arch of the aorta but never involve the root of the aorta

Front 116

Aside from aneurysm, what other vascular complications arise from tertiary syphilis?

Back 116

Insufficiency of the aortic valve leading to regurgitation to the left ventricle. This leads to cardiac overload and the heart undergoes massive hypertrophy (sometimes up to 3x normal weight). This condition is referred to as cor bovinum

Front 117

What signs and symptoms could arise due to a thoracic aortic aneurysm?

Back 117

Encroachment on mediastinal structures, respiratory difficulties, difficulty swallowing, pain caused by bone erosion, and persistent cough due to pressure on the recurrent laryngeal nerve

Front 118

Why is the term “dissecting aneurysm” really a misnomer?

Back 118

Because it doesn’t always lead to dilation of the aorta so isn’t a true aneurysm. It should be called a dissecting hematoma and is really a blood filled channel within the aortic wall between the laminar planes that can rupture outward

Front 119

What two groups of people are at risk for dissecting hematoma?

Back 119

Men 40-60 yrs old with antecedent hypertension and younger pts with CT disorders like Marfan syndrome. Much more rarely it occurs in pts following diagnostic catheterization (iatrogenic)

Front 120

What is a false channel or double-barreled aorta?

Back 120

It is when a dissecting hematoma re-ruptures into the lumen and a second channel is created. In chronic dissection this false channel can actually become endothelialized

Front 121

What is the most common preexisting histologically detectable lesion in aortic dissections?

Back 121

Cystic medial degeneration (CMD), which often accompanies Marfan syndrome

Front 122

T/F Abnormal medial histology is not prerequisite to dissection, and abnormal medial structure does not always lead to dissection.

Back 122

True

Front 123

What is the strongest predictor of serious complications in an aortic dissection?

Back 123

The level of the aorta affected. The most serious complications occur from the aortic valve to the arch

Front 124

Are proximal or distal aortic dissections more dangerous?

Back 124

Proximal because they involve either or both of the ascending and descending aorta

Front 125

What is the classic initial symptom of aortic dissection?

Back 125

Sudden onset of excruciating pain usually beginning in the anterior chest and radiating to the back. It will move down as the dissection progresses. This pain can be easily confused with that of acute MI

Front 126

What are the clinical manifestations of aortic dissection?

Back 126

Cardiac tamponade, aortic insufficiency, and MI

Front 127

What tx and sx have improved the prognosis or aortic dissection pts?

Back 127

Plication (folding and shorting of aortic wall) during surgery, and early administration of intensive antihypertensives

Front 128

What are the most common clinical manifestations of vasculitis?

Back 128

Fever, myalgia, arthralgias, and malaise

Front 129

What are the two most common mechanisms of vasculitides?

Back 129

Immune-mediated inflammation and direct invasion of vascular walls by infectious pathogens

Front 130

Why is it critical to distinguish which basic type of vasculitides a person has?

Back 130

Because if its immune-mediated you would administer immunosuppressive therapy, which would be disastrous if it was an infectious vasculitis

Front 131

Vasculitis lesions resemble lesions caused by which type of hypersensitivity reactions?

Back 131

Type III hypersensitivity reactions such as the local arthus phenomenon, serum sickness, and polyarteritis nodosa

Front 132

Review slide #10 of lecture 4

Front 133

Hypersensitivity to which drugs commonly cause vasculitic skin lesions?

Back 133

Penicillin and streptokinase. Hypersensitivity to drugs causes about 10% of vasculitic skin lesions due to antigen-antibody complexes depositing in vessel walls

Front 134

What is the most impressive example of vasculitis associated with viral infection?

Back 134

Hepatitis B and C where you have Hep antigen and anti-hep antibodies complexing and depositing

Front 135

When would you most commonly encounter antigen-antibody complexes with complement?

Back 135

In polyarteritis nodosa (PAN)

Front 136

What is a pauci-immune vasculitidy?

Back 136

One in which there are no immune complex deposits present

Front 137

What is an ANCA?

Back 137

Antineutrophil Cytoplasmic autoantibodies, which are commonly found in the plasma of pts with vasculitis. They are antibodies against enzymes found in neutrophils and monocytes and can be found in either of two forms in patients with small vessel vasculitis

Front 138

What are the two types of ANCA’s and how are they classified?

Back 138

C-ANCA and p-ANCA are classified by the pattern of cellular staining in neutrophils

Front 139

What is the staining pattern of c-ANCA?

Back 139

Cytoplasmic staining of PR-3, which is a component of neutrophils granules

Front 140

What is the staining pattern of p-ANCA?

Back 140

Perinuclear staining (around the periphery of the nucleus) of myeloperoxidase

Front 141

What vasculitidy is commonly associated with c-ANCA?

Back 141

Wegener granulomatosis

Front 142

What vasculitidy is commonly associated with p-ANCA?

Back 142

Microscopic polyangiitis

Front 143

Are all pts with small vessel vasculitis ANCA positive?

Back 143

No, about 10% are ANCA negative

Front 144

What is the relationship between ANCA titers and vasculitic disease activity?

Back 144

There is a close association, suggesting that ANCAs may play an important part in pathogenesis of these diseases

Front 145

Antibodies to endothelial cells may be induced by defects in immune regulation and predispose pts to which vasculitides?

Back 145

Systemic lupus erythematosus and Kawasaki disease

Front 146

How are systemic vasculitides classified?

Back 146

By size and anatomic site of the involved blood vessels, histologic characteristics of the lesion, and clinical manifestations

Front 147

Which vasculitides affect large vessels?

Back 147

Giant cell arteritis and Takayasu arteritis

Front 148

Which vasculitides affect medium-sized vessels?

Back 148

Polyarteritis nodosa and Kawasaki disease

Front 149

Which vasculitides affect small vessels?

Back 149

Microscopic polyangiitis and Wegener granulomatosis

Front 150

What is the most common vasculitis?

Back 150

Giant cell arteritis

Front 151

What arteries are principally affected in giant cell arteritis?

Back 151

Large arteries in the head, especially the temporal arteries but also the vertebral and ophthalmic arteries

Front 152

What is the dominant hypothesis of the cause of giant cell arteritis?

Back 152

T-cell mediated immune response to a vessel wall antigen. This is supported by the presence of a granulomatous inflammatory response with clonal population of T cells at affected sites

Front 153

What is the most common symptom presentation in giant cell arteritis?

Back 153

Facial pain or headache along the course of the temporal artery. Alternately, some have only vague symptoms like fever, fatigue, and weight loss

Front 154

What serious ocular symptoms can result in giant cell arteritis?

Back 154

Can range from diplopia to transient or complete vision loss and is usually due to involvement of the ophthalmic artery

Front 155

What happens in the most common variant of giant cell arteritis?

Back 155

There is granulomatous inflammation of the inner half of the media centered on the internal elastic membrane. It is marked by lymphocytic infiltrate, multinucleate giant cells, fragmentation of internal elastic lamina, macrophages close to the damaged elastic lamina, and both CD4 and CD8 lymphocytes.

Front 156

What gene polymorphism is associated with development of giant cell arteritis?

Back 156

The gene that encodes intercellular adhesion molecule 1

Front 157

Which arteries would be affected by PAN?

Back 157

Small or medium-sized muscular arteries (not arterioles, capillaries, or venules). Typically the renal and visceral vessels are involved, but pulmonary circulation is spared.

Front 158

What are the characteristics of classic PAN?

Back 158

Segmental transmural necrotizing inflammation of arteries of small to medium size in any organ

Front 159

What organ will usually never exhibit PAN?

Back 159

The lungs

Front 160

What are the organs most commonly affected by PAN?

Back 160

The kidneys, heart, and liver. Muscles, nervous system and skin are least affected

Front 161

What are some local consequences of PAN?

Back 161

Aneurysmal dilation and localized rupture. Also, impaired perfusion leading to ulcerations, infarcts, or ischemic atrophy

Front 162

What can be the first clue to existence of underlying PAN disorder?

Back 162

Hemorrhages in the area supplied by the affected vessels

Front 163

What are the histological features of PAN?

Back 163

In acute phase, transmural inflammation with neutrophils, Eosinophils, and mononuclear cells. Frequently fibrinoid necrosis and thrombosed lumen. In later phase the inflammatory infiltrate is replaced by fibrous thickening of vessel wall

Front 164

What age demographic are commonly affected with PAN?

Back 164

Usually young adults, but can occur in children too

Front 165

What are the clinical signs and symptoms of PAN?

Back 165

They are varied and non-specific, such as malaise, fever, weight loss, hypertension, abdominal pain, muscle aches, etc. Renal involvement is common, but not glomerulonephritis (no small vessel involvement)

Front 166

What viral antigen is associated with PAN?

Back 166

30% of pts have Hep B antigen is serum. There is no association with ANCA’s

Front 167

How would you diagnose PAN?

Back 167

You have to do a biopsy because the clinical symptoms are so diverse.

Front 168

What is the tx for PAN?

Back 168

Corticosteroids and cyclophosphamide will lead to remission or cure in 90%. If not treated can lead to death

Front 169

What is Kawasaki disease?

Back 169

Mucocutaneous lymph node syndrome. It is an acute illness of infancy and childhood that affects many organs including, skin, mucous membranes, lymph nodes, and blood vessel walls

Front 170

What are the most serious effects of Kawasaki disease?

Back 170

It causes severe aneurismal dilations in the heart (coronary arteries) that can be deadly without treatment

Front 171

What is thought to be involved in the underlying pathogenesis of KD?

Back 171

A pre-existing viral infection is thought to trigger the disease

Front 172

What vessels are involved in KD?

Back 172

Small, medium, and large vessels (especially coronary arteries)

Front 173

What is the leading cause of acquired heart disease in children?

Back 173

Kawasaki disease. 80% of KD pts are under 4 yrs old

Front 174

What are the most identifiable clinical presentations of KD?

Back 174

Conjunctival and oral erythema and erosion. Other signs include erythema and edema of hands and feet, rash, cervical lymphadenopathy, and fever.

Front 175

How do you treat KD?

Back 175

With intravenous immunoglobulin therapy

Front 176

KD vasculitis is believed to be due to activation of which immune cells?

Back 176

T-cells and macrophages that secrete cytokines and cause hyperactivity of B cells that create autoantibodies to EC’s and SMC’s

Front 177

What are the affects of Wegener granulomatosis?

Back 177

The triad of acute necrotizing granulomas of the upper respiratory tract (ear, nose, sinuses, throat, oral cavity), and/or lower respiratory tract (lungs), and glomerulonephritis. It is most prominent in the lungs and upper airways

Front 178

Which vessels are affected in WG?

Back 178

Small to medium-sized vessels, such as capillaries, venules, arterioles, and arteries

Front 179

What is limited WG?

Back 179

When the involvement is restricted to the respiratory tract only. Widespread WG can affect eyes, skin and sometimes heart as well.

Front 180

What are the oral manifestations of WG?

Back 180

Ulcerative lesions of the palate and pharynx

Front 181

Diagnosing WG based on lung lesions would lead to differential diagnosis of what other conditions?

Back 181

Mycobacterial or fungal infection. The granulomas can be very similar in appearance

Front 182

What type of renal lesions exist in WG?

Back 182

Early milder lesions of acute focal proliferation and necrosis and thrombosis and more advanced lesions of diffuse necrosis and proliferation with crescent formation (crescentic glomerulonephritis). The latter is called rapidly progressive glomerulonephritis (RPGN)

Front 183

What symptoms would exist in the 2 types of renal lesions in WG?

Back 183

Focal lesions may only cause hematuria or proteinuria, but diffuse lesions may lead to renal failure

Front 184

Describe the pathogenesis of WG?

Back 184

It is unsure but thought to be caused by some form of cell mediated hypersensitivity due to presence of granulomas and good response to immunosuppressive therapy. c-ANCA’s may also play a role in pathogenesis

Front 185

Presence of what antibody marker is found in 95% of WG cases?

Back 185

c-ANCAs

Front 186

What age demographic is affected by WG?

Back 186

40-50 year olds

Front 187

What are they typical clinical features of WG?

Back 187

Persistent pneumonitis, chronic sinusitis, mucosal ulcerations, and renal disease

Front 188

What is the prognosis of untreated WG?

Back 188

80% of people will die within 1 year if not treated. Immunosuppressive drugs work quite well, but following tx if c-ANCA titers rise then pt may be relapsing

Front 189

Which 2 vasculitides are often referred to as ANCA-associated small vessel vasculitides?

