Disease of blood circulation Flashcards

disease of blood circulation

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1
Q

Name the different types of edema

A

-pitting: extreme form of edema where indentation is formed if pressed on
-Ascites: fluid in stomach associated with liver faliur
-Hydrothorax: Fluid accumulates in pleural cavity – most commonly from cardiac failure

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2
Q

Pathogenesis of Edema

A

1) Increased capillary permeability:
Causes swelling of tissues with acute inflammation
Increase in capillary permeability from some systemic diseases
2)Low Plasma Proteins:Reduced protein levels (e.g., albumin) due to conditions like liver disease, kidney disease, or malnutrition lead to lower oncotic pressure, causing fluid to leak into the tissues and accumulate..
3)Increased hydrostatic pressure
Heart failure. Localized venous obstruction (blood clot, tumor)
Inferior/superior vena cava syndrome – fluid accumulation in lower/upper body due to blockage or compression of the vessel.
4)Increased hydrostatic pressure
Heart failure
Localized venous obstruction (blood clot, tumor)
Inferior/superior vena cava syndrome – fluid accumulation in lower/upper body due to blockage or compression of the vessel.

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3
Q

What is foreword faliur

A

when the left ventricle temporarily can’t pump blood effectively, leading to reduced blood flow to the body

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4
Q

What happens in Acute Pulmonary Edema

A

1) Foreword faliur
2)Since the left ventricle isn’t pumping enough blood, the right ventricle continues to pump blood into the lungs, but the left ventricle isn’t moving it out efficiently. This causes a backup of blood into the lungs.
3)The backup of blood increases pressure in the pulmonary capillaries. When capillary pressure rises, it forces fluid out of the blood vessels into the alveoli.
4)The fluid in the alveoli causes shortness of breath and impaired gas exchange.

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5
Q

What is circuiltory disturbance or shock and what are the types

A

-Shock is a state of insufficient blood flow or low blood pressure. Types include
1) Hypovolemic shock: Low blood volum
2) Cardiogenic shock:Reduced cardiac output
3) septic shock: Caused by an infection that releases toxins and causes widespread vasodilation
4) Anaphylactic Shock:immune system causes excessive vasodilation. This leads to low blood pressure and poor circulation.

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6
Q

What does Virchow’s triad state

A

Blood does not normaly clot in blood vessels but it can in conditions off
1) slow blood flow
2) Damaged blood vessel walls
3) Increased blood clotting.

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7
Q

What is Arterial thrombi related to

A

development of atherosclerosis, formation of lipid plaques causing narrowing and hardening of arteries

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8
Q

Explain how Venous Thrombosis
can happen and the MAIN issue with this. AND what is some common presentation of this

A

-Extended period of inactivity
-Cramped position for an extended period
-Varicose veins or any condition preventing normal emptying of veins.
Common presentation
-Leg swelling
MAIN PROBLEM IS THE Risk of detachment and further injury causing pulmonary embolism.

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9
Q

What is difference between DVT and phlebitis.

A

When it affects a vein close to your skin’s surface, it’s called superficial phlebitis. When it affects a deeper vein, it’s called deep vein thrombosis (DVT).

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10
Q

List some diseases of the veins

A

-Phlebitis
-Varicose veins: Damaged valves
Types of varicose veins include Hemmiroids. varicocele (scrotum),
-Aneurysms:weak spots in blood vessel walls that can bulge and rupture.

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11
Q

Explain Varicose veins/ how they happen

A

Dilated tortuous veins, usually in the leg - resulting from poor blood return
Result from incompetent valves
which leads to poor nutrition of the tissues served by the veins
-is genetic
-Superficial veins are susceptible -poorly supported by muscle contractions
If central veins are affected – can lead to poor nutrition and atrophy of limb, prone to rupture, thrombophlebitis

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12
Q

What is pulmonary embolism? how bad is it.

A

This happens when blood clot travels to lung. Collateral blood flow from other smaller arteries can still bring some blood to the lung tissue so it wont fully die. Overtime it can dissolve or get worse and become bigger collecting more debris.
Symptoms: Cyanosis and shortness of breath.

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13
Q

What can happen with a LARGE emboli

A

-complete block of pulmonary artery.
-Right side of heart ENLARGES and the PRESSURE INCREASES.
-Left ventricle unable to pump adequate blood to brain and vital organs
-Systemic blood pressure falls, and patient may go into shock

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14
Q

What can happen with a small emboli

A

-Small emboli (clots) can travel through the main arteries in the lungs and get stuck in the smaller arteries that supply the lower part of the lungs.
When this happens, it raises pressure in the lungs and causes poor blood flow to the affected area of the lung.
The part of the lung with blocked blood flow may die (this is called necrosis).
This causes a wedge-shaped area of lung damage, called a pulmonary infarct.

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15
Q

What is FAT embolism

A

Happens when fat particles enter the bloodstream, usually after a bone fracture. These fat particles can block small blood vessels in the lungs, brain, or other organs, leading to serious issues like breathing problems or organ damage.

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16
Q

what is AIR embolism how does it happen.

A

happens when air bubbles enter the bloodstream, which can block blood flow. Can happen by Large amount of air enters into circulation from lung injury due to a chest wound
May be accidentally injected into circulation (IDU).

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17
Q

What is Foreign Particulate Matter Embolism

A

When people inject crushed tablets, tiny particles can be left behind. These particles can travel to the lungs, get stuck in small blood vessels.

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18
Q

What happens in Amniotic Fluid Embolism

A

1)Amniotic fluid enters maternal circulation: ( tear in the placenta)
2)Blockage of pulmonary capillaries: The fetal debris and amniotic fluid can clog small blood vessels in the lungs, causing severe respiratory distress.
3)Activation of clotting: The amniotic fluid contains substances that trigger the body’s clotting system, leading to disseminated intravascular coagulation (DIC), a condition where widespread blood clotting occurs, followed by bleeding.
4)Immunostimulatory reaction: The amniotic fluid can also trigger a severe immune response, resembling toxic shock or anaphylaxis, which can cause shock, organ failure, and even death.

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19
Q

Explain main cause of arterial thrombosus. And things that arent a factor of it. AND examples of it.

A

-STASIS is not a factor due to rapid blood flow and high intravascular pressure
Main cause: Injury to vessel wall from arteriosclerosis, causing ulceration, roughening of arterial wall with thrombi formation
Blocks blood flow causing infarct
Coronary artery: Myocardial infarction
Major leg artery: Gangrene
Cerebral artery: Stroke

20
Q

What happens in Intracardiac thrombosis

A

Clot formation
Within atria: inappropriate contraction, atrial fibrillation
Surfaces of damaged heart valves
Wall of left ventricle (mural thrombi): on areas subject to myocardial infarction
May dislodge into systemic circulation and cause infarction of major organs: Spleen, kidneys, brain lung etc.

21
Q

What are some factors of Thrombosis by Increased Coagulability

A

-polycythemia
-post surgery
-Estrogen
-heredeitery including A mutation in the gene for factor V creates an abnormal form that is harder to turn off. This makes blood stay in a clotting state longer, increasing the risk of clot formation. AND Prothrombin mutation: (a protein involved in clotting) leads to higher levels of prothrombin.

22
Q

What is DIC

A

Disseminated Intravascular Coagulation, where excessive clotting is followed by widespread bleeding.

23
Q

What is the risk of thrombosis with pts with cancer

A

Tumors release substances like thromboplastic materials, microparticles, and inflammatory cytokines, which promote clotting.
Large tumors release clotting factors slowly but continuously, and some even express tissue factor and adhesion molecules, further increasing clot risk.

24
Q

DIFFERENCE BETWEEN Arteriosclerosis/Atherosclerosis

A

-Arteriosclerosis: refers to the general hardening and thickening of the arterial walls, often due to AGING or high blood pressure.
-Artherosclerosis: fatty plaques (cholesterol, calcium, and other substances) build up inside the arteries, causing them to narrow and harden. It can be triggered by factors like high cholesterol or smoking.

25
Q

How do monocytes contribute to CARDIOVASCULAR DISEASE.

A

1)Monocytes move into blood vessel walls when there is damage or inflammation, such as from high cholesterol or high blood pressure.

2)They turn into macrophages inside the vessel walls, which are the main cells in atherosclerotic plaques

3)Macrophages cause more inflammation and can make plaques grow larger, which can block blood flow, leading to heart attacks, stroke, and heart failure.

26
Q

HOW IS Cardiovascular disease diagnosed

A

Angiogram – to detect artery obstruction
Echocardiogram – to evaluate blood flow, structural abnormalities
Stress tests – measure cardiac function (ECG)

27
Q

What are some rise factors that can cause cardiovascular disease

A

Elevated blood lipids (most significant)
High BP
Smoking
Diabetes
Genetic – not modifiable - largest impact (40-60%)

28
Q

what do we measure in the blood to see risk of developing cardiovasular disease

A
  • fats, carbs, sugars
    -Trans and saturated are proinflamtory and can permote formation of artery-clogging plaques.
    -cholestrol
29
Q

How does cholestrol contribute to CVD

A

Cholesterol levels play role in premature atherosclerosis and cardiovascular disease (CVD) risk, and are transported by lipoproteins:
-Low-Density Lipoprotein (LDL): Often referred to as “bad” cholesterol, it is inflammatory and atherogenic, contributing to plaque buildup in arteries.
-High-Density Lipoprotein (HDL): Known as “good” cholesterol, it helps protect against CVD by removing excess cholesterol from the blood and transporting it to the liver for excretion. HDL also has anti-inflammatory, anti-atherogenic, and anticoagulatory properties.

30
Q

What is Dyslipidemia

A

Abnormal lipid levels in the blood.
Inflammatory monocytes, higher cytokines, and adhesion molecules—these stick to blood vessel walls and become foam cells, contributing to plaque.

31
Q

what is C-Reactive Protein and where is produced.

A

produced by the liver in response to inflammation. It’s a biomarker—meaning its levels in the blood can be measured to assess the level of inflammation in the body.
High CRP level predicts high cardiovascular disease risk
Reflects accumulation of macrophages, lymphocytes, lipids, products of tissue injury in unstable plaques in
coronary arteries

32
Q

What are some Cardiovascular risk indicators?

A

CRP and Homocysteine

33
Q

What is Homocysteine what does it do

A

Homocysteine:
Sulfur-containing aa formed from abundant in animal protein.
Elevated levels marked by early onset of severe atherosclerosis
High level is a risk factor for cardiovascular disease
Metabolism requires vitamins B6, B12, and folic acid, and deficiency can cause increased homocysteine levels.

34
Q

What is Bradycardia

A

When the heart rate is too slow.
can be caused from opiods.

35
Q

what is Tachycardia

A

When the heart beat is too fast

36
Q

what are some causes of hypertension

A

Cardiac effects:
Increased peripheral resistance → higher workload → heart enlargement → risk of heart failure.

Vascular effects:
Increased pressure → vessel damage → accelerates arteriosclerosis/atherosclerosis → risk of rupture and hemorrhage.

Renal effects:
Narrowed renal arterioles → reduced blood flow to kidneys → kidney damage → can lead to renal failure.

37
Q

What can cause hypertension

A

increased sympathetic stimulation can cause excessive vasoconstriction of small arterioles resulting in:
Increased peripheral resistance; increased diastolic blood pressure
Increased force of ventricular contraction
Compensatory increase in systolic pressure

38
Q

What is secondary hypertension and how to treat?

A

From a known disease (CVD, autoimmunity, chronic kidney disease, pituitary or adrenal tumor, hyperthyroidism)
Lifestyle: Diet (reduce salt/fat/sugar/alcohol intake/smoking cessation), exercise (weight/cardio), reduce stress, sleep
Diuretics - to remove salt/water

39
Q

What is it called when top number (systolic pressure) is high, but the bottom number (diastolic pressure) is normal or low.?

A

Isolated systolic hypertension (ISH)

40
Q

What does systolic pressure measure

A

Systolic pressure: Measures pressure when the heart beats.

41
Q

What does diastolic pressure measure

A

Measures pressure when the heart rests between beats.

42
Q

What happens in ISH or Isolated systolic hypertension.

A

In ISH, systolic pressure rises due to the aorta becoming stiffer with age, so it can’t expand as easily when the heart pumps blood.
The diastolic pressure stays normal because the small arteries (arterioles) aren’t constricting.

43
Q

What is an aneurysm?

A

aneurysm is when a part of an artery wall weakens and bulges out or dilates.

44
Q

What are the causes of an aneurysm?

A

-Arteriosclerosis (hardening of the arteries) is the main cause, making the vessel wall weaker.
-Congenital (present from birth) can also be a cause.

45
Q
  • what is A dissecting aneurysm of the aorta?
A

occurs when the layers of the aorta separate or tear due to degenerative changes over time.

46
Q
  • how does A dissecting aneurysm of the aorta happen?
A

-The inner lining of the aorta can tear, especially if there’s high blood pressure.
-Blood then gets forced into the wall of the aorta, creating a separation between its layers.