Pathology of Hypertension Flashcards
(80 cards)
1
Q
Hyaline Ateriolosclerosis
- Associated with what disease?
- Cause?
- Patient Profile?
- Appearance?
A
Disease Association:
• Benign Hypertension
Cause:
- Pressure pushes plasma proteins across injured endothelial cells
- Chronic Stress ^ increases matrix synthesis
Patient Profile:
• Hypertensive patients or Old people
Appearance:
• Thick Intima with very pink appearance from deposited proteins
2
Q
Hyperplastic Arteriolosclerosis
- Associated with what disease?
- Cause?
- Appearance?
A
Disease Association:
• SEVERE (malignant) Hypertension
Cause:
- Increased strain causes Muscle cells to become thickened and duplicated
- FIBRINOID NECROSIS may also occur
Appearance:
- Onion Skinning appearance
- Amphoric and pink in the case of fibrinoid necrosis
3
Q
Thrombosis
• cause of thrombosis in Vascular Disease?
A
Formation of a Blood Clot from Exposed ECM
• in this context Exposed ECM comes from ruptured plaque
4
Q
Embolus
• cause?
A
Thrombus is mobilized and can move throughout vasculature
5
Q
Atherolsclerosis
A
- Disease characterized by Intimal Lesions called artheromas
- these artheromas have a lipid core surrounded by a fibrous cap
6
Q
Medial Calcific Sclerosis
A
- Common in people over 50 y/o where Calcium is seen in the intima
- Don’t freak out if you see this on a radiograph or mammogram as long as it follows a vessel its okay
7
Q
What is the significance of: Turbulence, Dyslipidemia
A
• Two most common causes of endothelial injury leading to atherosclerosis
8
Q
What is a Fatty Streak?
A
i
9
Q
What is a Plaque?
A
i
10
Q
What is Stenosis?
A
Occlusion of an artery caused by large atherosclerotic plaque
11
Q
Aneurysm
A
Ballooning out of all 3 layers of a vessel due to weakening of the media
12
Q
Dissection
A
i
13
Q
T or F: Hypertension puts you at an increased risk for renal failure?
A
True, this risk is especially high in people with diabetes and hypertension
14
Q
What are the cutoffs for hypertension?
A
140 mmHg systolic 90 mmHg diastolic
15
Q
In what case might you place a patient with a blood pressure of lower than 140/90 on anti-hypertensive medication?
A
• High risk patients such as those with Diabetes may need treatment earlier than other people
16
Q
T or F: in the case of hypertension preventative medicine has proven to be extremely effective.
A
True
17
Q
What causes most cases of hypertension?
A
90% of cases are idopathic
18
Q
What are some diseases that often have a secondary effect of hypertension?
A
• Renal Disease
• Renal Artery Narrowing
• Adrenal Disorders
19
Q
Why is hypertension often a secondary result of many renal disorders?
A
- Macula Densa falsely Sense Low Blood Volume because of renal disease
- Increased Renin –> angiotensin I –> angiotensin II will lead to increased fluid volume and a heart that is beating harder
- Aldosterone may be secreted in too large amount in adrenal tumors etc. (pheochromocytoma)
20
Q
How do you calculate Cardiac Output?
A
CO = Heart Rate x Stroke Volume
21
Q
What is the standard response of the vascular wall to injury?
A
- Smooth Muscle Hyperplasia in INTIMA
- ECM is synthesized
- PERMANENT intimal thickening result
22
Q
Atherosclerosis
- Cause
- Vessels involved
- Disease Type
A
Cause:
• LIPID Accumulation with Cellular Reaction
Vessels Involved:
• Large and Medium Arteries
Disease Type:
• Considered an INFLAMMATORY DISEASE
23
Q
What are the most common arteries to see atherosclerosis in?
A
• Abdominal Aorta
• Coronary Arteries
• Cerebral
• Common Iliac
• Femoral Arteries
24
Q
****What is this?
• Clinical Significance
A
Monckebergs
• Typically not clinically significant
25
**\*\*Monckebergs**
* Cause
* Vessel type
* Appearance (radiology and H&E)
* Significance
Cause:
• **Cacification of Vessel Media**
Vessel:
• **Muscular Arteries**
Appearance:
* Dark **purple calcium deposits** in the media on H and E
* Follows the path of the vessel on Radiology
26
What patient population is Monckenbergs often seen in ?
• Ppl. **50 years and older** commonly have Monckebergs
27
**\*\*Arteriolosclerosis**
* Cause
* Vessel type
* Types
Cause:
• **Reduced lumen** size from thickening of vessel in response to **high pressure**
Vessel Type:
• **Small Arteries**
2 types:
**• Hyaline**
**• Hyperplastic**
28
What diseases are associated with arteriolosclerosis?
* Diabetes
* Hypertension
29
\*\*\*\*What is this?
• key features?
**Nephrosclerosis**
• Pitting Scars on the surface that should be smooth
30
\*\*\*\*What is this?
• Patients this is most commonly seen in?
**Onion Skinning** in Hyperplastic Arteriolosclerosis
• Most commonly seen in patients with **malignant hypertension** (\>200mmHg systolic)
31
\*\*\*\*\*What is this?
• Patients this is most commonly seen in?
**Hylaine arteriolosclerosis** - **intimal thickening** from ECM expansion
• seen in Elderly and people with Benign Hypertension
32
\*\*\*\*\*What is this?
• Patients this is most commonly seen in?
**Hyperplastic arteriolosclerosis** that has caused Fibrinoid Necrosis of Small Renal Arteries
33
What organs are most commonly damaged in Hyperplastic Arteriolosclerosis?
**Kidney Damage** is common
34
What is an atheroma?
• Plaques of LIPID CORES covered by a FIBROUS CAP • Lesions found in the INTIMA
35
What is the difference in etiology of an acute occlusion vs. chronic occlusion of a large vessel lumen?
Chronic:
• Plaque **slowly builds** up by binding more and more LDL
Acute:
• Cap ruptures and underlying collagen etc. is exposed and leads to acute **Myocardial Infarction**
36
How can atheroclerotic plaques increase the probability of aneurysm?
• Lipids and Necrotic Tissue may **weaken the intima** and media causing a ballooning out (aneurysm) of the vessel
37
What are some of the **constitutional** risk factors for atherosclerosis?
Genetics:
* Mendelian Disorders (like FH)
* Polygenic traits (like Diabetes, HTN)
Age:
• 40-60 pts. may start to become symptomatic Gender: • Premenopausal Women are protected
38
What are some **modifiable** risk factors for atherosclerosis?
* Hyperlipidemia
* Hypertension
* Cigarettes
* Diabetes
* Inflammation (CRP and Hyperhomocysteinemia)
39
What is the first gross sign indicating where a clot might form?
• Fatty Streak
40
\*\*What are the steps in formation an atherlosclerotic plaque?
* Chronic **Endothelial Injury**
* Endothelial Dysfunction **attracts leukocytes, monocytes, and platelets**
* Macrophages Recruit **Smooth Muscle to the intima**
* **Macrophages** and Smooth Muscle Cells **eat LIPIDS**
* Smooth muscle cells proliferate and **deposit Collagen and ECM**
41
What is secreted by T-cell in the atherlosclerotic plaque?
IFN-gamma
42
What does the fibrous plaque resemble underneath the microscope?
Granulation Tissue
43
What is the difference in stable and and unstable progression of atherloma?
Stable:
• **Slow** progression caused by accumulation of more and more lipid in the intima
\*\*\*Leads to stable angina
Unstable:
• RAPID progression caused by platelet and fibrin deposition that expands and causes thrombus formation
44
How do you know a plaque is becoming unstable?
• **70% or more** of the lumen is occluded - this characterizes and unstable plaque
45
What vessels are most commonly involved in Atherlosclerosis?
* INFRARENAL abdominal Aorta
* Coronary Arteries
* Popliteal Arteries
* Internal Carotid Arteries
* Circle of Willis
46
What are the ways in which **Athlerosclerosis** become clinically relevent?
• when does this happen?
**40-60 y/o** Disease Becomes Clinically Relevent 3 ways:
* **Aneurysm** (weakening of arterial wall)
* **Thrombosis** (ruptured plaque)
* **Critical Stenosis** (\>70% vessel occlusion)
47
\*\*\*\*What is this?
• Atherosclerotic Plaque
48
What are the 3 most common areas where plaques occur?
**• Ostia of Existing Vessels
• Branch Points
• Posterior Wall of Abdominal Aorta**
49
What roles does **dyslipidemia** play in formation of **atherosclerotic** plaque?
* Cholesterol **impairs endothelial cell function** causing an **increase in free radicals** that **scavenge NO** leading to less vasodilation
* **LIPID ACCUMULATION in the intima** becomes **oxidized LDL** and **cholesterol clefts form** - macrophages ingest this and become **foam cells**
50
\*\*\*\*What do you see here?
* Cholesterol Clefts
* Foam Cells
51
What is the importance of **cholesterol clefts** in atherosclerosis?
• Cholesterol Clefts **incite inflammation** and Subsequent Release of **IL-1**
52
\*\*\*\*What cell type is shown on the vessel surface seen here?
• Foam Cells
53
\*\*\*\*What is this?
• **Fibrous Cap** of an atherosclerotic Plaque resembling **granulation tissue**
54
What typically makes of the **cells of a plaque** and the **ECM**?
**Cells:**
• Smooth Muscle
• Macrophages
• T-cells
**ECM:**
• Collagen
• Elastic Fibers
• Proteoglycans
• Cholesterol Clefts
55
\*\*\*\*What is happening in this **coronary artery**?
* **Thrombosis** seen as **red**
* **Recanalization** of an old hemorrhage (seen as **darker pink**)
56
\*\*\*\*\*Would you consider this a stable or unstable plaque? why?
Stable because **only thickening of the wall** is seen and **no hemorrhage** or thrombosis is evident
57
\*\*\*\*\*Would you consider this plaque stable?
NO there is clear **evidence of thrombus**
58
\*\*\*\*\*What is this?
\*Thrombus formation in descending interventricular coronary artery
59
\*\*\*\*what process is seen here?
Thrombus from **Ruptured Plaque**
60
What are some of the **clinical** complications of atherosclerosis?
* Ischemia
* MI
* Stroke
* Aortic Aneurysms
* Peripheral Vascular Disease
61
What **layers** are involved in **aneurysms**?
All Three Layers
62
What is False Hematoma?
• Hematomas that communicate with the extravascular space
63
What are the characteristic **symptoms** of an **aneurysm**?
**• Deep constant pain in abdomen accompanied by back pain**
64
Why/How does **atherlosclerosis** put you at an increased risk of **aneurysm**?
* While atherlosclerosis is a disease of the intima but the plaque may **compress and cause thinning of the media**
* **Weakening** of the wall and **loss of elasticity** causes a predisposition for dilation and rupture
65
\*\*\*\*\*What is this patient about to get surgery for?
Abdominal Aneurysm
66
\*\*\*\*\*What disease causes a predisposition for the disease shown here?
Hypertension
• This is an ascending aortic dissection
67
\*\*\*\*\*\*what disease causes a predisposition for the disease seen here?
**Atherlosclerosis**
• this is an abdominal aortic aneurysm
68
What genetic disorders put you at an increased risk of aneurysm?
* Collagen Defects
* **Marfans** or **Type IV Ehlers-Danlos Syndrome**
69
Syphilis is most likely to cause what type of aneurysm? • why does this happen?
**Thoracic**
• Happens as a result of **inflammation around the VASO VASORUM**
• Inflammatory cells are often **plasma cells**
70
\*\*\*\*What pathological process is shown in this picture?
**\*Thoracic aneurysm**
\* Notice the **Tree Bark Appearance**
71
\*\*\*\*\*What pathological process is shown here?
• Who is at the greatest risk of experiencing this?
* **Abdominal Aortic Aneurysm**
* Male Smokers over 50 years old
72
Who is AAA typically seen in?
• complications?
**Typically Male smokers over 50**
Complications:
* Obstruction of Vessels Branching off of the aorta
* Embolism
* Impingement on Adjacent Structures
* Rupture
73
How does AAA feel?
**\* Feels like a pulsating tumor in the abdomen**
74
\*\*\*\*What processes is seen here?
• Dissection
75
\*\*\*\*What processes is seen here?
• main risk factor
* Dissection of **Ascending** Aorta
* Risk Factor - **Hypertension**
76
What is the role of TGF-ß in the pathogenesis of Dissection?
• What is unique about aneurysms in people with TGF-ß dysregulation?
* **TGF-ß regulates smooth muscle cell proliferation and matrix synthesis**
* Mutations in TGF-ß receptors or Downsteam signaling pathways result in **defective elastin and collagen synthesis**
* **ANEURYSMS** in these people tend to **RUPTURE even when SMALL**
77
What is the pathophysiology that links Marfan Syndrome to Aneurysm?
* **FIBRILLIN** is abnormally synthesized
* **TGF-ß is sequestered** in **aortic wall** due to abnormal FIBRILLIN
* this results in **DYSREGULATED SIGNALING** that causes progressive **loss of elastic tissue**
78
Cystic Medial Degreneration
* what is it?
* what causes it?
What is it:
• Change in medial smooth muscle phenotype
Cause:
• **ECM synthesis is defective** due to **ischemic changes** of the **outer media**
79
How can Dissection in a patient cause Cardiac Tamponade?
• Dissection can travel **Retrograde** into the heart valves
80
\*\*\*\*What is abnormal about the aortic wall shown here?
• Weak **disorganized collagen** can be seen which puts the patient at higher risk for **Dissection or Aneurysm** \*\*\*Disorganization at the top = major problem
