Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HSC 411 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Other Factors That Lead To Coagulation Defects (besides platelets)

A

Liver
Vitamin K Deficiency
Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Liver (Other Factors That Lead To Coagulation Defects)

A

Liver makes many coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Vitamin K Deficiency (Other Factors That Lead To Coagulation Defects)

A

Vitamin K is needed for clotting factor synthesis

May occur in:

  • newborn
  • those treated with broad spectrum antibiotics
  • liver/gall bladder disease - impaired fat absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Aspirin (Other Factors That Lead to Coagulation Defects)

A

Can cause impaired platelet aggregation (makes slippery)
Inhibits COX pathway
-and therefore the production of thromboxane AZ (which is needed for platelets to stick together; causes bleeding tendencies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Portal Hypertension

A

Increased resistance in the hepatic portal circulatory route due to liver disease

  • causes congestion in the veins
  • mainly seen in cirrhosis (scar tissue - hard for venous blood to get through)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Danger of Portal Hypertension and Liver Disease

A

Esophageal Varicies Rupture

Rupture when you swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Varicies

A

Engorged, twisted veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hereditary Defects In Coagulation

A

von Willebrand Disease (vWD)

Hemophilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

von Willebrand Disease (vWD)

A

MOST COMMON hereditary defect

Lacking vWF produced by endothelial cells - needed for platelet adhesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hemophilia

A

Sex-linked recessive disorder (x-linked, therefore all daughters of hemophiliac men are carriers) in which an insufficient quantity of the factor is produced (~90% of cases) or it is defective (~10% of cases)

Varying degrees of severity depending on the amount of factor produced (causing bleeding problems)

(Defect in coagulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Coronary Artery Disease (CAD)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Risk Factor

A

A risk factor is a characteristic, symptom, or sign that is associated with development of the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CAD Risk Factors

A

Determined mainly by Framingham Study

  1. High blood cholesterol: > LDLs and < HDLs
  2. High blood pressure - hypertension (normal is UNDER 120/80)
  3. Cigarette smoking - damages the endothelium
  4. Obesity (waist circumference >40” for men and >35” for women)
  5. Lack of physical activity (sedentary lifestyle)
  6. Diabetes mellitus
  7. Family history (genetics)
  8. Sex (men at higher risk, and women after menopause)
  9. Age
  10. Others (homocystine - influenced by diet, increased levels = increased risk and C Reactive Protein - a marker of inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Etiology of CAD

A
  1. Atherosclerosis: LEADING CAUSE

2. Coronary Artery Vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Coronary Artery Vasospasm

A

A condition in which the smooth muscle in the arterial wall constricts and blocks blood flow

-Endothelial dysfunction? (>endothelium and <N.O.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Atherosclerosis

A

Deposition of fatty plaque in the walls of the arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathogenesis/Atherosclerosis Mechanism:

A

Fatty Streaks -> Fibrous Plaques -> Complicated Lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Fatty Streaks

A

LDL’s and macrophages collect between endothelium and C.T.

Myointimal cells accumulate too.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Fibrous Plaques

A

Fibrous scar tissue forms around LDL’s and foam cells.

STABLE PLAQUE = intact endothelium overlying plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Complicated Lesion

A

Cells in plaques die and calcify.
If endothelium is damaged platelets stick forming overlying thrombus
Prone to ulceration, hemorrhage, and emboli.

This is UNSTABLE PLAQUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Common Sites of Atherosclerosis

A

Areas of turbulent blood flow

Aorta and main branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Symptoms may not occur until..

A

artery is 75% occluded

WHY?

  • for a time, compensatory vasodilation via nitric oxide release tires to compensate for the narrowing
  • eventually even a moderate increase in demand exceeds flow and ischemia results
  • symtoms vary greatly from individual to individual
  • with diabetics commonly experiencing NO symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Atherosclerosis Outcomes

A
  1. Occluding vessels over time
  2. Occluding vessels suddenly via rupture or thrombosis
  3. Weakening vessel walls to the point on aneurysm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CAD Leads To:

A
  1. Angina
  2. Sudden Cardiac Death
  3. Myocardial Infarctions
  4. Conduction Disturbance
  5. CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Angina Pectoris