Back 189

Wegener granulomatosis and microscopic polyangiitis

Front 190

Review slide 87 of lecture 4

Front 191

What is Buerger disease (thromboangiitis obliterans)?

Back 191

It is a distinctive disease often leading to vascular insufficiency. It is characterized by segmental, thrombosing, acute and chronic inflammation of medium and small arteries of the limbs

Front 192

What are the most commonly affected vessels in Buerger disease?

Back 192

The tibial and radial arteries. Sometimes secondarily extending into veins and nerves of the extremities

Front 193

What is the distribution of this disease?

Back 193

Mostly occurs in heavy smokers and begins before age 35 in most cases

Front 194

What evidence exists of a genetic basis for Buerger disease?

Back 194

It is much more common in Israel, Japan, and India than the USA

Front 195

What are the clinical features of Buerger disease?

Back 195

Superficial nodular phlebitis, Raynaud phenomenon in hands, pain in foot (instep claudication). Unlike ATH, this causes severe pain because there is neuronal involvement. Ulcers will develop over time and gangrene can develop

Front 196

What underlying disorders are often associated with BD?

Back 196

Rheumatoid arthritis, SLE, and malignancy

Front 197

What organisms are often implicated in infectious arteritis?

Back 197

Bacteria or fungi, particularly Aspergillus. Vascular lesions will often accompany bacterial pneumonia and occur adjacent to caseous tuberculosis or meningitis

Front 198

What complications can arise from vascular infections?

Back 198

Mycotic aneurysms, thrombosis, and infarction

Front 199

What is Rheumatoid vasculitis?

Back 199

It occurs predominantly after long-standing RA. It affects small and medium-sized arteries and leads to visceral infarction

Front 200

What is the difference between Raynaud disease and Raynaud phenomenon?

Back 200

The disease is due to an exaggerated vasomotor response to normal stimuli, such as cold. It happens in otherwise healthy people. The phenomenon is usually due to arterial narrowing secondary to SLE, scleroderma, ATH, or Buerger disease

Front 201

Which conditions account for 90% of clinical venous diseases?

Back 201

Varicose veins and phlebothrombosis/thrombophlebitis

Front 202

What causes varicose veins?

Back 202

Prolonged increased intraluminal pressure and loss of vessel wall support. This leads to abnormally dilated, tortuous veins usually in the upper and lower leg. This is usually due to occupations that require long periods of standing or long plane/car rides

Front 203

What is the prevalence of varicose veins?

Back 203

About 15-20% of people will develop them in the lower legs

Front 204

What demographic is at increased risk for varicose veins?

Back 204

People older than 50 yrs old, obese persons, and women (especially if they have been pregnant). There is also a familial tendency that is due to defective venous wall development

Front 205

What conditions are frequently discovered when a varicose vein is opened?

Back 205

Intraluminal thrombosis and valvular deformities. There is often scarring and thinning at points of maximal dilation

Front 206

What are the most disabling sequelae of varicose veins?

Back 206

Persistent edema in the extremity and trophic changes in skin that can lead to ulcers and poorly healing wounds.

Front 207

Are embolisms originating from varicose veins common occurrences?

Back 207

No, they are very rare (unlike deep leg vein thrombosis which frequently embolize)

Front 208

What are the most common veins to be affected by thrombophlebitis and phlebothrombosis?

Back 208

Deep leg veins account for more than 90% of cases

Front 209

What are the most important risk factors for TP and PT?

Back 209

Cardiac failure, neoplasia, pregnancy, obesity, postoperative state, and prolonged bed rest or immobilization.

Front 210

Which cancers are particularly likely to cause TP and PT?

Back 210

Adenocarcinomas of pancreas, colon, or lung

Front 211

What is the most common cause of superior vena caval syndrome?

Back 211

Neoplasms such as bronchogenic carcinoma or mediastinal lymphoma that compress the vena cava and often the pulmonary vessels as well. The signs are dusky cyanosis and dilation of veins of the head, neck, and arms

Front 212

What is the most common cause of inferior vena caval syndrome?

Back 212

Neoplasms such as hepatocellular carcinoma and renal cell carcinoma that can grow within veins. Also, thrombi from femoral or iliac veins can propagate upward and block the vein

Front 213

What are the signs of inferior vena caval syndrome?

Back 213

Marked edema of the legs and distention of superficial collateral veins of lower abdomen. If the renal veins are involved, massive proteinuria

Front 214

Which bacterial agents are most commonly implicated in lymphangitis?

Back 214

Group A b-hemolytic streptococci are most common, but any virulent pathogen can cause it

Front 215

What happens to infected lymphatics?

Back 215

They are dilated and filled with an exudates of neutrophils and monocytes

Front 216

How is lymphangitis recognized?

Back 216

By painful subcutaneous red streaks that extend along course of lymphatics or painful enlargement of regional nodes.

Front 217

What is the appearance of skin in areas of edema?

Back 217

Peau d’orange appearance of skin (orange peel look)

Front 218

What are the two types of cellular proliferations in vascular neoplasms?

Back 218

Endothelial cell derived and those derived from cells that support and/or invest blood vessels

Front 219

What is a hemangioma?

Back 219

A benign vascular tumor characterized by increased numbers of normal or abnormal vessels filled with blood. Can be localized (angioma) or an entire limb (angiomatosis).

Front 220

Where are the majority of hemangiomas located?

Back 220

They are most often superficial lesions of the head or neck. They can also occur internally and about 1/3 occur in the liver

Front 221

Do hemangiomas undergo malignant transformation?

Back 221

Rarely if at all

Front 222

When are hemangiomas most common?

Back 222

In infancy or childhood. Many of them regress spontaneously at or before puberty

Front 223

What are the histological characteristics of a hemangioma?

Back 223

Aggregated, closely packed, thin-walled capillaries filled with blood. There is often hemosiderin pigment found due to rupture of vessels in these lesions

Front 224

How do capillary and cavernous hemangiomas differ?

Back 224

Cavernous are characterized by formation of large, dilated vascular channels. Cavernous are less circumscribed and more frequently involve deep structures

Front 225

When is a cavernous hemangioma of greatest concern?

Back 225

In the brain where it may cause pressure symptoms or rupture

Front 226

What are the characteristics of a pyrogenic granuloma?

Back 226

Rapidly growing red nodule of the skin or gingival mucosa that is often ulcerated and bleeds easily. About 1/3 occur after trauma

Front 227

What other tissue proliferation is similar in appearance to a PG?

Back 227

Exuberant granulation tissue

Front 228

What is a lymphangioma?

Back 228

It is similar to a benign hemangioma of a blood vessel except in a lymphatic

Front 229

Where would you commonly find a simple (capillary) lymphangioma?

Back 229

In the head and neck region and axilla. It will appear as a slightly elevated, sometimes pedunculated lesion

Front 230

How do you distinguish a lymphangioma from a hemangioma histologically?

Back 230

They look almost identical except for the presence or absence of blood cells

Front 231

What is a cystic hygroma?

Back 231

It is also called cavernous lymphangioma and is analogous to cavernous hemangioma. It occurs in children and affects the neck and axilla mostly. It can get so large that it produces deformities in and around the neck

Front 232

What are the histological characteristics of a cystic hygroma?

Back 232

Massively dilated, cystic lymphatic spaces lined by ECs and separated by scant CT stroma

Front 233

What genetic disease is associated with higher incidence of cavernous lymphangioma (cystic hygroma)?

Back 233

Turner syndrome

Front 234

What does the term telangiectasia designate?

Back 234

That the vascular estasia is a congenital anomaly

Front 235

What is the most common ectasia?

Back 235

Nevus flammeus, or the common “birthmark.” They are commonly found on the head and neck

Front 236

Which type of nevus flammeus tends to grow proportionately with a child and become unsightly?

Back 236

Port wine stains

Front 237

What are the manifestations of Sturge-Weber syndrome?

Back 237

Port wine stains in the area of the trigeminal nerve. Often mental retardation, seizures, and hemiplegia

Front 238

What strange abnormality would you find radiographically in a Sturge-Weber pt?

Back 238

A calcified falx cerebri and meningeal masses

Front 239

What are spider telangiectasias?

Back 239

Non-neoplastic vascular lesions made up of an array of dilated subcutaneous arteries and arterioles. They tend to be on the face, neck and upper chest and are most frequent in pregnant women or pts with cirrhosis

Front 240

What is the inheritance pattern of hereditary hemorrhagic telangiectasia?

Back 240

Autosomal dominant

Front 241

Where are these lesions commonly located?

Back 241

They are widely distributed over skin and mucous membranes of the oral cavity, lips, respiratory, GI tract, and urinary tract

Front 242

What are the potential complications of HHT?

Back 242

Rupture of vessels that can lead to serious nosebleeds, bleeding into the gut, and hematuria

Front 243

What etiologic agent is responsible for bacillary angiomatosis?

Back 243

Gram-negative bacilli of the Bartonella family

Front 244

Bartonella henselae, one of the species implicated in bacillary angiomatosis causes what disease in immunocompetent persons?

Back 244

Cat scratch fever carried by domestic cats. Cat flea is its vector

Front 245

Who is most commonly afflicted with classic or chronic Kaposi sarcoma?

Back 245

90% occur in older men of Eastern European or Mediterranean descent. It is not associated with HIV virus

Front 246

Where do the lesions usually form in classic KS?

Back 246

Primarily in distal lower extremities spreading to more proximal sites with time.

Front 247

What is the prevalence of AIDS-associated KS?

Back 247

One in four AIDS pts, particularly male homosexuals

Front 248

What percent of AIDS KS pts will develop a second malignancy?

Back 248

About 1/3

Front 249

What are the 3 stages of KS lesions?

Back 249

Patch, plaque, and nodule

Front 250

What is the favored hypothesis for pathogenesis of KS?

Back 250

Virus associated neoplasm of primitive messenchymal cells or ECs. In AIDS, it is the HHV-8 virus

Front 251

What carcinogen has been well-documented as causing hepatic angiosarcomas?

Back 251

Polyvinyl chloride (PVC) and arsenic

Front 252

What is the common end point of many types of heart disease?

Back 252

Congestive heart failure

Front 253

What is the definition of congestive heart failure?

Back 253

Pathophysiologic state resulting from impaired cardiac function. The heart is unable to maintain an output sufficient for the metabolic requirements of the tissue and organs of the body

Front 254

What are the common causes of CHF?

Back 254

Coronary artery disease, hypertension, alcohol abuse, and heart valve disorders

Front 255

What types of medications can worsen CHF?

Back 255

NSAIDs, certain steroids, some diabetes meds (Avandia), and calcium channel blockers. These are things that affect the power of the heart muscle or sodium retention

Front 256

What venous effects result from CHF?

Back 256

Increased congestion of venous circulation and elevated venous pressure

Front 257

What is the histologic identifier of cardiac myocyte hypertrophy?

Back 257

Square “boxcar” looking nuclei

Front 258

Why would hypertrophied myocardium be more vulnerable to ischemic injury?

Back 258

Because the capillary beds don’t keep up with increased myocyte mass (which requires more oxygen)

Front 259

What is the end stage of CHF?

Back 259

Acute decompensated heart failure (ADHF). This is when the failing myocardium is no longer able to propel sufficient blood to meet the needs of the body, even at rest. The signs are pitting edema > 2mm, and presence of pulmonary rales

Front 260

What does backward failure refer to?

Back 260

Congestion of venous circulation secondary to CHF

Front 261

How can left-sided CHF eventually lead to right-sided CHF?

Back 261

Due to left ventricular insufficiency, blood gets backed up in to the pulmonary circulation. The increased pulmonary venous pressure leads to increased resistance for the right ventricle trying to push blood into the pulmonary circulation. This increased workload on the right side leads to HF

Front 262

What are the most common causes of left-sided HF?

Back 262

Systemic hypertension, mitral or aortic valve disease, ischemic heart disease, or primary diseases of the myocardium.

Front 263

With HF, there is less perfusion to the kidneys. What is the result of this?

Back 263

Secondary hyperaldosteronism. Aldosterone is released which causes renal tubules to reabsorb both sodium and water. Plasma volume increases along with systemic blood pressure increase

Front 264

What is the most common manifestation of left-sided HF?

Back 264

Dyspnea (shortness of breath)

Front 265

When is dyspnea most noticeable?

Back 265

During physical activity and when lying down (orthopnea)

Front 266

How does left-sided HF affect the left atrium?

Back 266

It becomes chronically dilated, leading to atrial fibrillation and “irregularly irregular” heartbeat

Front 267

What are rales?

Back 267

Inspiratory crackles heard in the lungs due to popping open of small airways and alveoli collapsed by fluid, exudates, or lack of aeration during expiration

Front 268

What are ronchi?

Back 268

Gurgling noises heard during inhalation or exhalation. Due to air flowing through mucous secretions in partially obstructed airways. This is usually heard in COPD

Front 269

What is the most common cause of right-sided HF?

Back 269

Left ventricular failure with associated pulmonary congestion and elevated pulmonary arterial pressure. It can also be caused by cor pulmonale or pulmonic or tricuspid valve disease.

Front 270

What is cor pulmonale?

Back 270

Any heart problem caused by an underlying intrinsic lung disease. “pulmonary heart disease”

Front 271

What are the changes in the liver secondary to CHF?

Back 271

Chronic passive congestion which causes atrophy and necrosis of hepatocytes around central veins. It will have a nutmeg-like appearance and may become fibrotic or possibly frankly cirrhotic

Front 272

What is the main clinical manifestation of right sided CHF?

Back 272

Distended neck veins caused by increased systemic venous congestion. Also, they have increased frequency of deep venous thrombi and pulmonary embolism

Front 273

Edema secondary to CHF will include fluid in what areas?

Back 273

Initially in feet and lower legs, then becomes more generalized. It can then lead to pericardial effusions and ascites

Front 274

How does inflammatory edema and CHF edema differ (in fluid content)?

Back 274

CHF edema fluid has low protein content (it’s a transudate)

Front 275

What is the most common cause of ischemic heart disease (IHD)?

Back 275

Narrowing of the coronary arteries by atherosclerosis. For this reason it is also called coronary heart disease and/or coronary artery disease

Front 276

What is the most common cause of death in economically developed countries?

Back 276

Ischemic heart disease

Front 277

What is the myocardial response to IHD?

Back 277

Angina pectoris, acute MI, sudden cardiac death, or chronic IHD w/CHF

Front 278

What will complete vessel occlusion by thrombus following ruptured atherosclerotic plaque lead to?

Back 278

Acute MI. If the obstruction is incomplete you may just have unstable angina or arrhythmia

Front 279

What is angina pectoris?

Back 279

Intermittent chest pain caused by transient, reversible myocardial ischemia

Front 280

What are the three variants of angina?

Back 280

Typical (stable), prinzmental (variant), and unstable

Front 281

What is the cause and manifestation of stable angina?

Back 281

Episodic chest pain associated with stress or exertion. Usually a crushing or squeezing substernal pain that may radiate down the left arm or jaw

Front 282

What degree of artery narrowing would lead to stable angina?

Back 282

Usually 75% narrowing or greater of the lumen

Front 283

How do you treat someone with symptoms of angina/MI?

Back 283

Give them three doses of nitroglycerin spaced ten minutes apart. If this doesn’t relieve the symptoms than its safe to assume it’s probably an MI, not angina

Front 284

How does nitroglycerin work to relieve angina symptoms?

Back 284

It is a vasodilator that reduces venous blood delivered to the heart by causing venous dilation. The reduced blood return to the heart lessens the workload of the heart. In larger doses it can actually cause coronary artery vasodilation and increase blood supply to the myocardium

Front 285

What is prinzmetal angina?

Back 285

It usually occurs at rest or awakens pt from sleep. It is associated with coronary artery spasm and will respond to administration of nitroglycerin

Front 286

How can unstable angina be identified?

Back 286

It is characterized by an increased frequency of angina pain that tend to be precipitated by progressively less exertion, are more intense, and often last longer than stable anginal episodes

Front 287

What is the most common cause of unstable angina?

Back 287

Acute plaque changes leading to superimposed thrombus or distal embolization of the thrombus, and/or vasospasm

Front 288

What percentage of MI patients will die?

Back 288

About 1/3, half million of the 1.5 million who have MI every year

Front 289

What are the two types of MI?

Back 289

Transmural, where the entire thickness of the ventricle wall dies, from the intima to the pericardium, and sub-endothelial which is not as serious due to only partial thickness of heart affected

Front 290

What is the most common cause of transmural infarct?

Back 290

90% caused by disrupted atherosclerotic plaque, mostly in the proximal 2 cm of LAD and left circumflex and proximal and distal thirds of right coronary artery

Front 291

What are the two coronary arteries most commonly affected by ATH plaque?

Back 291

The LAD is the most, followed by the right coronary artery then the left circumflex

Front 292

Why does complete vessel occlusion not always lead to MI?

Back 292

Due to anastomoses providing collateral blood flow

Front 293

What is the time interval between onset of complete myocardial ischemia and initiation of irreversible injury?

Back 293

20-40 minutes

Front 294

When would an external rupture of an infarct likely occur?

Back 294

During the first 2 weeks of the infarct, but most common between days 4-7

Front 295

What are the consequences of external rupture of transmural infarct?

Back 295

Massive hemopericardium leading to cardiac tamponade

Front 296

How long after an acute MI would acute pericarditis occur?

Back 296

Within 2-4 days after transmural infarct. This leads to significant pericardial effusion

Front 297

What is the late complication of large transmural MIs?

Back 297

Ventricular aneurysms of thin-walled, non-contractile, fibrous regions of the myocardium

Front 298

Where are the most common places for MI pain to radiate outside the chest?

Back 298

The neck, jaw, epigastrium, shoulder, and left arm

Front 299

How does MI pain differ from angina pectoris?

Back 299

MI pain typically last several hours to days and isn’t relieved by nitroglycerin

Front 300

How common are “silent” MIs that aren’t associated with chest pain?

Back 300

Happens in about 20-30% of pts and is more common in diabetes, hypertension, and elderly

Front 301

What is the most common cause of sudden cardiac death?

Back 301

Ischemic heart disease leading to ventricular fibrillation

Front 302

What are the three acute coronary syndromes?

Back 302

Unstable angina, acute MI, and sudden cardiac death

Front 303

What are the leads for an EKG?

Back 303

Lead I is from left arm to right arm, lead II is from left leg to right arm, and lead III is from left leg to left arm

Front 304

How would you check for AV node function from an ECG?

Back 304

By looking at the PR interval, which is the time that the impulse takes to travel from the SA node through the AV node and enter the ventricles. If its long then you may have a conduction problem

Front 305

How do you determine the absolute refractory period?

Back 305

It is the interval from the beginning of the QRS complex to the apex of the T wave

Front 306

What causes an arrhythmia?

Back 306

Electrical abnormalities of ischemic myocardium or conduction disturbances

Front 307

What is atrial flutter (AFL)?

Back 307

It is an abnormal heart rhythm usually associated with tachycardia. It is a supra-ventricular tachycardia that appears as recurring saw-toothed P waves between QRS complexes.

Front 308

What is atrial fibrillation?

Back 308

It is the most common arrhythmia, usually involves both atria. It is a quivering of heart muscle instead of a coordinated contraction.

Front 309

How do you identify atrial fibrillation?

Back 309

Presence of irregular pulse and absence of P waves on ECG

Front 310

What cerebral damage can A-fib cause?

Back 310

Cerebrovascular accident (CVA)

Front 311

What causes premature ventricular contractions (PVCs)?

Back 311

When the heartbeat is initiated by the ventricles rather than the sinoatrial node like normal. The impulse travels in reverse order basically so you get a reverse wave that dips down instead of spiking up

Front 312

What are the four regular patterns of PVC?

Back 312

Bigeminy when every other beat is a PVC, trigeminy when every third beat is a PVC, and quadrigeminy when every fourth beat is a PVC

Front 313

What is meant by unifocal PVC?

Back 313

The depolarization is triggered from one site in the ventricle every time so all the peaks PVC look the same on the ECG.

Front 314

What is meant by multifocal PVC?

Back 314

The depolarization is triggered from more than one site in the ventricles so all the PVC peaks look different on ECG

Front 315

What is it called when there are more than 3 PVCs in a row?

Back 315

Ventricular tachycardia, which is a dangerous rapid heartbeat. This type of arrhythmia can lead to ventricular fibrillation and sudden death

Front 316

How is ventricular fibrillation detected?

Back 316

It can’t be detected by palpating pulse points, it can only be confirmed by ECG

Front 317

What condition leads to sudden cardiac death?

Back 317

Lethal arrhythmias

Front 318

What is the mean electrical vector of the heart?

Back 318

The general direction of the heart’s depolarization wave front. It is estimated by the polarity of QRS complex in leads I, II, and III (the heart’s electrical axis in the frontal plane).

Front 319

What determines the heart’s cardiac axis in a healthy pt?

Back 319

Where the bulk of the major muscle is, usually the left ventricle with some contribution from the right ventricle

Front 320

What is the normal cardiac axis?

Back 320

-30 deg to 90 deg

Front 321

What happens when there is a left axis deviation?

Back 321

Left ventricle increases its activity or bulk. The axis will swing to the left beyond -30 deg

Front 322

What happens when there is a right axis deviation?

Back 322

The right ventricle is strained or hypertrophied and the axis swings beyond +90 deg

Front 323

What is a Q wave and what is its significance?

Back 323

It is any initially negative deflection of the QRS complex that can be related to myocardial injury

Front 324

What would cause ST segment depression?

Back 324

Myocardial ischemia, ventricular hypertrophy, acute posterior MI, pulmonary embolus, and left bundle branch block

Front 325

What is an ST elevation MI (STEMI)?

Back 325

It indicates a large amount of heart muscle damage secondary to total occlusion of coronary artery. Usually recognized by characteristics on ECG

Front 326

What causes a symmetric T-wave inversion?

Back 326

It is a sign of coronary ischemia, left ventricular hypertrophy, or CNS disorder

Front 327

What causes an asymmetric T-wave inversion?

Back 327

Toxicity of digoxin or similar drug

Front 328

What rule do you use to determine if there is a left bundle branch block?

Back 328

The rule of T-wave discordance. The T-wave and ST segment will be deflected opposite the QRS complex. So, if the QRS complex goes up, the T-wave goes down or vice versa.

Front 329

What are the diagnostic features of a right bundle branch block?

Back 329

Broad, M-shaped QRS complex

Front 330

What are the diagnostic features of a left bundle branch block?

Back 330

W or M pattern of QRS and inverted T waves.

Front 331

What disease processes are associated with left bundle branch block?

Back 331

Acute MI, aortic valve disease, cardiomyopathy, and cardiac surgery

Front 332

What disease processes are associated with right bundle branch block?

Back 332

IHD, acute massive PE, congenital disease, and cardiomyopathy

Front 333

What is the mnemonic to remember ECG changes indicating bundle branch blocks?

Back 333

WiLLiaM MaRRoW

Front 334

What is the major plasma marker of MI that can be detected by lab evaluation?

Back 334

Troponin (especially cardiac troponin T) is the major one, but also creatine kinase (CK)

Front 335

Does right-sided HF secondary to pulmonary hypertension caused by left-sided HF still count as cor pulmonale?

Back 335

No

Front 336

What causes acute cor pulmonale?

Back 336

Pulmonary embolism or right ventricular dilation leading to tricuspid regurgitation

Front 337

What causes chronic cor pulmonale?

Back 337

Pulmonary emboli, chronic obstructive and restrictive lung disease, and pulmonary vascular disease “Cor pulmonale, or right-sided heart failure, is an enlargement of the right ventricle due to high blood pressure in the lungs usually caused by chronic lung disease.”

Front 338

What is Jones criteria?

Back 338

Five conditions that are often present in pts with rheumatic fever. Two of these must be present in order to make the diagnosis of RF

Front 339

What are the five conditions of Jones criteria?

Back 339

Erythema marginatum, Sydenham chorea, carditis, subcutaneous nodules, and migratory large joint polyarthritis

Front 340

What is the histologic identifier for rheumatic fever?

Back 340

Aschoff bodies, which are foci of fibrinoid necrosis surrounded by mononuclear inflammatory cell infiltrate. This gets slowly replaced by fibrous scar tissue

Front 341

Where are you most likely to find Aschoff bodies?

Back 341

They are found most often in myocardium.

Front 342

Which valves are most commonly involved in rheumatic heart disease?

Back 342

Mitral valve alone in 65-70% of cases and mitral and aortic combined in 20-25% of cases (note, both of these valves are on the left side of the heart)

Front 343

What are the complications of untreated aortic stenosis?

Back 343

Death within 3-4 years of onset of symptoms either from CHF or lethal arrhythmia

Front 344

What conditions can lead to mitral regurgitation?

