Brainscape's Knowledge GenomeTM

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


See full index

Patho > Chapter 18 > Flashcards

Chapter 18 Flashcards

1
Q

Arteries have 3 layers, what are they?

A

Tunica Externa- collagen
Tunica Media- smooth muscle and elastin
Tunica Intima- single Endothelium layer

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

Tunica Externa

A

protective layer for artery
collagen
*anchors vessel to surrounding tissue
*small nerve fibers and VASA VASORUM

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

Tunica Media

A

smooth muscle and elasting

  • perfusion of tissue around it
  • controlled by nerve signals from externa, (Norepinephrin) Neurotransmitter that binds to receptors on smooth muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Tunica Intima

A

single layer of endothelium cells & small layer of connective tissue that sits beneath endothelial layer

  • Prevents clotting and big mediators of inflammation!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

One of the most important functions of the endothelium:

A

transports O2 to cells and takes waste away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Primary Hyperlipidemia

A

genetic based.

  • develops bc of mutation on LDL receptor
  • Prevents LDL from being taken up to tissue so you get a high serum LDL level.
  • creates Xanthomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Xanthoma

A

cholesterol deposits on tendons, skin, elbows

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

Secondary Hyperlipidemia

A

attributed to high calorie diet, ^ triglycerides levels.

  • Converts VLDL to LDL (bad cholesterol)
  • LDL’s don’t get taken up in blood so ^ LDL serum levels
  • need to exercise to prevent this.
  • diabetes, thyroid disease, renal disorders, Cushing syndrome, obesity, alcohol, estrogen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hyperlipidemia

A

high cholesterol

* can be categorized by which lipid is elevated.

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

fats are carried in the blood through____

A

lipoproteins

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

Lipoprotein structure

A
  • phospholipid membrane

* Apoliproteins- stabilize structure, activate enzymes necessary for lipoproteins to metabolize.

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

Apolipoproteins

A
  • stabilize lipoprotein structure
  • activate enzymes necessary for lipoprotein to metabolize
  • REACTIVE sites for receptors on tissue
  • Bind lipoproteins together.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

LDL

A

low-density lipoproteins (bad)

  • Lower density: less protein, more cholesterol
  • transports cholesterol from liver to cells
  • can be oxidized and deposited
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HDL

A

high-density lipoproteins (good)

  • Higher density: more protein, less cholesterol
  • transports cholesterol from cells to liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk factors for developing hyperlipidemia or atherosclerosis:

A 
smoking
diabetes
coronary artery disease
heart disease
low activity level / sedentary lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HDL lower than___ puts you at risk for hyperlipidemai

A

40

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

Health LDL us under

A

< 160

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

Endothelial Dysfunction

A

reversible changes in endothelial function that occur in response to environmental stimuli
- thrombosis, atherosclerosis, hypertensive vascular lesions

  • smoking/^BP/Insulin resistance/Diabetes etc..
    • produces inflammatory cytokines, GF, ROS, and other disease producing substances in endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Disorders of Arterial Circulation- Large, Medium, small arteris

A

large- aorta
medium- coronary and renal
small- arteries and arterioles that pass through the tissues

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

because lipids aren’t soluble in plasma, they get ___ by ___ for transport in blood

A

encapsulated, lipoproteins

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

4 types of lipoproteins

A
  1. Chylomicrons
  2. VLDL- very low density (^ triglycerid, not much chol/pr
  3. LDL- low density ( main carrier of cholesterol)
  4. HDL- high density ( 50% protein, less chol/tri)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

2 pathways in generation and transport of lipoproteins:

A
  1. Exogenous Intestinal- transport dietary cholesterol and lipids from intestine to liver chylomicron
  2. Endogenous Hepatic- Processing of triglycerides and cholesterol in liver and distributed to body for energy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

small, dense, LDL are more ___ and ___ to endothelium that larger LDL

A

atherosclerotic, toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Small LDL are:

A

more likely to enter the endothelium wall, become oxidized, and trigger atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Defect in HDL clearing system, results in accelerated atherosclerosis and little or no HDL

A

Tangier Disease

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

Hypercholesterolemia

A

^ levels of cholesterol in blood

2 categories:
1. Primary- genetic defect ( Familial Hypercholesterolemia)

  1. Secondary- obesity, high calorie diet, sendary life, diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Developmental Pathway of Atherosclerosis

A
  1. Fatty Streaks
  2. Fibrous Atheromatous Plaque
  3. Complicated Atherosclerotic Lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Fatty Streaks

A

thin yellow lines that run along the major arteries

  • made of smooth muscle cells filled with cholesterol and macrophages
  • begin in children 10-14 and develop till you’re 20.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Fibrous Atheromatous Plaque

A

basic lesion of atherosclerosis
- characterised by: accumulation of intracellular and extracellular lipids, proliferation of smooth muscle cells, formation of scar tissue, and calcification.

  • appear as grey, white or pearly elevated thickening in the intima
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Complicated Atherosclerotic Lesions

A

when the plaque breaks open/off, producing hemorrhage, ulceration, and scar tissue deposits.
- THROMBOSIS occurs at area of plaque break off

31
Q

Atherosclerosis process at a cellular level:

A
  1. macrophages attach to endothelium
  2. macrophages release ROS which damages endothel
  3. the damage creates a hole, exposing collage for platelet adhesion to area
  4. fibrin deposits in the area
  5. Deposition of extracellular matrix follows
  6. some macrophages die after eating cholesterol, then release the oxidized cholesterol back into the lesion (plaque build up)
32
Q

Non-traditional risk factors for atherosclerosis

A

C-Reactive protein (CRP)
Serum Homocysteine
Lipoprotein A

33
Q

Unstable plaques

A
  • thin fibrous caps that break off easily
  • plaque rupture –> clot formation (thrombus)
  • may completely block the artery or break free to become embolus
34
Q

Peripheral Arterial Disease (PAD)

A

atherosclerotic blockages of large arteries that supply peripheral structures, NOT central structures like heart, brain.
- mainly effects men (60-70’s)

35
Q

Principle symptom of chronic obstructive arterial disease:

A

Claudication

36
Q

Claudication

A

pain when walking (bc of large clot in extremity)
symptoms: weak popliteal/pedal pulse, foot numb

  • seen in gastrocnemius bc of highest O2 consumption when walking
  • when blood flow is cut off completely: can get ischemic ulceration, gangreen, bc of loss of blood flow
37
Q

Thromboangitis Obliterans (Beurger Disease)

A

nonatherosclerotic inflammation and thrombosis
* effects blood flow to extremities but in small arteries/veins. Tobacco use is main predisposing factor.

  • predominant symptom: pain in lower extremity just sitting
  • weak pulse in pedal/popliteal
  • skin atrophy, ulceration, and gang green
38
Q

Raynaud Phenomenon

A
  • intense vasospasm of arteries, arterioles in fingers and toes.
  • Primary- hyper activity in sympathetic NS. emotional response. attacks all 10 fingers/toes at once. NOT asymetric.
  • Secondary- assoc. with previous vessel injury, collagen disease, asymmetric finger involvement, very painful
  • frostbite, occupational trauma, intense heat/cold
39
Q

Aneurysm

A

pathological outpouching or sac-like dilation in the wall of a blood vessel usually caused by weakening of the vessel wall.

  • most common in arteries
40
Q

The weakness in epithelium that creates aneurysms is caused by:

A 
congenital defectors
Trauma
Infections
atherosclerosis
^BP
41
Q

True Aneurysm

Fals Aneurysm

A
  • bounded by a complete vessel wall. Blood remains in vascular compartment
  • localized dissection or tear in the inner wall of the artery w/formation of an extravascular hematoma that causes vessel enlargement
42
Q

Berry Aneurysm

A

small, spherical dilation of the vessel bifurcation

* Circle of Willis*

43
Q

Fusiform Aneurysm

A

involves entire circumference of the vessel and is characterized by a gradual and progressive dedication of the vessel.

  • thoracic or abdominal aorta aneurysm*
44
Q

Sacular Aneurysm

A

appear saclike over part of the vessel

45
Q

Dissecting Aneurysm

A

false aneurysm
results from a tear in the intima layer of the vessel that allows blood to enter the vessel wall, dissecting its layers to create a blood-filled cavity

46
Q

thoracic and abdominal aneurysms

A

worst thing it can do is rupture

  • thoracic- mainly due to atherosclerosis. usually asymptomatic
  • BUT* may present as substernal, neck, or back pain.
47
Q

Arterial BP healthy number:
Diastolic:
Systolic:
Pulse Pressure:

A

120/80
diastolic: ventricular relaxation ( ^ BP: above 120)
Systolic: ventricular contraction (^ BP: above 180)

Pulse Pressure: (systolic - diastolic)

48
Q

Mean Arterial Pressure:

A

1/3 systolic + 2/3 diastolic

49
Q

Cardiac output:

A

HR x SV

50
Q

Blood pressure:

A

CO x total peripheral resistance

51
Q

Systolic

A

measures the pressure in your blood vessels when your heart beats

52
Q

Diastolic

A

Measures the pressure in your blood vessels when your heart rests

53
Q

short term Blood Pressure Regulation is meant to:

A
  • correct temporary imbalances in BP (exercise, body position)
  • maintain BP at survival levels during life-threatening situation
54
Q

the neural control of BP is vested in centers that are located in the ____ of the ___ and lower third of the ___ where integration and modulation of _____ response occurs

A

reticular formation
medulla
pons
autonomic NS

55
Q

Parasympathetic pathway for nerve impulses to the heart

A

vagus nerve

56
Q

Sympathetic pathway for nerve impulses to the heart

A

Spinal cord and peripheral sympathetic nerves

57
Q

Extrinsic reflexes for ANS

A
  • mediate the cardiovascular response to stimuli originating from outside body. ( Pain, Temp)
  • response channeled through hypothalamus
58
Q

Intrinsic reflexes for ANS

A
  • baroreceptor (pressure) and chemoreceptor (chemical)
  • stimuli originates iwthin the cardiovascular system
  • essential for rapid short-term regulation of BP
59
Q

Baroreceptors

A

high and low pressure reeptors.

-low pressur baroreceptors ^ BP by telling kidney to reabsorb salt and water

60
Q

Chemoreceptors

A

sense an imbalance in gas levels and change respiratory rate
* too much CO2, slow down breathing*

61
Q

Epinephrin

A
  • sympathetic neuro transmitter

- ^ HR, Cardiac Contractility, and vascular tone

62
Q

Renin- Angiotensin- Aldosterone System

A

renin–> Angiotensin I –> Angiotensin II

  • renin released due to ^ in sympathetic NS activity and low BP/fluid volume
  • Renin converts Angiotensinogen to Angiotensin I.
  • Angiotensin I goes to lungs __> Angiotensin II.
63
Q

Angiotensin II does what?

A
  • Strong vasoconstrictor of arterioles to ^ BP
    _ Reduces sodium excretion by ^ sodium reabsorption by kidney.
  • Stimulates Aldosterone secretion from adrenal gland (long term regulation of BP) ^ salt and H2O retention.
64
Q

Vasopressin

A

Antidiuretic Hormone (ADH)

  • released to Increase BP and act as vasoconstrictor.
  • tells kidney to not release any water.
65
Q

Hypertension is classified as:

A
  • consistent 140/ 90 mmHg or higher
66
Q

Hypertensive Crisis
Hypertensive Urgency
Hypertensive Emergency

A
  • crisis: >180/120mm Hg either/or, doesn’t have to be both
  • Urgency: have ^ BP but don’t see organ damage yet.
  • Emergency: see organ damage and neurological effects. Vision, kidney, heart damage, very bad.
67
Q

Hypertension is classified as:

A
  • consistent 140/ 90 mmHg or higher
68
Q

Treatment of Hypertension: (drugs)

A
  1. Beta Blockers- Lower HR, decrease release of renin. Long term effect is a chronic cough.
  2. ACE inhibitors- inhibit conversion of angiotensin I to II.
  3. Calcium Channel blockers- decrease peripheral vascular resistance. inhibit movement of calcium to smooth muscle cells
  4. a-2 Agonists: decrease sympathetic outflow from CNS
69
Q

Hypertension in Pregnancy

A
  1. Pre-eclampsia/eclampsia- hypertension after 20 wks. Proteinuria, elevated serum creatinin and liver enzymes, decreased platelets
  2. Gestational Hypertension- ^BP after 20 weeks. NO proteinuria, resolves by 12 weeks postpartum
  3. Chronic Hypertension- occurs during pregnancy but regular hypertension
70
Q

Orthostatic Hypotension

A

abnormal drop in BP that occurs when a person stands after having been in seated or supine position.

71
Q

Vericose Veins

A

most commonly seen vein issue.

  • more women than men (pregnant women especially)
  • veins that are dilated and twisted in legs, overfilled, and have lack of movement of blood in them.
72
Q

the most common cause of secondary varicose veins

A

Deep vein thrombosis

73
Q

Primary varicose veins

Secondary varicose veins

A

primary- superficial saphenous veins

secondary- deep venous channels

74
Q

A patient with a systemic bacterial infection is at risk of developing ___

A

Immune Thrombocytopenic Purpura

Patho (18 decks)

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