Patho Flashcards For Exam 4

Front 1

What is coronary artery disease?

Back 1

A disease in which blood flow to the myocardium is diminished due to narrowing of one of more of the coronary arteries

Front 2

What are the risk factors for CAD?

Back 2

1. High blood cholesterol
2. High blood pressure
3. Cigarette smoking
4. Obesity
5. Lack of physical activity
6. Diabetes mellitus
7. Family history of heart disease
8. Sex
9. Age
10. Others (emerging risk factors)

Front 3

What are the non-traditional / emerging
risk factors for CAD?

Back 3

1. homocysteine
- increased levels = increased risk
- damages endothelium
- strongly influenced by diet and genetics

2. C-Reactive Protein
- marker of inflammation

3. Endolthelial dysfunction
- < NO so less vasodilation
- enodthelian vasoconstricts, and is overproduced
so it increases CAD risk

Front 4

Etiology of CAD

Back 4

1. ATHEROSCLEROSIS
- leading cause; 90% of CAD people have plaque

2. Coronary Artery Vasospasm
- condition in which smooth muscle in the arterial wall
constricts and blocks blood flow
- 10% from this

Front 5

Pathogenesis of CAD

Back 5

[refer to BB notes]

1. Fatty streaks
2. Fibrous Plaques
3. Complicated lesion

Front 6

Common sites of CAD

Back 6

Areas of turbulent blood flow
- aorta and main branches
- coronary arteries

Front 7

Symptoms of CAD may not occur until the
artery is what percent occluded?

Back 7

75%

Front 8

What allows for compensatory vasodilation?

Back 8

Nitric Oxide - released from endothelium

- eventually a moderate increase in demands exceeds
flow and ischemia results

Front 9

What kind of symptoms do diabetics usually experience in CAD?

Back 9

No symptoms

Front 10

Three outcomes of atherosclerosis

Back 10

1. Occluding vessels over time
- allows for collateral circulation
- ischemia

2. Occluding vessels suddenly
- anoxia
- thrombi move to smaller branches and occlue
- or plaque ruptures and occludes

3. Weakening vessel walls to the point of aneurysm

Front 11

Sequela / Complications of CAD

Back 11

1. Angina
2. Sudden cardiac death
3. Myocardial infarctions
4. Conduction disturbance
5. CHF

Front 12

What is angina pectoris?

Back 12

Symptomatic, paroxysmal chest pain due to transient myocardial ischemia

Front 13

Where does the chest pain usually radiate to?

Back 13

Arms, chin or shoulder

Usually radiates left

Front 14

What are the three types of angina?

Back 14

1. Stable
2. Variant
3. Unstable

Front 15

Stable Angina

Back 15

- "Classic Angina"
- Frequently occurs during activity
- Occurs with exertion

- Stress, cold, exercise exacerbate it

- Associated with fixed obstruction in the coronary arteries
- Stable plaques (covered with endothelium, no collagen exposed)

Front 16

What is stable angina alleviated by?

Back 16

Rest

Front 17

Pain in stable angina is described as?

Back 17

Pressure, heaviness, tightness

Typically follows ulnar nerve

Front 18

How are stable anginas treated?

Back 18

With NITROGLYCERIN
- vasodilates the coronary vessels and brings relief to many patients

Front 19

Warnings! for stable angina treatment

Back 19

It it lasts more than 5-10 minutes,
or if not relieved by nitrolglycerin
it is NOT angina
(its a possible MI)

Front 20

Prinzmetal's or Variant Angina

Back 20

- Vasospastic
- Can occur when arteries are stenotic or patent
- Occurs more often in women
- May be due to vasospasm

Front 21

What are some suspected etiologies of variant angina?

Back 21

Endolthelial Dysfunction likely

Hormones possible
- estrogen
- more MI during period

Front 22

Unstable Angina

Back 22

- Occurs without trigger
- Results from atherosclerotic plaque disruption
- May lead to MI

* thrombi superimposed on plaque
- stuttering pain pattern
(occlusion, then not, etc)

Front 23

What is sudden cardiac death?

Back 23

sudden loss of cardiac function in someone who's been previously asymptomatic

Front 24

What is the most common underlying cause of sudden cardiac death?

Back 24

CAD

- can also be related to exertion, vasospasm, occlusion of
coronary artery, thrombosis, arrhythmia, or congenital defects

Front 25

What percent of people have had symptoms leading up to sudden cardiac death?