Back 344

Rheumatic heart disease, IHD, CHF, and mitral valve prolapse (the most common of the 4)

Front 345

What is mitral valve prolapse?

Back 345

It is one of the most common cardiac disorders that is characterized by accumulation of loose ground substance within leaflets and chordae of mitral valve that leads to a floppy valve that doesn’t function properly during systole.

Front 346

What CT disorder can often lead to mitral valve prolapse?

Back 346

Marfan syndrome where the collagen in the mitral valve is disordered so valve is defective

Front 347

What condition would result in ballooning of the mitral valve leaflets into the left atrium?

Back 347

Mitral valve prolapse

Front 348

What are the clinical manifestations of mitral valve prolapse?

Back 348

Most pts are asymptomatic, but some will have palpitations, fatigue, or atypical chest pain. On auscultation you would hear a sharp mid-systolic click followed by late systolic murmur

Front 349

What are potential complications of mitral valve prolapse?

Back 349

Can lead to CHF but the largest complication is the increased risk for developing infective endocarditis. Pt must be prophylaxed prior to dental tx if they are symptomatic

Front 350

What are the characteristics of nonbacterial thrombotic endocarditis (NBTE)?

Back 350

Small fibrin and platelet thrombi (vegetations) loosely adherent to valve leaflets along lines of closure. Frequently found in cachectic pts, particularly in setting of cancer, so its commonly called “wasting away” endocarditis. It is commonly attributed to disseminated intravascular coagulation (DIC)

Front 351

What is Libman-Sacks endocarditis?

Back 351

It refers to sterile vegetations on cardiac valves of pts with systemic lupus erythematosus. These will occur most frequently on ventricular surfaces of mitral and tricuspid valves and do not have predilection for lines of valve closure

Front 352

What organisms are generally associated with acute infective endocarditis?

Back 352

Highly virulent bacteria such as Staph aureus that can infect even structurally normal valves. They cause rapid infection

Front 353

What organisms are generally associated with subacute infective endocarditis?

Back 353

Bacteria that are less virulent such as a-hemolytic streptococci that usually infect abnormal valves. They cause slower progressing infection that is accompanied by local inflammatory reaction and granulation tissue in the affected valve

Front 354

What are some causative events for Bacteremia that can lead to infective endocarditis?

Back 354

IV drug abuse, dental or surgical procedures, or injuries to gut, urinary tract, oropharynx, or skin

Front 355

Why is infective endocarditis difficult to eradicate?

Back 355

Due to the avascular nature of heart valves there isn’t much of an inflammatory response to the infection. Without effective antibiotics it would almost always be fatal.

Front 356

What is the hallmark of infective endocarditis?

Back 356

Presence of valvular vegetations containing bacteria or other organisms

Front 357

What are the most common sites of infection in infective endocarditis?

Back 357

Aortic and mitral valves (left side of heart)

Front 358

What side of the heart is more often infected in IV drug abusers?

Back 358

The right side because they are injecting into veins usually. They will often become infected with Staph aureus

Front 359

What are the two types of prosthetic heart valves used?

Back 359

Bio valves (pig/cow/human) and mechanical valves

Front 360

What will any pt with a mechanical valve need to take?

Back 360

Anti-coagulation meds due to exposure of non-biologic surfaces

Front 361

What is the main advantage of mechanical valves?

Back 361

They will last indefinitely until the pt dies

Front 362

What is the main advantage of bio valves?

Back 362

They don’t require use of anti-coagulation meds

Front 363

What are the complications associated with all prosthetic valves?

Back 363

Para-valvular leakage, thrombosis, infective endocarditis, and structural deterioration

Front 364

What are primary myocardial diseases?

Back 364

They affect the muscles of the heart but aren’t necessarily caused by vascular problems. This includes inflammatory disorders (myocarditis), immunologic diseases (rheumatic fever), systemic metabolic disorders (hemochromatosis), and muscular dystrophies

Front 365

What is the difference between myocarditis and MI damage?

Back 365

MI damage is caused by ischemia, in myocarditis the damage is actually caused by the inflammatory process

Front 366

What are the major causes of myocarditis?

Back 366

Infections (viruses, bacteria, fungi, helminthes, protozoa, etc), immune-mediated (post-viral, rheumatic fever, SLE, drug hypersensitivity, transplant rejection), and others such as sarcoidosis (giant cell myocarditis)

Front 367

What are the most common cause of infective myocarditis in the USA?

Back 367

Viruses such as Coxsackieviruses A and B and other enteroviruses. Adenoviruses also common

Front 368

Which layers of the hear are affected in myocarditis?

Back 368

Only the myocardium, the endocardium and valves are unaffected

Front 369

What form of myocarditis is Chagas disease?

Back 369

It is due to a protozoan called Trypanosoma cruzi transmitted to humans via insect vector

Front 370

What heart condition can Lyme disease cause?

Back 370

Lyme myocarditis caused by spirochetes. This is usually mild and reversible

Front 371

What is cardiomyopathy?

Back 371

Literally means heart muscle disease, could be applied to almost any heart disease. By convention it is used to describe heart disease resulting from a primary abnormality in the myocardium

Front 372

What are the three categories of cardiomyopathy?

Back 372

Dilated, hypertrophic, and restrictive

Front 373

What are the major causes of hypertrophic cardiomyopathy?

Back 373

Infants of diabetic mothers, storage diseases, and Autosomal dominant inheritance of 50% (this is due to mutation in gene for myosin heavy chain and other contractile proteins

Front 374

What are the characteristics of a hypertrophic cardiomyopathy?

Back 374

Heavy, muscular, hypercontractile heart that is poorly compliant and has poor diastolic relaxation

Front 375

What is restrictive cardiomyopathy?

Back 375

Decrease in ventricular compliance leading to stiff and inelastic ventricle that can be filled only with great effort. Result is impaired ventricular filling during diastole

Front 376

What are the common causes of restrictive cardiomyopathy?

Back 376

Cardiac amyloidosis (usually a result of multiple myeloma), endocardial fibroelastosis, hemochromatosis, and radiation injury

Front 377

What is the most common cause of heart disease in children in western world?

Back 377

Congenital heart disease

Front 378

What is the most common acquired heart disease in children?

Back 378

Kawasaki disease

Front 379

What is one of the most important environmental factors in congenital heart disease?

Back 379

Congenital rubella infection. Still, this accounts for only a small percentage. Most of the cases are idiopathic

Front 380

What are the three major groups of congenital heart disease?

Back 380

Left-to-right shunt, right-to-left shunt (cyanotic), and obstruction

Front 381

What is the most common malformation in congenital heart disease?

Back 381

Ventricular septal defect followed by atrial septal defect and patent ductus arteriosus

Front 382

What is the most well defined genetic association with congenital heart disease?

Back 382

Trisomies 13, 15, 18, 21, and Turner syndrome

Front 383

What types of diseases can occur in the pericardium?

Back 383

Inflammatory conditions and effusions usually in conjunction with local myocardial or mediastinal diseases as well as uremia

Front 384

What is the etiologic agent responsible for most cases of primary pericarditis?

Back 384

Viruses usually, but can be pyrogenic bacteria or fungi

Front 385

What is the most common systemic disorder associated with pericarditis?

Back 385

Uremia

Front 386

What dictates the appearance of acute pericarditis?

Back 386

It depends on what caused it. For uremia or RF it is fibrinous and has a shaggy appearance (“break and butter”), for viral it is a “violin string” exudate, for bacteria it is fibropurulent, and for TB it is caseous

Front 387

What is constrictive pericarditis?

Back 387

It is a form of chronic disease where the heart is completely encased in dense scar tissue to the point that it can’t expand normally during diastole

Front 388

What are the clinical manifestations of pericarditis?

Back 388

Atypical chest pain that is often worse on reclining and has a high-pitched friction rub on auscultation

Front 389

What are the major types of pericardial effusions?

Back 389

Serous, serosanguineous, and chylous

Front 390

What causes serous effusions?

Back 390

CHF and hypoalbuminemia

Front 391

What causes serosanguineous effusions?

Back 391

Blunt chest trauma and malignancy

Front 392

What causes chylous effusions?

Back 392

Mediastinal lymphatic obstruction

Front 393

What can occur is effusions develop rapidly?

Back 393

Cardiac tamponade

Front 394

What type of tumor would most likely develop on the heart?

Back 394

Metastatic secondary tumor in pts with disseminated cancer. Usually involve the pericardium and cause hemorrhagic effusions

Front 395

Which primary neoplasms most commonly metastasize to the heart?

Back 395

Carcinoma of the lung and breast, melanocarcinoma, and hematopoietic malignancies.

Front 396

What are the most common primary tumors of the heart?

Back 396

Myxoma, lipoma, rhabdomyoma, angiosarcoma, and rhabdomyosarcoma (these are all very rare though)

Front 397

What is the most common primary cardiac tumor of infancy and childhood?

Back 397

Cardiac rhabdomyoma, best known for their association with tuberous sclerosis (neurocutaneous syndrome)

Front 398

What are the four categories of atelectasis and which ones are reversible?

Back 398

Resorption, compression, and microatelectasis are reversible. Contraction atelectasis is irreversible

Front 399

What is the most common cause of resorption atelectasis?

Back 399

Obstruction of a bronchus postoperatively by a mucous or mucopurulent plug

Front 400

What is the most important contribution to the development of microatelectasis?

Back 400

Loss of surfactant

Front 401

What is the effect on expiratory flow rate of obstructive lung diseases?

Back 401

It is decreased

Front 402

What is the effect on FVC and FEV1 of restrictive lung diseases?

Back 402

FVC and FEV1 are both reduced

Front 403

What is the only difference on a PFT between restrictive and obstructive lung disease?

Back 403

FVC is increased in obstructive and decreased in restrictive

Front 404

What does FEV1/FVC ratio tell you and how does it indicate disease state?

Back 404

It is the portion of total lung capacity exhaled in the first second. This should be about 80% in healthy people. In obstructive disease FEV1 is reduced due to obstruction to air escape, so the ratio is reduced. In restrictive disease both FEV1 and FVC are reduced so the ration stays about the same

Front 405

What are the major obstructive lung diseases?

Back 405

Asthma, emphysema, chronic bronchitis, bronchiectasis, cystic fibrosis, and bronchiolitis

Front 406

What lung condition results from obstructive disease?

Back 406

Hyperinflation, not collapse

Front 407

What are the two general conditions where restrictive defects would be present?

Back 407

Extra-pulmonary disorders such as obesity, kyphoscoliosis, and Guillain-Barre and acute or chronic interstitial diseases (ARDS, pneumonoconioses, sarcoidosis, idiopathic pulmonary fibrosis)

Front 408

Is bronchial asthma considered acute or chronic inflammatory disorder?

Back 408

Chronic

Front 409

What are the two categories of asthma?

Back 409

Extrinsic and intrinsic, based on presence or absence of underlying immune disorder

Front 410

Which one of the above is IgE mediated (atopic)?

Back 410

Extrinsic

Front 411

What are the three types of extrinsic asthma?

Back 411

Atopic, occupational, and allergic bronchopulmonary aspergillosis

Front 412

Which of the above is the most common?

Back 412

Atopic

Front 413

What are the major histologic identifiers of asthma?

Back 413

Curschman spirals and Charcot-Leyden crystals

Front 414

What obstructive lung disease is the 4th leading cause of death is USA?

Back 414

COPD

Front 415

What conditions are encompassed by COPD?

Back 415

Small airway disease (SAD), chronic bronchitis, and emphysema

Front 416

How is COPD distinguished from asthma?

Back 416

COPD is irreversible airflow obstruction while asthma is reversible largely “Emphysema is more common and more severe in men”

Front 417

What part of the lung is affected by emphysema?

Back 417

The alveoli become permanently enlarged and the septal walls get destroyed. This leads to loss of elastic recoil and air becomes trapped

Front 418

What are the first symptoms of emphysema?

Back 418

Usually dyspnea is the first symptom unless the pt has underlying chronic bronchitis or asthmatic bronchitis. In that case they would likely initially complain of cough and weezing

Front 419

How does the pattern of distribution of affected tissue differ in bronchitis and emphysema?

Back 419

Chronic bronchitis mainly affects large and small airways while emphysema affects the acinus (distal to terminal bronchioles)

Front 420

What are the three types of emphysema?

Back 420

Centriacinar, panacinar, and distal acinar (the first two are more important)

Front 421

What is the most common type of emphysema?

Back 421

Centriacinar

Front 422

How is centriacinar emphysema classified?

Back 422

By the pattern of involvement in lobules. The central parts of the acinus formed by the respiratory bronchioles are affected first and distal alveoli are spared

Front 423

Are the upper or lower lobes more severely affected by centriacinar emphysema?

Back 423

Lesions are more severe and more common in the upper lobes

Front 424

What is the likely cause of centriacinar emphysema?

Back 424

Cigarette smoking in people who don’t have congenital deficiency in a1-antitrypsin (AAT)

Front 425

What are the characteristics of panacinar emphysema?

Back 425

The acini are uniformly enlarged and disease is more diffuse from the bronchiole to the terminal alveoli

Front 426

What is the likely cause of panacinar emphysema?

Back 426

Happens most frequently in pts with a1-antitrypsin deficiency (ATT) and also in smokers with centriacinar emphysema

Front 427

Are the upper or lower lobes more severely affected in panacinar emphysema?

Back 427

The lower lobes

Front 428

What is the predominant theory on the mechanism of emphysema destruction of lung tissue?

Back 428

Proteinases vs anti-proteinases. If there is a deficiency in anti-proteinases then tissue destruction will result via proteinase activity

Front 429

What is the major function of a1-antitrypsin?

Back 429

It protects tissues against the enzyme neutrophil elastase

Front 430

What effect does cigarette smoking have on anti-proteases?

Back 430

It creates a functional rather than congenital deficiency in AAT due to production of reactive oxygen species that inactivate ATT

Front 431

What are “pink puffers”?

Back 431

Pts with emphysema and no bronchitis component. They are barrel-chested and dyspnic and have prolonged expiration with noticeable effort

Front 432

What are “blue bloaters”?

Back 432

Pts with emphysema and chronic bronchitis. They have less prominent dyspnea but retain a lot of CO2 and become hypoxic and cyanotic. They tend to be obese

Front 433

Where do most pts fit in with respect to the two above categories?

Back 433

Somewhere in between these two extremes

Front 434

What is the end result of all COPD cases?

Back 434

Secondary pulmonary hypertension, right-sided heart failure, and death related to pulmonary failure eventually

Front 435

How is chronic bronchitis diagnosed?

Back 435

It is defined clinically as a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years

Front 436

There are several forms of chronic bronchitis, what is the most common?

Back 436

Simple chronic bronchitis where the productive cough raises mucoid sputum

Front 437

What is the defining feature of chronic bronchitis?

Back 437

Mucus hyper-secretion usually beginning in the large airways“Chronic bronchitis with significant airflow obstruction is almost always complicated by emphysema”

Front 438

What are the histologic characteristics of chronic bronchitis?

Back 438

Edema of mucous membranes, mucous secretions filling airways, increase in size of mucous glands, and squamous metaplasia or dysplasia of bronchial epithelium

Front 439

What is bronchiectasis?

Back 439

Permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic supporting tissue. This is usually due to chronic necrotizing infections or bronchial obstructions (so it isn’t a primary disease)

Front 440

What are the main symptoms of bronchiectasis?

Back 440

Cough with expectoration of purulent sputum

Front 441

How is bronchiectasis diagnosed?

Back 441

By radiographic demonstration of bronchial dilation

Front 442

What congenital or hereditary condition can often lead to bronchiectasis?

Back 442

Cystic fibrosis

Front 443

What are the two critical processes involved in the pathogenesis of bronchiectasis?

Back 443

Obstruction and chronic persistent infection

Front 444

What is one very notable external sign of bronchiectasis?

Back 444

Clubbing of fingers

Front 445

What is the major characteristic of restrictive lung disease?

Back 445

Reduced lung compliance resulting in greater pressure requirement to expand the lungs because they are stiff due to interstitial lung disease

Front 446

What are the manifestations of acute respiratory distress syndrome?

Back 446

Acute onset of dyspnea with tachypnia and rales, hypoxemia, bilateral pulmonary edema, and diffuse symmetrical lung involvement

Front 447

What are common causes of ARDS?

Back 447

Pneumonia, aspiration of gastric contents, sepsis, and severe trauma with shock

Front 448

What is the most common cause of non-cardiogenic pulmonary edema?

Back 448

ARDS, the edema is due to PMN’s releasing oxygen radicals that cause damage to alveolar capillary membrane. It is not caused by left-sided heart failure

Front 449

What are the two sequences of events in diffuse alveolar damage (ARDS)?

Back 449

Acute (exudative) for the first few days and fibroproliferative for a week to a month.

Front 450

What is the most characteristic finding in diffuse alveolar damage (ARDS)?

Back 450

Hyaline membranes lining the distended alveolar ducts. These are only present during the acute stage though and disappear during the fibroproliferative stage

Front 451

What is the prognosis of ARDS?

Back 451

Grim, used to be 100% mortality rate, but now is down to 30-40%

Front 452

What is the end stage of most chronic restrictive lung diseases?

Back 452

Diffuse interstitial pulmonary fibrosis with or without honeycombing

Front 453

What is the most common subtype of chronic interstitial lung disease?

Back 453

Idiopathic pulmonary fibrosis (cause largely unknown). There are over 150 causes that are known though

Front 454

Existence of granulomas histologically would implicate what causes of ILD?

Back 454

Exposure to coal, asbestos, and silica. Could be CWP, sarcoidosis, Wegener granulomatosis, or hypersensitivity pneumonitis

Front 455

What is the histologic identifier of sarcoidosis?

Back 455

Non-caseating granulomas in many tissues and organs

Front 456

What other diseases can cause non-caseating granulomas, thus complicating diagnosis of sarcoidosis?

Back 456

Mycobacterial and fungal infections and berylliosis

Front 457

What is the hallmark of acute sarcoidosis?

Back 457

Erythema nodosum (raised, red, tender nodules on the legs)

Front 458

What demographic groups have highest incidence of sarcoidosis?

Back 458

Danes/Swedes and US blacks (10 times > US whites)

Front 459

Are smokers are higher risk for developing sarcoidosis?

Back 459

No

Front 460

What are the etiologic factors in sarcoidosis?

Back 460

Immunologic and genetic mostly. There isn’t any evidence to suggest involvement of an infectious agent

Front 461

What is the histologic morphology of sarcoidosis?

Back 461

Non-caseating epitheliod granulomas full of histiocytes and rimmed by CD4+ helper T cells

Front 462

What are the manifestations of Wegener granulomatosis?

Back 462

Necrotizing vasculitis, parenchymal necrotizing granulomatous inflammation, necrotizing granulomas of the pulmonary vessels, and acute and chronic inflammation intermingled with fibrinoid necrosis

Front 463

Collagen vascular disorders affecting the lungs can lead to what?

Back 463

Diffuse interstitial fibrosis culminating as end-stage honeycomb lung. At this point the only tx is to get a lung transplant

Front 464

What is the most common preventable cause of death in hospitalized pts?

Back 464

Pulmonary thromboembolism

Front 465

What are the risk factor for pulmonary thromboembolism?

Back 465

Prolonged bed rest, surgery on legs, severe trauma, CHF, disseminated cancer, and birth control pills for women

Front 466

What are the cardiac consequences of a pulmonary embolism?

Back 466

Acute right-sided HF ensues due to increased pulmonary arterial pressure. Right-to-left shunting of blood can occur in pts with a patent foramen ovale

Front 467

What is a saddle embolus?

Back 467

A clot that is lodged in a bifurcation of the pulmonary artery

Front 468

Why are most pulmonary emboli clinically silent?

Back 468

Because they are small and are quickly removed by fibrinolytic activity

Front 469

At what point does a pulmonary embolism cause serious morbidity/mortality?

Back 469

When 60% or more of vasculature gets obstructed. This can lead to right-sided HF, cardiovascular shock, or sudden death (this is one of the few things that can cause instant death, even before any symptoms appear)

Front 470

What is the biggest risk factor for pulmonary embolism?

Back 470

Previous pulmonary embolism, over 30% will develop a second

Front 471

What are the prophylactic measures taken to prevent thromboembolism?

Back 471

Early ambulation for post-op/post-partum pts, elastic stockings, leg exercises for bedridden pts, and anticoagulation/thrombolytic meds for persons at high risk

Front 472

What are the most frequent causes of pulmonary hypertension?

Back 472

Chronic obstructive or interstitial lung disease, recurrent pulmonary emboli, heart disease with a left-to-right shunt

Front 473

What demographic would most likely exhibit pulmonary vascular sclerosis?

Back 473

Young person, commonly women. This will accentuate the effects of heart problems, causing fatigue, syncope, dyspnea, and chest pain

Front 474

What is the incidence and mortality of pneumonia?

Back 474

It is responsible for one sixth of deaths in USA

Front 475

What is the most common pathogen to cause upper respiratory infections?

Back 475

Rhinoviruses

Front 476

Why is it important to quickly identify and treat Streptococcal tonsillitis?

Back 476

Because a peritonsillar abscess, glomerulonephritis, or acute rheumatic fever can develop

Front 477

What is the biggest concern for children that have acute bacterial epiglottitis?

Back 477

Maintaining an open airway as airway obstruction is common

Front 478

What pathogen causes a grey pseudomembrane in the upper respiratory tract?

Back 478

C. diptheriae

Front 479

What is the most common cause of croup (laryngotracheobronchitis)?

Back 479

Parainfluenza

Front 480

What is one of the most frightening manifestations of croup?

Back 480

Stridor, which is a high pitched sound resulting from turbulent airflow in the upper airway during inspiration or expiration

Front 481

What is consolidation (referring to the lungs)?

Back 481

Loss of air space and replacement of fluid, often due to inflammatory response to infection

Front 482

What are the characteristics of bronchopneumonia (lobular pneumonia)?

Back 482

It is termed “hospital acquired” and is often caused by Staph aureus, Klebsiella, E. coli or Pseudomonas. It results in multiple patchy foci of acute consolidation and usually affects one or more lobes

Front 483

What are the characteristics of lobar pneumonia?

Back 483

It is termed “community acquired pneumonia” and is caused by Strep >90% of the time. It results in consolidation of an entire lobe or multiple lobes

Front 484

What is more important, determining the type of pneumonia or the organism causing it?

Back 484

The causative agent and the extent of damage are the more important things to assess

Front 485

What are the seven types of pneumonia syndromes?

Back 485

Community acquired acute and atypical, nosocomial, aspiration, chronic, necrotizing, and immunocompromised

Front 486

What is the most common cause of community acquired pneumonia?

Back 486

Strep pneumonia

Front 487

Deficiency of what organ will predispose to pneumococcal infections?

Back 487

The spleen because it’s the major organ responsible for removing pneumococcus from the blood

Front 488

What are the 4 stages of pneumococcal pneumonia?

Back 488

Congestion, red hepatization, gray hepatization, and resolution

Front 489

What is the most common cause of atypical pneumonias?

Back 489

Mycoplasma pneumonia (Eaton agent). This will present very similar to viral pneumonia and Chlamydiae pneumonia

Front 490

What histologic feature differentiates atypical pneumonia?

Back 490

Alveolar spaces are remarkably free of cellular exudate and the organisms attach to cilia

Front 491

Look at slide 90 of lecture 14

Front 492

What are the characteristics of influenza virus?

Back 492

Genome composed of eight segments of ssRNA and helical ribonucleo-protein

Front 493

Which types of pts would more commonly develop nosocomial pneumonia?

Back 493

Severe underlying disease, immunosuppression, prolonged antibiotic tx, invasive catheters, or pts on mechanical ventilation (ventilator-associated pneumonia (VAP)

Front 494

Who is at greatest risk for aspiration pneumonia?

Back 494

Patients who have an abnormal gag and swallowing reflex that facilitates aspiration. This is a frequent cause of death in these patients.

Front 495

What causes the lung damage in aspiration pneumonia?

Back 495

The irritating nature of stomach acids as well as aerobic bacteria

Front 496

What kind of disease is TB?

Back 496

Chronic granulomatous disease with caseous necrosis

Front 497

What is the term for disseminated TB infection?

Back 497

Miliary TB, can affect many other organs such as spleen and liver

Front 498

Where are primary and secondary TB lesions generally located?

Back 498

In the apex of one or both upper lobes of the lungs

Front 499

What is a Ghon complex?

Back 499

A calcified focus (lesion) and an associated lymph node in the lung of pt with TB

Front 500

What is non-reactive TB?

Back 500

This is when an immunocompromised persons has TB that doesn’t elicit a granulomatous response

Front 501

What are the species of dimorphic fungi?

Back 501

Histoplasma capsulatum, Coccidioides immitis, and Blastomyces dermatitidis

Front 502

What are some species of opportunistic fungi?

Back 502

Molds (Aspergillus and mucormycosis), and yeasts (Candida and Cryptococcus neoformans)“All systemic fungi, either deep seated or opportunistic, can infect the lungs.”

Front 503

What is the most frequent disease causing fungus?

Back 503

Candida albicans

Front 504

What is an important histologic diagnostic clue for Candida albicans?

Back 504

Presence of pseudohyphae (they will also demonstrate true hyphae and yeast-like forms)

Front 505

What special fungal stain is commonly used to highlight the pathogens?

Back 505

Periodic acid-Schiff (PAS)

Front 506

What tissues can candidiasis invade?

Back 506

Skin, mucous membranes, and deep organs (invasive candidiasis). The most common is superficial infection of mucosal surfaces, but most serious is invasive form

Front 507

What complications can arise from taking oral corticosteroids for asthma?

Back 507

Candida infection

Front 508

What predisposes a woman to vaginal candidiasis?

Back 508

Diabetes, pregnancy, and birth control pills

Front 509

Who is at greatest risk for invasive candidiasis?

Back 509

Cancer pts who are severely neutropenic following chemo.

Front 510

What is the most common fungal endocarditis?

Back 510

Candida endocarditis that usually occurs in pts with prosthetic heart valves or IV drug abuse

Front 511

How does candida and Cryptococcus differ histologically?

Back 511

Cryptococcus is budding yeast only, no hyphae or pseudohyphae

Front 512

What organs are affected by Crypto?

Back 512

Pulmonary, CNS, or disseminated disease. Usually localizes in the lungs by inhalation and disseminates to other sites from there, especially the meninges

Front 513

What population is at risk for mucormycosis and invasive aspergillosis?

Back 513

These are uncommon infections because they only affect immunocompromised people. Those commonly affected include hematolymphoid malignancies, profound neutropenia, corticosteroid therapy, and transplant pts

Front 514

What causes mucormycosis?

Back 514

Zygomycetes, which are non-septate fungi. The two major fungi of this class are Rhizopus and Mucor

Front 515

What are the morphologic characteristics of Aspergillus?

Back 515

Septate hyphae that branch at acute angles

Front 516

What is the risk of fungal infection for diabetic ketoacidotic pts?

Back 516

They are more likely to develop fulminant invasive form of mucormycosis that invades the nasal cavity, sinuses, and eventually the orbit and brain

Front 517

What is an aspergilloma?

Back 517

It is a fungus ball where fungi have colonized a preexisting pulmonary cavity (lung cyst, post-tuberculous cavity, etc) caused from a previous disease

Front 518

What is the geographic distribution of the dimorphic fungi H. capsulatum?

Back 518

Ohio and central Mississippi river valleys and along the Appalachian mountains in southeast US

Front 519

What is the geographic distribution of the dimorphic fungi C. immitis?

Back 519

Southwest and far west US, particularly San Joaquin Valley

Front 520

What is the geographic distribution of B. dermatitidis?

Back 520

Areas overlapping with H. capsulatum

Front 521

What are primary pulmonary nodules?

Back 521

Aggregates of macrophages stuffed with dimorphic fungi that develop into small granulomas complete with giant cells. They may develop central necrosis and later fibrosis and calcification

Front 522

What other lung disease is very similar to acute pulmonary infection of dimorphic fungi?

Back 522

Primary tuberculosis

Front 523

What condition will develop in a vulnerable host from prolonged infection of dimorphic fungi?

Back 523

Chronic cavitary pulmonary disease with perihilar mass lesions that can resemble bronchogenic carcinoma radiologically

Front 524

When blastomyces (dimorphic fungus) infections become disseminated, what is a common manifestation?

Back 524

Cutaneous infections that can induce pseudoepitheliomatous hyperplasia (PEH) which may be mistaken for squamous cell carcinoma

Front 525

What is the most likely cause of a lung abscess?

Back 525

Aspiration of infective material from carious teeth or infected sinuses or tonsils. The most frequently encountered anaerobes are commensals normally found in the oral cavity

Front 526

What are the clinical manifestations of a lung abscess?

Back 526

Prominent productive cough, spiking fever and malaise, clubbing of fingers, weight loss, and anemia

Front 527

When a lung abscess is suspected in an older pt, what other disease must be considered?

Back 527

Underlying carcinoma, owing to the fact that bronchogenic carcinoma often leads to lung abscesses

Front 528

For whom is CMV pneumonitis a serious problem?

Back 528

For AIDS and transplant pts

Front 529

What is the most common opportunistic viral pathogen in AIDS?

Back 529

CMV

Front 530

What is the most common form of opportunistic CMV disease?

Back 530

CMV retinitis

Front 531

What type of organism is Pneumocystis?

Back 531

It was once believed to be protozoa, but now thought to be fungus

Front 532

Are bacterial or fungal pneumonias more common in AIDS pts?

Back 532

Bacterial are more common and more severe and often associated with Bacteremia

Front 533

How does CD4 count help you determine the cause of pneumonia in AIDS pts?

Back 533

>200 is likely bacterial or TB, <200 is likely Pneumocystis, and CMV/Mycobacterium avium is <50

Front 534

What type of cancer makes up the majority of lung tumors?

Back 534

95% arise from bronchial epithelium (bronchogenic carcinomas)

Front 535

What is the most common benign lesion of the lungs?

Back 535

Hamartomas that consist mainly of mature cartilage mixed with bronchiolar epithelium, fat, fibrous tissue, and blood vessels

Front 536

What is the number on e cause of cancer related death in industrialized countries?

Back 536

Bronchogenic carcinoma (lung cancer)

Front 537

What is the demographic trend for lung cancer in the USA?

Back 537

Rate is decreasing in males and increasing in females

Front 538

What is the age of peak incidence?

Back 538

Between the ages of 55-65 years

Front 539

Where do bronchogenic carcinomas usually originate?

Back 539

In the large bronchi, therefore the mass is usually around the hilar region

Front 540

What are the two groups or distinctions of bronchogenic carcinomas?

Back 540

Divided into small cell and non-small cell cancers. This distinction arises due to the difference in how they respond to tx.

Front 541

How would you treat small vs. non-small lung cancers?

Back 541

The small cells have likely metastasized by dx and are not amenable to surgery. They are best treated with chemo. The non-small cell cancers usually respond poorly to chemo and are better treated with surgery

Front 542

What are the 4 major histologic classifications of lung cancer?

Back 542

The non-small cell cancers include squamous cell carcinomas, Adenocarcinomas, and large cell carcinomas. The other group is small cell carcinoma

Front 543

Which type of cancer has a better prognosis?

Back 543

Non-small cell cancers, as long as they haven’t metastasized. This is because surgery can provide a cure via lobectomy or pneumonectomy

Front 544

What is the most common primary lung tumor?

Back 544

Adenocarcinoma, not squamous cell carcinoma. This trend is particularly true for women, non-smokers, and those under 45 y/o

Front 545

What percentage of lung cancers occur in smokers or recently quit smokers?

Back 545

About 90%

Front 546

Does quitting smoking eventually provide even risk levels for lung cancer compared to people who have never been smokers?

Back 546

No, they may never return to baseline levels

Front 547

What genotypes would make someone more prone to lung cancer caused by smoking?

Back 547

Certain polymorphisms of the P 450 genes as well as peripheral blood lymphocyte phenotype

Front 548

Which types of lung cancer have the strongest association with cigarette smoking?

Back 548

Adeno, squamous, and small cell carcinomas

Front 549

How does asbestos exposure affect lung cancer risk of smoker and non-smokers?

Back 549

Non-smokers have a 5 times increased risk, smokers have a 55 times greater risk

Front 550

What are the characteristics of squamous cell carcinoma of the lung?

Back 550

It is more common in men and usually begins as a central hilar mass and grows peripherally into the parenchyma and spreads to local lymph nodes. It commonly undergoes cavitary necrosis and usually takes longer to disseminate outside the thorax than other types

Front 551

How are SSC of the lung identified?

Back 551

They are commonly asymptomatic at first but can be identified by cytologic smear of sputum or bronchial lavage fluids. When it gets larger it will begin to be symptomatic as it obstructs lumen of a major bronchus and starts to cause atelectasis

Front 552

What are the characteristics of Adenocarcinomas of the lung?

Back 552

They are usually more peripherally located than SCC and are slower growing. Despite slow growth, they metastasize widely at an early stage

Front 553

What is bronchoalveolar cancer?

Back 553

A sub-category of adenocarcinoma that isn’t truly bronchogenic. It arises from cells lining small airways (bronchioles) and/or cells lining the alveoli. The cells affected in the bronchioles are the “clara cells” and the cells affected in the alveoli are the type 2 cells. These tumors are usually peripherally located

Front 554

Which type of BAC is related to tobacco smoking?

Back 554

The non-mucinous type

Front 555

What are large cell carcinomas?

Back 555

A group of neoplasms that are too undifferentiated to permit categorization. They may be squamous cell or glandular in origin. The prognosis is poor due to early metastasis

Front 556

What are the characteristics of small cell lung carcinomas?

Back 556

They are called oat cell carcinomas due to the shape and appearance of the cells. They are generally centrally located masses that extend into lung parenchyma and have early involvement in hilar and mediastinal nodes.

Front 557

What is the prognosis of small cell lung carcinoma?

Back 557

It is generally a silent, insidious lesion that has a grim prognosis if symptoms have begun. Usually it has already spread by that point so it can’t be surgically resected. It’s common for the first symptoms to be due to metastatic spread to other organs

Front 558

How do you treat an oat cell lung cancer?

Back 558

Surgery doesn’t work, so you have to do chemo and radiation. Even with this though, the lesion invariably recurs and pt won’t live more than 2 years

Front 559

What histologic finding can distinguish a small cell (oat cell ) carcinoma?

Back 559

Extensive necrosis and “crush artifact” from fragmentation. Also nuclear molding is common

Front 560

What paraneoplastic syndromes can develop from lung cancers?

Back 560

SCC can lead to increased PTH and hypercalcemia, adenocarcinoma can lead to hematologic syndromes like DIC and thrombophlebitis, and other carcinomas may lead to neuromuscular syndromes. SCLCs may lead to increased ADH or ACTH

Front 561

What is a bronchial carcinoid tumor?

Back 561

A Neuroendocrine tumor that can lead to Neuroendocrine secretions that cause carcinoid syndrome. Not as malignant as oat cell tumor but still malignant

Front 562

What lung tissue gives rise to mesothelioma?

Back 562

The parietal or visceral pleura

Front 563

Does cigarette smoking increase risk of developing mesothelioma in persons exposed to asbestos?

Back 563

No, the increased risk is for development of bronchogenic carcinoma

Front 564

Which form of asbestos causes mesothelioma?

Back 564

Amphibole asbestos, not serpentine

Front 565

Presence of what virus is associated with 60-80% of pleural malignant mesotheliomas?

Back 565

Simian virus 40 (SV40) due to a carcinogenic antigen that it produces

Front 566

What is the appearance of the lung at autopsy of a mesothelioma pt?

Back 566

Lung is ensheathed by a yellow-white layer of tumor that obliterates the pleural space

Front 567

What is the most common histologic pattern of mesothelioma?

Back 567

Epithelial pattern, most likely to be confused with pulmonary adenocarcinoma

Front 568

Are benign mesotheliomas related to asbestos exposure?

Back 568

No

Front 569

Which virus is strongly related to nasopharyngeal carcinoma?

Back 569

EBV

Front 570

How do nasopharyngeal and Burkitt lymphoma tumors differ?

Back 570

While they are both associated with EBV, nasopharyngeal tumors almost always have the EBV genome present (not so with Burkitt)

Front 571

What is the most common variant of nasopharyngeal carcinoma?

Back 571

Undifferentiated form, characterized by large epithelial cells with syncytial growth and prominent nucleoli

Front 572

What is a lymphoepithelioma?

Back 572

Large neoplastic cells in a background of reactive lymphocytes that appears similar to non-Hodgkin lymphoma. The neoplasm is epithelial in nature, lymphocytes are not neoplastic. This is not a benign tumor

Front 573

How do you treat nasopharyngeal carcinomas?

Back 573

Radiation therapy

Front 574

What is the most common initial symptom of laryngeal cancer?

Back 574

Persistent hoarseness of voice is usually the first symptom, and hemoptysis is common if the lesion is on the free edge of the vocal cord

Front 575

How do laryngeal papillomas differ between children and adults?

Back 575

In adults there is usually only one, in kids they have multiple and it is referred to as juvenile laryngeal papillomatosis

Front 576

What is the distribution of laryngeal cancers?

Back 576

Occur in men 7 times more often than women, occur usually after 40 years of age, and almost always occur in smokers

Front 577

What type of cancer is most common in the larynx?

Back 577

Squamous cell lesions, rarely adenocarcinoma. They usually occur directly on vocal cords

Front 578

Which laryngeal cancers have better prognosis, supraglottic or subglottic?

Back 578

Subglottic because the supraglottic larynx is rich in lymphatics and metastases are more common

Front 579

What is function of the majority of the pancreas?

Back 579

Exocrine pancreas is about 85-90% of the pancreas

Front 580

What is the function of the exocrine pancreas?

Back 580

Secrete digestive proenzymes such as trypsinogen and active enzymes such as amylase and lipase. It also secretes bicarbonate rich fluid and mucin that transport enzymes to duodenum

Front 581

What regulates the secretions from the exocrine pancreas?

Back 581

Duodenal humoral factors such as secretin and cholecystokinin

Front 582

How and where is trypsinogen activated?

Back 582

In the duodenum, enteropeptidase converts it into the active form trypsin

Front 583

What is the function of trypsin?

Back 583

It is a digestive enzyme as well as an activator enzyme for other proenzymes

Front 584

What are zymogen granules?

Back 584

They are where trypsinogen is stored and constitute one of the mechanisms that protect the pancreas from the enzymes it produces.

Front 585

What are the more common causes of acute pancreatitis?

Back 585

Biliary tract disease due to obstruction from gallstones or other objects and alcoholism. This is usually reversible if the cause is removed

Front 586

What is the critical trigger event in acute pancreatitis?

Back 586

Inappropriate activation of trypsin leading to autodigestion of the pancreas

Front 587

When is acute pancreatitis a medical emergency?

Back 587

When it is “full blown” acute pancreatitis called “acute abdomen”. Pts experience unrelenting pain, rigid abdomen, and absence of bowel sounds

Front 588

What lab findings would indicate acute pancreatitis?

Back 588

Increased pancreatic enzymes in urine and blood. Serum amylase is the first to become elevated followed by lipase. These are very specific markers for this condition

Front 589

What are the histologic identifiers of acute pancreatitis?

Back 589

Edema, fat necrosis, acute inflammation, proteolytic destruction of pancreatic tissue, and hemorrhage

Front 590

What is the long term sequelae of acute pancreatitis?

Back 590

Development of pancreatic pseudocyst, which is an area of necrosis surrounded by fibrous tissue. There is a cystic space that can enlarge over time, resolve, or become secondarily infected

Front 591

What is the major difference between acute and chronic pancreatitis?

Back 591

In chronic there is irreversible damage to pancreatic function, in acute the changes are reversible.

Front 592

What is the most common cause of chronic pancreatitis?

Back 592

Alcohol abuse, followed by mutation in the cystic fibrosis transmembrane conductance regulator gene (CFTR). It can also come about following repeated bouts of acute pancreatitis from long standing ductal obstruction

Front 593

What are the clinical features of chronic pancreatitis?

Back 593

Abdominal pain, indigestion, jaundice, and diabetes (due to destruction of endocrine islets)

Front 594

How do you diagnose chronic pancreatitis?

Back 594

It is difficult and requires a high degree of suspicion. You will only have mildly elevated serum amylase and lipase during attacks. Radiographic calcifications in the pancreas would indicate this condition

Front 595

What are the histologic characteristic of chronic pancreatitis?

Back 595

Fibrosis, dilation of pancreatic ducts, loss of acinar cells and chronic inflammation

Front 596

What are the two kinds of cystic neoplasms of the pancreas?

Back 596

Serous cystadenomas, and mucinous cystic neoplasms. These are mostly benign and not very common

Front 597

What are the characteristic of carcinoma of the pancreas?

Back 597

Epithelial malignancy arising from the exocrine pancreas. It is quite lethal, the 4th highest mortality rate for neoplasms. Usually affects those from 60-80 years old

Front 598

What are the risk factors for pancreatic carcinoma?

Back 598

Smoking doubles the risk, chronic pancreatitis, and diabetes

Front 599

What mutations are found in pancreatic carcinoma?

Back 599

K-RAS, and p16 are responsible 90% of the time. Others include SMAD4 and TP53

Front 600

What type of carcinoma would you most likely find in the pancreas?

Back 600

Adenocarcinomas that are highly invasive locally

Front 601

Why is carcinoma of the head of pancreas usually better prognosis?

Back 601

It’s still bad prognosis (<5% survival) but better because it is usually caught earlier as a tumor in that area will likely obstruct biliary flow and jaundice will ensue

Front 602

What are the functions of the endocrine pancreas?

Back 602

It constitutes about 10-15% of the pancreas and secretes insulin, glucagon, and other hormones

Front 603

What are Islets of Langerhans?

Back 603

Collections of cells (~1000) that consist of 5-20% alpha, 70% beta, 5% delta, and 1% pancreatic polypeptide secreting cells

Front 604

Which cells secrete insulin?

Back 604

Beta cells

Front 605

What is somatostatin?

Back 605

It is made by delta cells of the pancreas and suppresses insulin and glucagon secretion

Front 606

What triggers insulin synthesis and release?

Back 606

Rise in blood glucose triggers both, intestinal hormones and certain amino acids trigger release but not synthesis

Front 607

Which immune cells destroy beta cells in type 1 diabetes?

Back 607

CD4+ cells activate macrophages that produce cytokines that damage the cells. CD8+ cells directly kill beta cells. Also, autoantibodies produced by B cells damage beta cells

Front 608

What happens in diabetic ketoacidosis?

Back 608

Dehydration resulting from hyperglycemia and production of ketone bodies as a result of lipase activation which increases free fatty acids. These are oxidized by liver to ketone bodies. If these aren’t used fast enough they end up in the blood and urine and metabolic ketoacidosis results from increased plasma hydrogen ion concentration“Type 2 DM is a true multifactorial disease that involves multiple genetic and environmental factors”

Front 609

What are the most important environmental factors in the pathogenesis of type 2 DM?

Back 609

Sedentary lifestyle, dietary habits, and OBESITY

Front 610

How does obesity contribute to insulin resistance?

Back 610

Increases circulating free fatty acids that have a lipotoxic effect on muscle and liver tissue. This tend to reduce the activity of insulin signaling proteins and increase insulin resistance. Also, altered levels of hormones released by adipocytes such as adiponectin and resistin contribute.

Front 611

What condition is responsible for most of the complications experienced by diabetics?

Back 611

Hyperglycemia that leads to formation of AGEs and activation of protein kinase C

Front 612

What are advanced glycosylation end products?

Back 612

In hyperglycemic conditions glucose is attached to proteins irreversibly and these accumulate in vessel walls

Front 613

What pathologic conditions result from AGE deposition in vessels?

Back 613

In large vessels they promote cholesterol deposition leading to atherosclerosis. In small vessels like renal glomeruli, they accumulate in the basement membrane and cause it to thicken

Front 614

What are the histologic characteristics of the DM type 1 pancreas?

Back 614

Reduction in number and size of islets and T-lymphocyte infiltration (insulitis)

Front 615

What are the histologic characteristics of the DM type 2 pancreas?

Back 615

Amyloid deposits in islets

Front 616

What are the two types of endocrine pancreas tumors?

Back 616

Insulinomas (most common) and gastrinomas are the two islet cell tumors. They are very rare

Front 617

What conditions result from the above tumors?

Back 617

Insulinomas result in hyperinsulism and are benign 90% of the time. Gastrinomas result in Zollinger-Ellison syndrome due to hypersecretion of gastric acid that causes severe peptic ulcers

Front 618

Are gastrinomas benign or malignant?

Back 618

Half are benign and half are malignant

Front 619

Apthous ulcers all have what feature in common?

Back 619

Located on non-keratinized tissue and they are surrounded by an erythematosus halo

Front 620

What triggers apthous ulcers?

Back 620

Stress, fever, certain foods, and inflammatory bowel disease

Front 621

How can herpes virus infections be diagnosed histologically?

Back 621

Balooned cells with intra-nuclear acidophilic viral inclusions. Cells may fuse to form giant cells or polykaryons. Presence of Tzanck cells

Front 622

What percentage of Kaposi sarcoma pts will develop intraoral purpuric masses?

Back 622

>50%

Front 623

What underlying condition would you suspect in a pt that presents with oral hairy leukoplakia?

Back 623

HIV infection as this is seen almost exclusively in HIV pts

Front 624

What virus is associated with hairy leukoplakia?

Back 624

EBV, which in this case is infecting epithelial cells

Front 625

Can chronic friction or irritation lead to development of leukoplakia?

Back 625

Nope, this is a dirty lie perpetuated by the authors of our textbook

Front 626

What percentage of leukoplakia lesions will progress to SCC?

Back 626

25% of all sites in the oral cavity, 50% if the lesion is on the floor of the mouth or lateral borders of the tongue

Front 627

Has oral hairy leukoplakia been related to the development of oral cancer?

Back 627

No, which is in direct contrast to regular oral leukoplakia

Front 628

What percentage of erythroplakia will likely transform to SCC?

Back 628

>90% so recognition of these lesions is extremely important. They will appear red and velvety, and often granular with poorly defined or irregular boundaries

Front 629

Are SCCs well or poorly differentiated?

Back 629

Moderately to well-differentiated to the point where they are keratinized usually (or have keratin pearls)

Front 630

Tumors in which locations of the mouth are more likely to result in spread to regional lymph nodes?

Back 630

Half of tongue cancers and 60% of those in FOM will have spread by initial dx

Front 631

What are the possible causes of sialedenitis?

Back 631

Viral, bacterial, or autoimmune in origin.

Front 632

What is the most common cause of sialedenitis?

Back 632

Viral disease called mumps, usually caused by paramyxovirus

Front 633

What conditions may lead to bacterial sialedenitis?

Back 633

Ductal obstruction by stone formations (sialoliths) or if a pt is severely dehydrated. Those with chronic debilitating medical conditions, compromised immune function, or medications that lead to oral or systemic dehydration are also are risk for acute bacterial sialedenitis

Front 634

What conditions would lead to chronic sialedenitis?

Back 634

Decreased production of saliva with subsequent inflammation, usually related to autoimmune problems (Sjogren syndrome)

Front 635

Which salivary glands are more commonly affected by tumors?

Back 635

80% of the time the parotid glands are involved, most others are in the submandibular glands

Front 636

Are males or females more affected by salivary gland tumors?

Back 636

Females have higher incidence

Front 637

Which salivary gland tumors have better prognosis?

Back 637

70-80% of parotid tumors are benign but only 50% in submandibular are benign. In general, those in the submandibular are more ominous than the parotids

Front 638

What two tumors make up 75% of all parotid tumors?

Back 638

Pleomorphic adenomas and Warthin tumors

Front 639

What is the classic presentation of a parotid tumor?

Back 639

Mass causing painless swelling at the angle of the mandible“Parotid tumors arise most often in the superficial lobe”

Front 640

Do pleomorphic adenomas of the parotid always have well defined and encapsulated borders?

Back 640

Not always, sometimes the tumor can penetrate the capsule and so a larger margin or tissue must be resected in order to prevent recurrence.

Front 641

What is the concern when removing a parotid tumor?

Back 641

Resecting the facial nerve and causing Bell’s palsy

Front 642

What cellular derivation do pleomorphic adenomas usually have?

Back 642

Even though they may have epithelial, glandular, and CT elements, they are all derived from myoepithelial cells

Front 643

Which type of salivary gland tumor is often bilateral and more common in males?

Back 643

Warthin tumors and they are usually associated with smoking. They are very rare over all though

Front 644

What are the microscopic features of Warthin tumors?

Back 644

They have 2-tiered epithelial layer lining cystic spaces. They also have well-developed lymphoid tissue sometimes forming germinal centers

Front 645

What are the malignant tumors of the parotid?

Back 645

Malignant mixed tumors that can arise de novo or from preexisting benign pleomorphic adenomas, and mucoepidermoid carcinoma (which is the more common of the two).

Front 646

What are the morphologic and histologic characteristics of hepatocytes?

Back 646

Cords of cuboidal cells with granular cytoplasm radiating around the central vein

Front 647

What are the macrophages in the liver called?

Back 647

Kupffer cells

Front 648

What are Ito cells?

Back 648

Storage cells in the space of Disse that store fat and Vit A and can transform into myofibroblast-like cells

Front 649

What are the serum aminotransferases of the liver?

Back 649

AST and ALT (aspartate and alanine)

Front 650

What are the serum proteins made in the liver?

Back 650

Albumin and PT factors (Factors V, VII, X, prothrombin, and fibrinogen)

Front 651

What two values are used to evaluate biliary excretion function?

Back 651

Serum bilirubin and serum alkaline phosphatase

Front 652

What are the synonyms for direct and indirect bilirubin?

Back 652

Direct is conjugated bilirubin and indirect in unconjugated bilirubin. Delta is conjugated bilirubin bound to albumin

Front 653

What type of inflammation in the liver would be caused by foreign bodies, organisms, or drugs?

Back 653

Granulomatous inflammation from aggregates of macrophages and other inflammatory cells

Front 654

What are the two types of hepatocytes degeneration?

Back 654

Balooning degeneration and steatosis

Front 655

What happens in ballooning degeneration?

Back 655

Cells enlarge and cytoplasm becomes clumped. Often there will be accumulations of biliary material, iron, or copper in the cytoplasm

Front 656

What happens in steatosis?

Back 656

Hepatocytes accumulate fat droplets in the cytoplasm, can be small droplets (microvesicular) or large droplets (macrovascular).

Front 657

What types of cell death can occur with significant insult to the liver?

Back 657

Coagulative necrosis, apoptosis, and lytic necrosis

Front 658

Where would you expect to find necrosis in the liver lobules?

Back 658

In the centrilobular zone and rarely in the mid-zonal area. These areas are the last to receive oxygenated blood so are more susceptible to ischemic injury

Front 659

What is the range of necrosis that can happen in the liver?

Back 659

It can range from focal to massive, involving parts of lobules, entire lobules, or most of the liver

Front 660

What is the most serious consequence of fibrosis in the liver?

Back 660

The deposition of collagen can affect blood flow and perfusion to hepatocytes. Also, fibrosis is generally irreversible

Front 661

What is cirrhosis of the liver?

Back 661

When the liver gets nodules of regenerating hepatocytes surrounded by fibrosis. This usually constitutes end-stage liver disease and carries increased risk of malignancy

Front 662

What is the definition of liver failure?

Back 662

Loss of at least 80-90% of hepatic functional capacity

Front 663

What are the 3 categories of hepatic failure?

Back 663

Acute liver failure with massive necrosis, chronic liver disease, and hepatic dysfunction without necrosis

Front 664

What would be considered acute liver failure?

Back 664

When progression from symptom onset to hepatic encephalopathy happens in 2-3 weeks and there is massive hepatic necrosis

Front 665

Which type of liver failure is the most common?

Back 665

Chronic liver disease, acute is pretty rare. This is what results from cirrhosis

Front 666

What is happening with the hepatocytes in dysfunction without necrosis?

Back 666

Hepatocytes are viable, but unable to function normally. This is usually caused by fatty liver

Front 667

What are the clinical symptoms of liver failure?

Back 667

Jaundice, peripheral edema (due to hypoalbuminemia) and cerebral compromise (due to hyperammonemia from defective urea cycle function), spider angiomas, hypogonadism, gynocomastia, and fetor hepaticus.

Front 668

What are the serious complications of liver failure?

Back 668

Sepsis from accumulation of toxic metabolites, multiple organ failure (respiratory and renal), coagulopathy due to lack of clotting factors, hepatic encephalopathy, and hepatorenal syndrome

Front 669

What is hepatic encephalopathy?

Back 669

It is a complication of acute and chronic liver failure. In acute cases it is due to elevated ammonia that impairs neuronal function and causes generalized brain edema. In chronic cases it is due to alterations of CNS amino acid metabolism that causes abnormal neurotransmission

Front 670

What are the symptoms associated with hepatic encephalopathy?

Back 670

CNS dysfunction, confusion, stupor, coma, rigidity, hyperreflexia, seizures, and asterixis

Front 671

What is asterixis?

Back 671

A pattern of non-rhythmic, rapid extension and flexion movements of the head and extremities that is commonly seen in hepatic encephalopathy

Front 672

What happens to the liver in cirrhosis?

Back 672

Progressive and diffuse fibrosis of the liver. The architecture of the liver is altered and abnormal nodules develop. This starts with hepatocellular death followed by fibrosis and regeneration

Front 673

What are the most common causes of liver cirrhosis?

Back 673

Alcohol abuse accounts for 60-70% and hepatitis B and C are the other main ones

Front 674

What is the difference in collagen deposition and distribution in normal and cirrhotic livers?

Back 674

In normal liver there is only type IV collagen in the space of Disse. In cirrhosis there is type I and III in the space of Disse and collagen deposited diffusely throughout the liver

Front 675

What cell type in the liver is responsible for fibrosis?

Back 675

The perisinusoidal stellate cells (Ito cells)

Front 676

What are the vascular changes that follow fibrosis in cirrhosis?

Back 676

Sinusoidal cells lose fenestrations and protein/solute movement between plasma and hepatocytes is impaired. Shunts also develop (portal vein-hepatic vein for example)

Front 677

What is the most common cause of portal hypertension?

Back 677

Cirrhosis is the most common, but can also be caused by thrombus or portal vein sclerosis and severe right sided heart failure

Front 678

What are the consequences of portal hypertension?

Back 678

Ascites, portosystemic venous shunts, congestive splenomegaly, and hepatic encephalopathy

Front 679

What are the functions of bile flow?

Back 679

Elimination of bilirubin, cholesterol, and xenobiotics and promotion of dietary fat absorption in the gut via emulsification

Front 680

What is bilirubin?

Back 680

The end product of heme degradation following RBC breakdown

Front 681

What is the process of heme degradation?

Back 681

Heme oxygenase converts heme into biliverdin and biliverdin reductase converts biliverdin into bilirubin

Front 682

How is bilirubin conjugated in the liver?

Back 682

The enzyme UGT conjugates bilirubin with glucuronic acid“The rate of systemic bilirubin production is equal to rate of bilirubin hepatic uptake, conjugation, and excretion.”

Front 683

What are the characteristics of unconjugated bilirubin?

Back 683

It is pre-hepatic and tightly bound to albumin. It is insoluble in water and can’t be excreted in the urine. If it gets into CNS, it is toxic and will cause severe damage (kernicterus)

Front 684

What are the characteristics of conjugated bilirubin?

Back 684

It is post-hepatic and can be excreted in urine. It is water soluble and loosely bound to albumin, not toxic like unconjugated form

Front 685

What serum level of bilirubin constitutes jaundice?

Back 685

>2.0 mg/dL (normal is <1.2)

Front 686

What are the 2 forms of hereditary hyperalbuminemia?

Back 686

Gilbert syndrome, which is due to reduced liver UGT and causes increased unconjugated bili. Dubin-Johnson sundrome, which is reduced hepatocellular excretion and causes increased conjugated bili

Front 687

What is cholestasis?

Back 687

Impaired bile flow leading to retention of bili, bile salts, and cholesterol

Front 688

What are the two causes of cholestasis?

Back 688

Hepatocellular dysfunction (non-obstructive) and biliary obstruction (obstructive)

Front 689

What lab values would indicate cholestasis?

Back 689

Increased serum alkaline phosphatase

Front 690

What are the clinical features of cholestasis?

Back 690

Jaundice, pruritis (itching of the skin), and xanthomas (focal accumulations of cholesterol)

Front 691

What histologic features would be present in cholestasis?

Back 691

Enlarged hepatocytes containing bile pigments in the and bile canaliculi. In obstructive cholestasis you will also get distension of the bile ducts

Front 692

How do you treat cholestasis?

Back 692

Obstructive form can be alleviated by surgery, but non-obstructive is difficult to treat and can be exacerbated by biliary surgery. Liver transplant may be the only option

Front 693

What is the prognosis of Hep A?

Back 693

It is self-limiting and benign, even asymptomatic in some individuals. It isn’t cytotoxic to the hepatocytes and doesn’t cause any chronic carrier state

Front 694

What is the best diagnostic marker for HAV?

Back 694

IgM anti-HAV

Front 695

What type of virus is HAV?

Back 695

ssRNA picornavirus

Front 696

What type of virus is HBV?

Back 696

dsDNA hepadnaviridae family

Front 697

What are the common modes of transmission of HBV?

Back 697

Horizontal transmission such as transfusion, dialysis, needle stick accidents, IV drug abuse, and sexual transmission

Front 698

What serum markers are used to track the progress of HBV infection?

Back 698

HBsAG is present at symptom onset and peaks in acute dz. HBeAg indicates that active viral replication is happening and pt will be extremely infectious. Anti-HBs is the marker that may persist for life, may indicate protection

Front 699

What does the presence of IgM and IgG indicate?

Back 699

Cessation of liver damage

Front 700

What is the major determining factor in the outcome of HBV infection?

Back 700

The host immune response. If the host has a good T cell response by IFN-g producing cells, then acute infection is usually resolved. If cytotoxic T cells predominate then hepatocytes damage will ensue

Front 701

What antigen is administered in the HBV vaccine?

Back 701

Purified HBsAg

Front 702

What type of virus is HCV?

Back 702

ssRNA flavivirus

Front 703

What are the two main causes of chronic liver disease in the western world?

Back 703

HCV and alcoholism

Front 704

What is the big mode of transmission of HCV?

Back 704

IV drug abuse

Front 705

What symptoms do most HCV pts have?

Back 705

75% are asymptomatic

Front 706

What is the identifying serologic marker in HCV infection?

Back 706

HCV RNA. They also will likely have anti-HCV antibodies

Front 707

What are the two outcomes of HCV infection?

Back 707

Persistent infection in 85% of pts with asymptomatic infection, and cirrhosis in 20% of pts

Front 708

If a person is infected with delta hepatitis, what other co-infection would you expect?

Back 708

HBV must encapsulate the HDV virus in order for it to multiply. So you can’t have HDV without HBV

Front 709

What is the most reliable serum marker indicating recent HDV exposure?

Back 709

IgM anti-HDV

Front 710

What are the outcomes of HDV infection?

Back 710

If the virus was acquired concurrently with HBV (coinfection), then most pts will clear the viruses and recover completely. Pts who already have HBV, then get HDV superinfection will likely progress to more severe, chronic hepatitis

Front 711

How is HEV generally transmitted?

Back 711

It is generally water borne due to fecal contamination of water

Front 712

What are the clinical features of HEV?

Back 712

Self-limiting disease not associated with chronic liver disease or persistent viremia

Front 713

Which demographic group are at a higher risk of death from HEV?

Back 713

Pregnant women

Front 714

Which two types of viral hepatitis don’t progress to chronic hepatitis and don’t cause a chronic carrier state?

Back 714

HAV and HEV

Front 715

Which type of hep is most likely to demonstrate viral persistence and chronic disease?

Back 715

HCV

Front 716

When do all hep viruses have peak infectivity?

Back 716

During the last few days of incubation period to early period of acute symptoms

Front 717

How would you classify chronic hepatitis?

Back 717

Evidence of hepatic disease for more than 6 months and histologic evidence of inflammation and necrosis of the liver

Front 718

What is the major lab finding in chronic hepatitis?

Back 718

Persistent elevation of serum aminotransferases

Front 719

What is the definition of the carrier state?

Back 719

An asymptomatic pt who harbors and can transmit the virus. They develop non-progressive liver damage with little disability

Front 720

When are people especially at risk for developing carrier state from HBV infection?

Back 720

Early infection via vertical transmission (mother to child). There is a 95% chance of becoming a carrier in that case. It is rare to become a carrier in adulthood

Front 721

Which types of hepatitis can result in fulminant hepatitis?

Back 721

A, B, and E. This is basically liver failure resulting from massive hepatic necrosis

Front 722

Most types of viral hepatitis are similar to each other histologically and similar to drug-induced liver disease. Considering this, how can you determine the cause?

Back 722

You have to perform serologic studies to distinguish viral and drug induced liver disease

Front 723

What bacteria can cause pyrogenic liver abscesses?

Back 723

E. coli and Klebsiella

Front 724

How would you end up with solitary or multiple abscesses?

Back 724

Solitary abscesses are often the result of a penetrating injury. Multiple abscesses are the result of vascular seeding or biliary infection