A

Symptomatic , paroxysmal chest pain due to transient (short-lived) myocardial ischemia.
Pain may radiate to the arms, chin, shoulder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

3 Types of Angina

A
  1. Stable
  2. Varient
  3. Unstable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Stable Angina

A

Frequently occurs during activity.
Alleviated by rest
“Classic” angina

-usually follows physical exertion/stress = increase in myocardial demand

Associated with fixed obstructions in the coronary arteries
(stable plaques)

As HR increases, diastolic filling time is decreased = decreased flow through atherosclerotic coronary vessels, which leads to myocardial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Stable Angina - pain described as:

A

pressure, heaviness, tightness

Why is it associated with exertion?
-increased demand for blood, but not enough flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Stable Angina - Treatment

A

Nitroglycerin - to vasodilate coronary vessels - brings relief to many patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Warning! (stable angina)

A

If it lasts for more than 5-10 minutes or is not relieved by Nitro — NOT ANGINA

(Possibly a MI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Prinzmetal’s or Varient Angina (vasospastic)

A

May occur when coronary arteries are stenotic or patent.
Occurs more often in women and may be due to vasospasm

  • occurs most often between midnight and 6 am (when person is sleeping)
  • exercise tolerant (not caused from exercise)

Mechanism unknown - endothelia dysfunction?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Unstable Angina

A

Occurs without trigger
Results from atherosclerotic plaque disruption and may lead to MI
Thrombi superimposed on plaque (dangerous)

  • Associated with complicated plaque
  • -no endothelium so thrombus develops (thrombus gets bigger and smaller, causing angina randomly)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Sudden Cardiac Death

A

Death Sudden

-loss of cardiac function (in someone who is PREVIOUSLY ASYMPTOMATIC)

Responsible for ~450,000 deaths per year in North America

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Most Common Underlying Cause of Sudden Cardiac Death

A

CAD (with no warning signs)

Incident may be related to increased exertion, vasospasm, occlusion of coronary artery, thrombosis or arrhythmia, congenital malformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Sudden cardiac death is first indication of CAD for many patients…. BUT

A

there is almost always at least SOME warning (in the weeks beforehand)

36
Q

Myocardial Infarction

A

Cell death resulting from prolonged ischemia

37
Q

(MI) Blood Flow Obstructed from:

A
  1. Thrombosis (80-90% of the time)
  2. Ulceration and hemorrhage from atherosclerotic plaque
  3. Prolonged vasospasm
  4. Sudden increase in oxygen demands of tissue
38
Q

Right Coronary Artery (MI Artery Obstruction)

A
  • inferior infarct
  • posterior infarction
  • involves posterior septum
  • 30% of cases
39
Q

Left Anterior Descending Artery

A
  • anterior infarction
  • apical (apex)
  • artery of “sudden death”
  • 50% of cases
40
Q

Left Circumflex Artery

A
  • lateral infarction
  • can also be LAD
  • 20% of cases
41
Q

Characteristics/S&S of MI (listed)

A
  1. Pain and autonomic nervous system responses
  2. Weakness and other signs of imparied cardiac function
  3. ECG alterations
42
Q

Pain and Autonomic Nervous System Responses (S&S of MI)

A

-Severe, crushing, suffocating pain (not relieved by rest or nitroglycerine), GI problems (nausea and vomiting), SOB, diaphoresis

Pain and sympathetic stimulation lead to:
-Tachycardia, anxiety, restlessness

NOTE: most common S&S for WOMEN are: weakness, SOB, fatigue
-1/3 of women die from MI

43
Q

Weakness and Other Signs of Impaired Cardiac Function

A

Fatigue and weakness
Skin: pale, cool, and moist
Hypotension and shock

44
Q

ECG Alterations:

A

ST segment elevation or depression

Q waves

45
Q

Cell Death Causes

A

-Release of intracellular proteins and enzymes therefore fever and leukocytosis

46
Q

(MI) Enzymes/Proteins Released Include

A

CPK: creatine kinase
CK-MB: cardiac specific
T: Troponin (now accepted as standard biomarker)

47
Q

Myocardial Necrosis to Repair

A

1-2 days old:

  • beginning acute inflammation
  • marked by changes in the electrocardiogram and by a rise in the MB fraction of creatine kinase

1 to 2 weeks:

  • many macrophages
  • little collagenization

Necrotic tissue is repaired with scar tissue = fibrous CT

48
Q

Diagnosis of MI

A

Requires two out of three components (history, EKG, and enzymes)

49
Q

Post MI Complications

A

Determined by extent and location of injury

  1. Sudden death occurs in ~20% due to arrhythmias
  2. Heart failure. Blood becomes congested
  3. Cardiogenic shock - decreased CO below level required to perfuse tissue adequately
  4. Pericarditis
  5. Thromboemboli from stasis/inactivity
  6. Ventricular aneurysms: from scar tissues inelasticity
  7. Rupture of the heart
  8. Arrhythmias - most serious being ventricular fibrillation
50
Q

Treatment of MI

A
  1. Coronary Artery Bypass Graft (CABG) of occluded artery
    - Saphenous vein or internal thoracic artery
    - LIMA preferred
  2. Percutaneous Transluminal Coronary Angioplasty (PTCA) with stents
    - open vessel and keep it from collapsing
    - problem is restenosis
51
Q

Diabetes Mellitus

A

Metabolic disorder of carbohydrate, protein, and lipid metabolism

Most common endocrine disorder
1-2% of US population

52
Q

Diabetes Background Information

A

Affects 24 million in US and is under diagnosed!
Affects all age groups
Incidence is on the rise
Decreases life expectancy and can have a profound impact on quality of life

53
Q

Normal Fasting Blood Glucose

A

Levels are <100 mg/dL

54
Q

Glucose is the primary energy source for _______ and the only energy source for ______

A
  • cell metabolism

- the brain

55
Q

Blood glucose is controlled by the opposing effects of 2 hormones:

A

insulin and glucagon

secreted from the Islets of Langerhans (alpha and beta cells)

The antagonistic effects of tehse two hormones allow for careful regulation of this important plasma variable

56
Q

Actions of Insulin:

A
  1. promote glucose uptake
  2. promote fat storage in form of FFAs
  3. prevent fat and glycogen breakdown
  4. prevent gluconeogenesis
  5. prevent protein breakdown
57
Q

Blood Glucose Too High =

A

Pancreas secretes insulin

58
Q

Blood Glucose Too Low =

A

Pancreas secretes glucagon

59
Q

Notes on Insulin Receptors and GLUT

A
  • Glucose cannot enter muscle cells without insulin
  • In order for insulin to work, it must bind to insulin receptors on the C.M.
  • Once bound, intracellular mechanisms are activated
  • Which cause the cell to transport glucose transport proteins to the C.M.
  • -the main glucose transporter in muscle is GLUT 4
  • GLUT 4 binds to glucose
  • Glucose is transported into the cell
  • Glucose is used for metabolism
60
Q

Diabetes Mellitus is a syndrome involving _____ and characterized by ____

A
  • disordered metabolism

- chronic hyperglycemia

61
Q

Hyperglycemia Stems from:

A
  1. Insulin deficiency
  2. Impaired release of insulin
  3. Inadequate or defective insulin receptors
  4. Production of inactive form of insulin
  5. Destruction of insulin
62
Q

Type 1 DM

A

10% of cases
Absolute insulin deficiency
T cell mediated AUTOimmune attack

63
Q

Type 2 DM

A

90% of cases
Combination insulin deficiency and/or resistance
Slow gradual progression and development of symptoms
Previously a disease of older individuals (>40)
-age is dropping as obesity becomes a childhood epidemic

64
Q

Etiology of Type 1

A

Autoimmune destruction of beta cells in the islets of Langerhans

Why the beta cells self-antigens become altered and vulnerable to immune attack is unclear

Suspicions:

  • Genetic - HLA’s
  • Viral Exposure

NOTE: there are some people who develop Type 1 who show no evidence of immune dysfunction = idiopathic

65
Q

Signs and Symptoms Emerge when

A

Most beta cells are destroyed, resulting in an absolute insulin deficiency

66
Q

Pathogenesis of Type 1

A
  1. Hyperglycemia (may reach 1,200 mg/dL at extreme)
  2. Glycosuria as glucose is lost in the urine. Recall that glucose is removed from filtrate via carrier molecules that have a TM (transport maximum)
    - osmotic diuresis occurs as the glucose exerts a substantial osmotic pressure and water is not reabsorbed from the renal tubules
  3. Polyuria and
  4. Polydipsia result
67
Q

Low insulin stimulates ____ and ____ to release more glucose into the blood

A

glycogenolysis
gluconeogenesis

But without insulin, the cells cannot take up glucose. Gluconeogenesis promotes the conversion of protein to glucose which results in fatigue, weakness, and muscle and weight loss

68
Q

Lipid metabolism increases leading to ____ and production of _____.