Back 25

about 50%

Front 26

What is a myocardial infarction?

Back 26

Necrosis resulting from prolonged ischemia

Front 27

What are the different ways blood flow is obstructed during MI?

Back 27

1. thrombosis (80-90% of the time)

2. ulceration & hemorrhage from atherosclerotic plaque

3. prolonged vasospasm

4. sudden increase in oxygen demands of tissue

Front 28

Right coronary artery obstruction
would result in damage to?

Back 28

inferior infarct

posterior infarct

posterior septum

Front 29

LAD obstruction is often termed?

Back 29

The "Widow Maker" or "Artery of Sudden Death"

accounts for 50% of MIs

Front 30

What part of the heart does LAD occlusion infarct?

Back 30

Anterior Infarction

Front 31

Left circumflex artery occlusion results in?

Back 31

Lateral infarction

20% of cases

Front 32

which part of the heart has the highest metabolic demands?

Back 32

the left ventricle

Front 33

Describe the pain experienced during MI

Back 33

Severe
Crushing
Suffocating
Elephant on chest
Severe sweating (diaphorisis)
Nausea and vomitting

Front 34

What happens to the sympathetic NS during a MI?

Back 34

Increases sympathetic NS

Front 35

Pain and Symp NS stimulation lead to?

Back 35

Tachycardia, anxiety and restlessness

Feels like an impending sense of doom

Front 36

What are the most common symptoms for women's MIs?

Back 36

Weakness
Shortness of Breath
Fatigue

Front 37

What happens to the ECGs during an MI?

Back 37

ST segment elevation or depression

Q waves

Front 38

Lactic Acid during MI

Back 38

increased production during ischemia because cells resort
to anaerobic metabolism

decrease blood volume = decreased O2 = anaerobic

Front 39

Why do we see Potassium increases during MI?

Back 39

Because potassium is generally kept inside the cells,
and when they die the membranes are disrupted and it leaks out

This causes pH to rise

It hyperpolarizes cells and puts them closer to threshold
leading to ECG abnormalities and conduction defects

Front 40

What different enzymes show up during MI?

Back 40

CPK
- creatine kinase
- prominent 3-4 hours after MI

CK-MN
- cardiac specific
- appears within 1st hour and
stays elevated longer

TROPONIN
- released when muscles are damaged
- preferred test enzyme

Front 41

What are the three components needed to diagnose MI?

Back 41

History
ECG
Enzymes

(need two out of the three)

Front 42

What is the damage by MI determined by?

Back 42

Extent and location of injury

Front 43

What are the post MI complications?

Back 43

1. Sudden death
2. Heart failure
3. Cardiogenic shock
4. Pericarditis
5. Thromboemboli
6. Ventricular Aneurysm
7. Rupture of the heart
8. Arrhythmias

Front 44

What are the 5 ways MIs are treated?

Back 44

1. Coronary Artery Bypass Graft
2. PTCA
3. Pharmacological
4. Management of life threatening complications
5. Rehabilitation and Lifestyle

Front 45

1. Coronary Artery Bypass Graft
(CABG)

Back 45

Mammary or LIMA

Left internal mammary artery is preferred

Front 46

Why is the LIMA preferred?

Back 46

it has superior latency
- doesn't occlude
- same size as LAD
- doesn't damage the endothelium

Front 47

Percutaneous Transluminal
Coronary Angioplasty (PTCA)

Back 47

- don't have to put you completely out
- threat it up through the femoral a.
- pump up balloon and crush plaque
- can also apply a stent

Front 48

What is the problem with PTCA?

Back 48

Restenosis (reocclusion)

Front 49

Pharmacological: MONA

Back 49

M: morphine for the pain
O: oxygen
N: nitroglycerin to vasodilate
A: aspirin

also use thromboemblolytics like TPA, or beta adrenergic blockers

Front 50

What is diabetes mellitus?

Back 50

a metabolic disorder of carbohydrate, protein, and lipid metabolism

Front 51

it is characterized by what condition?

Back 51

hyperglycemia

(high blood glucose)

Front 52

Describe a person with insulin resistance's insulin levels

Back 52

They may be high, low, or normal

Front 53

What are normal fasting blood glucose levels?

Back 53

< 100 mg/dL

100 - 125 mg/dL is prediabetes

and >125 mg/dL is diabetes

Front 54

Blood glucose is controlled by which two hormones?

Back 54

Insulin and Glucagon

Front 55

When blood glucose is too high, which is secreted?

Back 55

Insulin

Front 56

In which two ways does insulin help lower blood glucose?

Back 56

- It allows glucose to enter into muscle cells

- It stimulates the liver to take up glucose and
store it as glycogen
(glucogenesis)

Front 57

When blood glucose is too low, what is secreted?

Back 57

Glucagon

Front 58

In what three way does it help lower blood glucose?

Back 58

It causes the liver to do two things:
1) Glucogenolysis - breakdown of stored glycogen to glucose
2) Gluconeogensis - production of new glucose

- It also can cause adipose tissue to undergo lipolysis,
which releases FFA
- The increased fat metabolism produces ketones which
stimulate gluconeogenesis

Front 59

What are the two types of diabetes?

Back 59

TYPE I
- absoulte insulin deficiency
- T cell mediated autoimmune attack

TYPE II
- combination of insulin deficiency and/or resistance

Front 60

What is the etiology of Type I?

Back 60

Genetics: HLA's

Viral Exposure


For some, it is idiopathic

Front 61

What are the symptoms of Type I diabetes?

Back 61

1. Hyperglycemia

2. Glycosuria
(excretion of glucose in the urine)

3. Polyuria
(excessive passage or urine)

4. Polydipsia
(increased thirst)

Front 62

What does Type I have to be treated with for life?

Back 62

Exogenous insulin

Front 63

What is the etiology of Type II Diabetes?

Back 63

Strong genetic component
(even stronger than type I)
with multiple genes involved

Sedentary Lifestyle also contributes

Front 64

Defective genes create two major problems
in those with NIDDM?

Back 64

1. Beta cell dyfunction
(response is sluggish or muted)

2. Insulin reistance
(inability of cells to take up G)

Front 65

What chronic disease is a major contributer to NIDDM?

Back 65

Obesity

80% of Type II are obese

Obese people have fewer insulin receptors
and produce resistin
(resistin: promotes insulin resitance)

Front 66

What happens to the beta cells during Type II Diabetes?

Back 66

Hyperinsulinemia fatigues them over time, and evnetually
they undergo apoptosis

Front 67

What are the beta cells replaced with after apoptosis?

Back 67

Fibrous CT

Front 68

What are the symptoms of type II diabetes?

Back 68

1. Hyperglycemia

2. Glycosuria
(excretion of glucose in the urine)

3. Polyuria
(excessive passage or urine)

4. Polydipsia
(increased thirst)

Front 69

Which part of Diabetes is a strong indicator for CVD?

Back 69

Insulin resistance

Front 70

What are the secondary complications of diabetes?

Back 70

1. Peripheral Neuropathy
2. Nephropathy
3. Retinopathesis
4. Vascular Complications
5. Infections

Front 71

Peripheral Neuropathy

Back 71

Ischemia and demyelination causes a decrease
in impulse conduction

* PINS and NEEDLES type of nerve pain

Front 72

Nephropathy

Back 72

Renal vascular complication and impaired blood flow causes
progressive desctruction of nephrons and
loss of renal function

(often the cause of death)

Front 73

Retinopathesis

Back 73

Diabetes is the leading cause of blindness in the US

Capillaries rupture or form aneurysms that tend to leak/burst

Scar tissue develops leading to:
- renal detachment
- cataracts
- glaucoma

Front 74

Vascular Complication

Back 74

accelerated rate of atherosclerosis causes:
- CAD
- CVD
- PVD
- Renal Stenosis
- Ulceration, poor wound healing, and gangrene

Front 75

Infections

Back 75

poor circulation, poor immune function, and high glucose concentration favor the growth of microbes

Front 76

How do we manage Type I Diabetes?

Back 76

LIFESTYLE
- maintain ideal weight
- work with a dietitian to adjust insulin
therapy accordingly to lifestyle
- caloric intake based on body weight

Front 77

How do we manage NIDDM?

Back 77

Early on we can control it with diet, exercise, and weight loss

As it progresses, insulin therapy may be needed
to offset the loss of beta cells

Front 78

How does weight loss and exercise help?

Back 78

It increases the number of insulin receptors
therby decreasing insulin resistance

Exercise contribute to weight loss and increasing the insulin receptors