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patho finals > mod 5 > Flashcards

mod 5 Flashcards

1
Q

hardening of large and medium arteries

A

atherosclerosis

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2
Q

hardening of small arteries

A

arteriolosclerosis

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3
Q

hardening of any artery

A

arteriosclerosis

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4
Q

inflammation of any artery

A

arteritis

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5
Q

a progressive chronic inflammation of arteries are characterized by:

A

1.Inflammation (Macrophages engulf LDLs > Foam Cells
2. Fibrosis( Conn. tissue/Collagen/Elastin
3.Liquid deposition(Cholesterol esters & cholesterol in cells

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6
Q

Etiology of Atherosclerosis

A

-BEGINS with Endothelial Injury
-Big Inflammatory Component
-Risk Factors:

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7
Q

Non-Modifiable

A

Age (40-60), Male, FamHx, Indigenous

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8
Q

Modifiable

A

cholesterol, HTN, Smoking, Diabetes, Obesity, Metabolic Syndrome

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9
Q

Gruel/Porridge (ie. The fat in the blood)

A

Athero

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10
Q

Hardening

A

Sclerosis

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11
Q

Proliferation & Fibrosis

A

Conversion of Fatty Streak into a Mature Atheroma

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12
Q

Complicated plaque formation

A

Thin Fibrous Cap > Rupture > Thrombus > ACS

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13
Q

a.Heart > IHD (Angina, MI).
b.Brain > Cerebral Infarction (Stroke)
c.Kidneys > Renal Infarction
d.GIT > GI-Ischemia/Infarction
e.Lower Extremities > PVD (Eg. Claudication, Gangrene of Legs, Arterial Leg Ulcers)

A

Multi-Organ Disease:

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14
Q

Characterized By Accumulation

A

1.Lipids
2.Fibrous Elements
3.Local Inflammatory Response (Macrophages engulf LDLs > “Foam Cells”)

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15
Q

-Cause of 90% Myocardial Ischemia, Due to Occlusion of Coronary Circulation
-Cause ≈50% of deaths in Western Society.

A

Principal cause of Heart Disease & Stroke

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16
Q

3 Types of Lipids in Plasma:

A

1.Cholesterol + Ch. Esters
2.Phospholipids
3.Triglycerides (Fatty Acids + Glycerol)

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17
Q

-Insoluble In Water > Must be Packaged to be suspended in plasma.

A

Lipid Transport:

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18
Q

attribute to atherosclerosis

A

LDLs

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19
Q

help prevent atherosclerosis

A

HDLs

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20
Q

Vessel Injury – Endothelial Damage:
a. Risk Factors:

A

i.High Cholesterol
ii.Hypertension
iii.Smoking
iv.Toxins/Poisons
v.Virus
vi.Bacteria
vii.Immune Reaction
viii.Diabetes

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21
Q

a. fat deposition under the tunica-intima vessel-layer.
b. the typical early atherosclerotic lesion.
i. majority are clinically silent
ii. are reversible – eg. if diet changes
c. yellow color reflects:
i. oxidized lipids
ii. presence of ‘foam cells

A

Fatty Streak Formation

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22
Q

a. fatty streak gets more profound
b. foam cells unable to digest lipid contents → die
c. oxidized ldls – attract immune cells, cytokines, platelets, smooth muscle, connective tissue

A

Lipid Plaque

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23
Q

fat deposition under the

A

tunica-intima vessel-layer

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24
Q

the typical early atherosclerotic lesion.

A

i. majority are clinically silent
ii. are reversible – eg. if diet changes

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25
Q

yellow color Fatty Streak Formation reflects

A

i. oxidized lipids
ii. presence of ‘foam cells

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26
Q

a. fatty streak gets more profound
b. foam cells unable to digest lipid contents → die
c. oxidized ldls – attract immune cells, cytokines, platelets, smooth muscle, connective tissue

A

Lipid Plaque:

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27
Q

-Consistent Systolic of +130mmHg.
AND/OR
-Consistent Diastolic of +80mmHg

A

HYPERTENSION

28
Q

Primary “Essential” Idiopathic Hypertension

A

95%

29
Q

Idiopathic ʹ Likely multifactorial

A

not curable

30
Q

▪Genetics/Family Hx
▪High Cholesterol/Salt Diet
▪Diabetes/Obesity
▪Smoking/Alcohol
▪Stress
▪Age

A

risk factors of HTN

31
Q

Isolated Diastolic HTN

A

typically in older men

32
Q

Due to Overactive Sympathetic NS > inc CO

A

Isolated Systolic HTN - in young adults

33
Q

Due to dec Arterial Compliance- Calcification/Fibrosis

A

Isolated Systolic HTN - in older adults

34
Q

-rapid inc in BP (>200/120mmhg) sufficient to cause vascular damage

A

Malignant Hypertension

35
Q

Rupture of Artery/Arterioles in brain

A

Intracerebral Hemorrhage

36
Q

hardening of kidney blood vessels) > Renal Failure

A

Nephrosclerosis

37
Q

a “flow” limitation, typically due to coronary artery stenosis (narrowing)

A

ischemia

38
Q

an oxygen limitation, typically due to high-altitude/respiratory insufficiency/etc.

A

hypoxia

39
Q
  • irreversible cell-death, typically due to sustained ischemia.
A

infarction

40
Q

Regional Ischemia

A

local

41
Q

Global Ischemia

A

entire heart

42
Q

-Initially Subendocardial Ischemia /Infarction (ST-Depression & T-Wave Inversion)
-Progresses to Transmural͛-Ischemia/Infarction (ST-Elevation & Pathological Q-Waves)

A

myocardial ischemia

43
Q

Metabolic Changes - (Aerobic → Anaerobic)

A

Inc. Lactate, (Anaerobic Metabolism) dec. pH

44
Q

-Decreased Myocardial Perfusion (relative to demand) due to Coronary Insufficiency.

A

Angina pectoris

45
Q
  • Stable Atherosclerotic Coronary Obstruction (No Plaque Disruption)
    -Presentation: Chest Pain on Physical Exertion, which fades quickly with Rest (minutes)
A

Stable Angina

46
Q

-Due to: Coronary Vasospasm (May not be Atheroma).
-Presentation: Angina Unrelated to Activity (Ie. At Rest)

A

Variant/Prinzmetal Angina

47
Q

-Unstable Atherosclerotic Plaque (+/- Plaque Disruption & Thrombus).
-Presentation: Prolonged Angina @ Rest (Either New Onset /inc Severity/inc Frequency).
-Red Flag that MI may be Imminent

A

Unstable Angina “Preinfarction Angina”

48
Q

-Due to: Ischemia masked by neuropathy (eg. Diabetes/dec. B12/etc)
-Presentation: Painless, but may have Nausea, Vomiting, Diaphoresis + Abnormal ECG

A

silent ischemia

49
Q

-Smoking
-Hypertension
-Hyperlipidaemia
-Diabetes
-Obesity

A

Prevention/Management of CV Risk Factors

50
Q

Anti-Anginal Therapy

A

a.Nitrates (GTN)
b.B-Blockers (Metoprolol)
c.Ca-Channel Blockers

51
Q

Antiplatelet Therapy

A

Aspirin / Clopidogrel

52
Q

Lipid-Lowering Therapy

A

Atorvastatin/Simvastatin

53
Q

Delayed Autoimmune Complication of a GROUP A BETA HEMOLYTIC STREPTOCOCCI Tonsillo - Pharyngitis.

A

Rheumatic Fever (RF

54
Q

Acute Phase of Rheumatic Fever

A

Acute Rheumatic Fever / Carditis

55
Q

Typically > Mitral Stenosis

A

Chronic Rheumatic Heart Disease (RHD)

56
Q

Licks joints but bites heart! (Temporary Arthritis, but Permanent Valvular Damage)

A

Rheumatic Fever (RF)

57
Q

Licks heart but bites joints! (Mild Myocarditis, but permanent Severe Arthritis

A

Rheumatoid Arthritis (RA)

58
Q

Jones Criteria Rules - Must Have:

A

a.Evidence of Previous GABH-Strep (Strep. Pyogenes) Infection
b.(2x Major Criteria) OR (1 Major + 2 Minor)

59
Q

(Evidence of Previous Strep Infection):

A

a.Anti-Streptolysin-O Titre
b.Anti-DNaseB Antibodies
c.Positive Throat Swab Culture

60
Q

a.Joints (Migratory Polyarthritis ʹ Not necessarily arthralgia)

b.Carditis (Incl. Pericarditis - Friction Rub, Quiet Heart Sounds, Tachy)

c.Nodules (Subcutaneous, painless, on extensor surfaces)

d.Erythema Marginatum (Non-Pruritic, Tinea-like Rings on Trunk & Limbs)
Sydenham’s Chorea (Rapid, Involuntary Movements)

A

(Major Criteria) – the JONES Criteria

61
Q

-(Fever)
-(Arthralgia)
-(Elevated ESR)
-(Prolonged PR-Segment)

A

(Minor Criteria)

62
Q

also called a defect, refers to one or more problems with the heart structure that are present at birth.

A

CONGENITAL HEART DISEASE

63
Q

where problems with the heart mean there isn’t enough oxygen present in the blood. Babies born with cyanotic heart disease generally have a blue-coloured tinge to areas such as their fingers, toes and lips because of a lack of oxygen. They may also experience symptoms of: breathlessness. chest pain.

A

Cyanotic

64
Q

where the blood contains enough oxygen but it’s pumped abnormally around the body. Babies born with acyanotic heart disease may not have any apparent symptoms but, over time, the condition can cause health problems.

A

Acyanotic

65
Q

yellow color reflects

A

i. oxidized lipids
ii. presence of ‘foam cells

66
Q

Rupture of Artery/Arterioles in brain

A

Intracerebral Hemorrhage

67
Q

hardening of kidney blood vessels

A

Nephrosclerosis

patho finals (5 decks)

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