A

hyperlipidemia
ketone bodies

This leads to metabolic acidosis called diabetic ketoacidosis

69
Q

DKA (diabetic ketoacidosis) produces ___

A

nausea, vomiting, and brain toxicity

70
Q

Ketones can be detected on the breath as ___

A

a sweet fruity odor.

An acidotic coma can result

71
Q

Etiology Type 2

A

Strong genetic component (even stronger than Type 1) with multiple genes involved

72
Q

Defective genes create two problems (diabetes type 2)

A
  1. Beta cell dysfunction - response is sluggish or muted
  2. insulin resistance - inability of cells to take up glucose
  • glucose carriers are not cycled to the cell surface as readily
  • defective cell use of the glucose that does enter the cells
73
Q

Obesity (type 2 diabetes)

A

Over 80% of Type 2 are obese
-seem to have fewer insulin receptors

as obesity and genetics interact over time, type 2 emerges

74
Q

Other strong etiological contributors

A

sedentary lifestyle - reduces the need for glucose uptake, so response is subnormal

75
Q

Pathogenesis of Type 2

A

Genetic beta cell defect is operating before there are signs of the disease. This combines with insulin resistance to contribute to hyperglycemia

During the years as the disease progresses, the hyperglycemia acts as a strong insulin secretion stimulates promoting hyperinsulinemia that may create a fatiguing of the beta cells

Over time, the beta cells undergo apoptosis and a replaced with fibrous CT. Loss leads to the classic signs and symptoms of DM

76
Q

Classic S&S of DM

A

Hyperglycemia
Glycosuria
Polyuria
Polydipsia

Other S&S may occur as acute or chronic complications arise

77
Q

Complications of DM

A

Emergence of complications varies, depending on the length of time, severity, and compliance. Average onset is 15 years. Can be delayed by tight glucose control.

78
Q

Theory (DM)

A

Abnormal glycoprotein (glycosolated protein) formation and attachment to basement membranes throughout the body to cause injury to target organs/structures

Within blood vessels, this leads to endothelial damage, atherosclerosis, and ischemia. Causes microvascular and macrovascular complications

Abnormal proteins also attach to hemoglobin = HbA1c

This leads to:

  1. Peripheral neuropathy
  2. Nephropathy
  3. Retinopathies
  4. Vascular Complications
  5. Infections
79
Q

Peripheral Neuropathy

A

Ischemia and demyelination causes a decrease in impuls conduction (pins and needles type of nerve pain)

80
Q

Nephropathy

A

Renal vascular complications (often the cause of death) impaired blood flow causes progressive destruction of nephrons and loss of renal function

81
Q

Retinopathies

A

Diabetes is the leading cause of blindness in the US.
Capillaries rupture or form aneurysms that end to lead/burst. Scar tissue develops leading to retinal detachment, cataracts, and glaucoma

82
Q

Vascular Complications

A

Accelerated rate of atherosclerosis causes
CAD
CVD
PVD (peripheral vascular disease) - resulting in intermittent claudication - pain in legs due to ischemia
Renal Stenosis
Ulceration, poor wound healing and gangrene

83
Q

Infections

A

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

84
Q

Management/Treatment of DM

A

Goal is tight glucose control (avoid wide fluctuations)

Type 1:

  • maintain ideal weight
  • work with dietician to adjust insulin therapy to lifestyle
  • caloric intake based on body weight

Type 2:

  • Early on, Type 2 can be controlled with diet, exercise, and weight loss
  • weight loss increases numbers of insulin receptors thereby decreasing insulin resistance
  • exercise will contribute to weight loss and increase in insulin receptors
  • as the disease progresses, insulin therapy may be required to offset the loss of beta cells
85
Q

Future of Diabetes?

A

Stem cell transplants

HSC 411 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions