Blood Vessels - Class Flashcards

Question

Effects of Physical Activity on Venous Return

Answer 1

*Effects of Exercise on Venous Return* - ↑ Heart rate and contractility → ↑ cardiac output and blood pressure - Vasodilation of vessels in muscles, lungs, and heart → ↑ blood flow - ↑ Respiratory rate → enhances thoracic (respiratory) pump - ↑ Skeletal muscle activity → activates skeletal muscle pump *Venous Pooling with Inactivity* - Venous pressure alone is insufficient to move blood upward - Prolonged standing may reduce cardiac output enough to cause dizziness - Prevented by: - **Tensing leg muscles** → activates skeletal muscle pump - **Pressure suits** (e.g., for jet pilots) → support venous return

Answer 2

- **Veins** hold ~**64–70%** of total blood volume → Act as **volume reservoirs** due to high distensibility → Can expand **~8× more** than arteries at same pressure - **Arteries + capillaries** hold only **~20** of total volume - Arteries: ~15% - Capillaries: ~5% - Blood distribution is **uneven**: most is stored in **systemic veins**, not evenly across all vessels

Answer 3

- The **force of blood** distending arterial walls 1. **Systolic Pressure** - **Highest pressure** in arteries - Occurs during **ventricular contraction** (systole) 2. **Diastolic Pressure** - **Lowest pressure** in arteries - Occurs during **ventricular relaxation** (diastole) 3. **Blood Pressure Reading** - Reported as **systolic/diastolic** - Normal: **120/80 mmHg** 4. **Korotkoff Sounds (Cuff Sounds)** - Cuff inflated above systolic pressure → **no sound** (no flow) - **1st sound = systolic pressure** (turbulent flow begins) - **Sounds disappear = diastolic pressure** (laminar flow restored) - Used during auscultatory blood pressure measurement

Answer 4

- Average pressure in arteries over a full cardiac cycle - Reflects **driving force** of blood through the vasculature **Pulse Pressure (PP)** - PP = **SBP − DBP** **Formulas to estimate MAP** - *At rest* (diastole lasts longer): **MAP = DBP + (SBP − DBP) / 3** - *During exercise* (systole and diastole nearly equal): **MAP = DBP + (SBP − DBP) / 2** **Clinical relevance** - Important for assessing tissue perfusion, especially in critical care - Normal MAP ≈ **70–110 mmHg** - Minimum of **60 mmHg** needed to perfuse vital organs

Answer 5

1. **Cardiac Output (CO)** - CO = **Stroke Volume × Heart Rate** - ↑ CO → ↑ BP 2. **Peripheral Resistance** a. **Vessel Diameter**: Vasoconstriction ↑ resistance → ↑ BP. Vasodilation ↓ resistance → ↓ BP b. **Blood Viscosity**: ↑ viscosity (e.g. polycythemia) → ↑ resistance → ↑ BP c. **Total Vessel Length**: ↑ vessel length (e.g. obesity) → ↑ resistance → ↑ BP 3. **Arterial Blood Volume** - More blood in arteries → ↑ pressure against vessel walls 4. **Arterial Compliance / Vessel Elasticity** - ↓ compliance (stiff arteries) → ↑ systolic pressure - Elastic vessels buffer pressure fluctuations

Answer 6

- *CO = HR × SV* - ↑ **Cardiac Output** → ↑ **Systolic BP** - ↓ **Cardiac Output** → ↓ **Systolic BP** - ↑ HR or SV = ↑ CO → proportionally increases BP *(as CO ↑, BP ↑ if resistance is constant)* **Frank-Starling Law** - ↑ **Venous return** → ↑ **EDV** (end-diastolic volume) - ↑ EDV → ↑ **stretch** of ventricular wall (↑ **preload**) - ↑ Stretch → ↑ **cross-bridge formation** in sarcomeres - ↑ Cross-bridges → ↑ **force of contraction** - ↑ Force → ↑ **SV** → ↑ **CO** → ↑ **BP** - *Proportional relationship*: More filling = more ejection = higher pressure - *Moderator band* limits overexpansion of right ventricle

Answer 7

- *Definition*: Friction between blood and vessel walls that opposes flow; BP must overcome PR to maintain circulation - *Affects*: **Afterload** – resistance heart must work against to eject blood **3 Primary Sources of PR:** 1. **Vessel Diameter** - *Smaller diameter = much greater resistance* (inverse to radius⁴) - Flow is slower and more turbulent in narrow vessels → more resistance - Arterioles control this dynamically through vasoconstriction and vasodilation - **Most powerful influence** on PR 2. **Blood Viscosity** - Thicker blood = greater resistance - *Increased by*: dehydration, polycythemia (↑ RBCs), high protein content - *Decreased by*: anemia, dilution with IV fluids 3. **Total Vessel Length** - Longer vessels = more surface area = greater resistance - *↑ Fat tissue* adds capillary length (~200 miles/lb) → raises PR **Systemic Vascular Resistance (SVR)** - Total PR in the systemic circulation - Major regulator: **arterioles**, by changing radius **Summary (Poiseuille’s Law)** - PR is governed by: - **↑ Resistance** if radius ↓ (to the 4th power), viscosity ↑, or length ↑ - **↓ Resistance** if radius ↑ (vasodilation has a major impact) - *Key takeaway*: **Vessel diameter** is the most effective and rapid way to change resistance and blood pressure.

Answer 8

Widespread or localized changes in vessel diameter to adjust **blood pressure** and **flow distribution** 1. **Regulate Systemic Blood Pressure** - *↑ BP*: Via vasoconstriction (narrowing vessels) - Requires **medullary vasomotor center** or **hormonal signals** - *↓ BP*: Via vasodilation - *Clinical importance*: Maintains **cerebral perfusion** during hemorrhage or dehydration 2. **Redistribute Blood Flow (Perfusion)** - *Central control*: Sympathetic NS directs blood away from kidneys/digestive organs → toward muscles during exercise - *Local control*: Metabolites (e.g., CO₂, H⁺, adenosine) in tissues trigger local vasodilation to increase perfusion - No systemic pressure change needed 3. **Localized Vasoconstriction** - *Constriction of one artery*: - ↓ pressure downstream - ↑ pressure upstream - *Effect*: Routes blood away from some organs and toward others based on need

Answer 9

- *Highly variable* depending on activity level - Controlled by both **systemic sympathetic input** and **local metabolite signals** *Receptor Distribution and Function* - **Skeletal muscle arterioles express both**: - **α₁-adrenergic receptors** → vasoconstriction (dominant **at rest**) - **β₂-adrenergic receptors** → vasodilation (activated **during exercise**) *Resting State* - **Sympathetic tone** is mediated by **norepinephrine** from postganglionic sympathetic neurons → binds **α₁ receptors** on skeletal muscle arterioles → causes **vasoconstriction**, ↓ perfusion to inactive muscle → most **capillary beds closed**, total skeletal muscle flow ~**1 L/min** *Exercise State* 1. **Epinephrine** released from **adrenal medulla** into bloodstream → binds **β₂ receptors** on skeletal muscle arterioles → causes **vasodilation**, **overrides α₁ tone** in active tissue → effect is **receptor-selective**: **epinephrine has high affinity for β₂**, unlike norepinephrine 2. **Local metabolites** (↑ CO₂, H⁺, lactate) accumulate in working muscle → trigger additional **vasodilation**, independent of neural control 3. **Sympathetic stimulation to non-muscle organs** (e.g., gut, kidney): → activates **α₁ receptors**, causing **vasoconstriction** → **redistributes blood** to skeletal muscle *Additional Notes* - **β₁-adrenergic receptors** are found in the **heart**, not vessels → ↑ heart rate and contractility → ↑ cardiac output - **Isometric contractions** impede local blood flow → cause **faster fatigue** than isotonic exercise

Answer 10

*Total Cardiac Output* - **At rest**: ~**5 L/min** - **Moderate exercise**: ~**17.5 L/min** *Major Shifts During Exercise* 1. **Skeletal muscle** - At rest: **20%** (~1,000 mL/min) - Exercise: **~71%** (~12,500 mL/min) - ↑ Perfusion via **β₂-receptor activation** and **local metabolites** (CO₂, H⁺, lactate) 2. **Digestive + Renal systems** - Digestive: ↓ from **27%** to **3.4%** - Renal: ↓ from **22%** to **3.4%** - ↓ Flow via **α₁-mediated vasoconstriction** 3. **Cutaneous (skin)** - ↑ Absolute flow: 300 → 1,900 mL/min - Helps dissipate **heat** - %CO increases modestly 4. **Cerebral circulation** - **Constant flow** (~750 mL/min) - % of CO ↓ due to larger CO - Maintained by **tight autoregulation** → *ensures brain perfusion* 5. **Coronary circulation (heart)** - %CO remains **stable** (~4%) - Absolute flow ↑ in proportion to cardiac output - Matches **increased oxygen demand** from myocardium *Key Point* - Exercise redistributes blood to **active muscle and skin**, while maintaining **brain and heart perfusion**, and reducing flow to **kidneys and GI tract**.

Answer 11

**Blood Pressure: Arm vs. Leg Exercise** - **All skeletal muscle arterioles** have **α₁ receptors** (vasoconstriction) and **β₂ receptors** (vasodilation) - Sympathetic tone is **systemic** and does **not differ** between arms vs. legs - **Key difference** lies in: - **Local metabolite accumulation** (↑ CO₂, H⁺, lactate) in **active muscles** - → Triggers **vasodilation** in **working muscle**, lowering **total peripheral resistance (TPR)** - **Leg exercise**: - **Large muscle mass** → more local vasodilation - → **Greater ↓ TPR** → **smaller increase in BP** - **Arm exercise**: - **Smaller muscle mass** → less local metabolite production - → **Less vasodilation** → **higher TPR maintained** - → Leads to **greater rise in BP** for the same workload - *Summary*: - BP rise is **greater during arm exercise** due to **less metabolically driven vasodilation**, not because of different sympathetic output

Answer 12

- Formed when two or more **arteries connect** to supply the same region → introduces **redundancy** - Ensures **continuous blood flow** to vital areas (brain, heart, stomach) even if one vessel is blocked - Example: **Cerebral arterial circle (Circle of Willis)** - Connects **internal carotid** and **vertebral-basilar** systems via anterior and posterior communicating arteries - Allows blood rerouting if one artery is obstructed - Only ~¼ of people have a **complete circle** - Function: If one arteriole is blocked, another can still supply blood to the capillary bed

Answer 13

- Brain receives ~700 mL/min of blood — more stable than any other organ - Just seconds of interruption → loss of consciousness - 4–5 minutes → irreversible brain damage (neurons are non-mitotic) - Blood flow is constant overall but dynamically redistributed to active regions - Brain **autoregulates its own blood flow**. VASOMOTOR CENTER - Cerebral arteries **dilate** when systemic BP drops - **Constrict** when BP rises - Main regulator = **pH of brain tissue** → CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (via carbonic anhydrase) → ↑ CO₂ → ↓ pH → **vasodilation** to increase perfusion

Answer 14

- A **direct connection** between an arteriole and a venule, bypassing capillaries - Allows blood to be **rerouted quickly**, especially in areas where vessels may be **compressed** or **obstructed** (e.g., joints, visceral organs during movement) - Ensures continuous blood flow even when capillary routes are unavailable - Common in areas needing **rapid blood flow adjustment** (e.g., skin for thermoregulation) - Contrast with **thoroughfare channels**: those still pass through a capillary bed, while arteriovenous anastomoses do not

Answer 15

- **Transient Ischemic Attacks (TIAs)**: brief episodes of cerebral ischemia - Caused by spasms of diseased cerebral arteries - Symptoms: dizziness, vision loss, weakness, paralysis, headache, aphasia - Last minutes to a few hours, fully reversible - Often an **early warning sign** of impending stroke - **Stroke (Cerebrovascular Accident, CVA)**: sudden death of brain tissue due to ischemia - Causes: **atherosclerosis**, **thrombosis**, **ruptured aneurysm** - Effects: vary from mild to fatal → May include blindness, paralysis, loss of speech or sensation - Recovery depends on **surrounding neurons** and **collateral circulation**

Answer 16

Tissues can regulate their own blood supply based on local conditions **Metabolic Theory** - Inadequate perfusion → accumulation of **CO₂, H⁺, lactate** → **Stimulates vasodilation** → increases local blood flow. Oxygen delivery clears metabolites → Once cleared → vasoconstriction resumes **Vasoactive Chemical** - Paracrines secreted by by nearby cells platelets, endothelial cells, mast cells, perivascular tissue-> stimulate vasamotion. **Vasodilators** 1. **Nitric oxide (NO)** – from endothelial cells in response to shear stress 2. **Prostacyclin** – inhibits platelet adhesion and promotes dilation 3. **Histamine, bradykinin, prostaglandins** – from mast cells, basophils **Vasoconstrictor** - **Endothelins** – potent constrictors secreted from endothelial cells *Clinical Note* - This local vasodilation overrides sympathetic α₁-mediated vasoconstriction during exercise. Especially important in active skeletal muscle, ensuring perfusion where needed

Answer 17

Sudden increase in blood flow following a period of ischemia - *Mechanism*: - Occlusion → ↓ flow → metabolite buildup (CO₂, H⁺, adenosine) - Upon restoration → **intense vasodilation** → transient **↑ perfusion above baseline** - *Examples*: Skin flushing after cold exposure, limb reperfusion after compression

Answer 18

Formation of new blood vessels from existing vasculature - *Triggers*: - **Chronic low oxygen** (e.g. exercised muscle, tumor growth) - **Tissue regrowth** (e.g. uterine lining, wound healing, fat, muscle growth) - **Obstructed blood flow** (e.g. coronary collateral development) - *Mediated by*: Growth factors (e.g. **VEGF**, FGF) released by hypoxic or injured tissue

Answer 19

*Sympathetic Vasomotor Tone* - Sympathetic nerves fire at baseline frequency to maintain partial vasoconstriction ("vasomotor tone") - **↑ Sympathetic firing** → **vasoconstriction** (via α₁-adrenergic receptor*) - **↓ Sympathetic firing** → **vasodilation** - NE (norepinephrine) is secreted by most sympathetic postganglionic neurons *Adrenergic Receptor Distribution* - Vessel effect depends on receptor type expressed: - **α₁ receptors** (most systemic arterioles) → **vasoconstriction** - **β₂ receptors** (skeletal muscle, coronary vessels) → **vasodilation** - **Epinephrine** (from adrenal medulla) has high affinity for β₂, allowing vasodilation in active tissues - **NE** (from sympathetic nerves) favors **α₁**, maintaining vasoconstriction elsewhere *Medullary Vasomotor Center (in medulla oblongata)* - Integrates autonomic reflexes that regulate BP: 1. **Baroreflex**: ↑ BP → ↑ baroreceptor firing → ↓ HR, ↓ sympathetic tone (→ vasodilation) 2. **Chemoreflex**: triggered by hypoxia, hypercapnia, or acidosis → ↑ sympathetic output 3. **Medullary ischemic reflex**: ↓ perfusion to brainstem → extreme sympathetic output *Clinical Note* - **Loss of sympathetic tone** (e.g. neurogenic shock) → **dangerous hypotension** - Neural control can redistribute blood flow, e.g., shunting from gut to muscle during exercise

Answer 20

eflex to maintain stable blood pressure via autonomic adjustments in heart rate and vessel tone - **Baroreceptors** in carotid sinus and aortic arch detect arterial stretch → send signals via glossopharyngeal (CN IX) and vagus (CN X) nerves to the nucleus of the solitary tract in the medulla -> sends signals to vasomotor center and cardioinhibitory center./ *When blood pressure is high*: - ↑ Stretch → ↑ baroreceptor firing → activates **cardioinhibitory center** (medulla) → ↑ **parasympathetic (vagal)** output to heart → ↓ heart rate - Also inhibits **vasomotor center** → ↓ **sympathetic tone** → vasodilation → ↓ TPR → ↓ blood pressure *When blood pressure is low*: - ↓ Stretch → ↓ baroreceptor firing → less activation of cardioinhibitory center → ↓ parasympathetic tone → ↑ heart rate - Activates **vasomotor center** → ↑ **sympathetic tone** → ↑ heart rate, ↑ contractility, ↑ vasoconstriction → ↑ TPR → ↑ blood pressure

Answer 21

- **Chemoreceptors** in **carotid bodies** and **aortic bodies** - *Monitored variables*: **pH**, **CO₂**, **O₂** **Primary role**: - Adjust **respiration rate** to correct blood gas levels **Secondary role**: - Regulate **vasomotion** when chemical imbalance is detected **Triggered by**: - The chemoreceptor reflex responds primarily to changes in pH, which are influenced primarily by CO₂ (via carbonic acid) and indirectly by low O₂ (via lactic acid from anaerobic metabolism). **Responses**: 1. Signal to **vasomotor center** → **vasoconstriction** → **↑ BP**, ↑ lung perfusion and gas exchange → enhances CO₂ clearance, O₂ delivery

Answer 22

- *Trigger*: ↓ perfusion to **medulla oblongata** (e.g. brain ischemia) **Detection**: - Medulla monitors **its own blood flow** **Response**: - Activates **sympathetic output** from cardiac & vasomotor centers: - ↑ HR and contractility - **Widespread vasoconstriction** **Goal**: - ↑ **BP** to restore perfusion to brain - Short-term emergency reflex to protect **cerebral circulation**

Answer 23

Hormones regulate BP by: Vasoactive effects (vasoconstriction/dilation) and by Water & Na⁺ balance → affects blood volume **Angiotensin II** Formed via **RAAS pathway** from **angiotensinogen (liver)** → Converted to angiotensin I by **renin** (kidney), then to **angiotensin II** by **ACE** 1. Vasoconstrictor → ↑ peripheral resistance → ↑ BP. 2. Stimulates aldosterone (adrenal cortex) → ↑ Na⁺ reabsorption, water follows → ↑ blood volume and pressure 3. Stimulates ADH (vasopressin) release from the posterior pituitary → Promotes water reabsorption in the collecting ducts → Contributes to increased blood volume and pressure **Aldosterone** *regulated primarily by angiotensin II, to a leser extent high blood K+* Acts on distal tubule & collecting duct in kidney→ ↑ Na⁺ reabsorption, K⁺ excretion → Water retained → ↑ blood volume and BP **ADH (Vasopressin)** *primary stimulate is plasma osmolarity deceted by osmolarity receptors in hypothalamus, also stimulated by angiotensinII* Secreted fromposterior pituitar -> Promotes water retention only via aquaporins in collecting duct. At high levels, also acts as vasoconstrictor → ↑ blood volume and ↑ BP **Epinephrine and Norepinephrine** - Cause vasoconstriction in most vessels via α₁-adrenergic receptors - Cause vasodilation in skeletal and cardiac muscle arterioles via β₂-adrenergic receptors → Redistributes blood to muscles during stress or exercise **Atrial Natriuretic Peptide (ANP)** - Released by **atria** in response to stretch (↑ BP/volume) -> Promotes **Na⁺ excretion** → water loss and Causes **vasodilation** → ↓ blood volume and ↓ BP

Answer 24

- **Viscosity** = resistance of fluid to flow; determined by **hematocrit** (RBC concentration) - **Peripheral resistance (PR)** is **directly proportional** to viscosity → ↑ viscosity → ↑ resistance → ↑ BP **Factors that increase viscosity**: 1. ↑ **RBC count** (e.g., polycythemia) - primary driver 2. **Cold temperature** (slows flow, increases aggregation) → ↑ hematocrit → ↑ viscosity → ↑ BP 3. Hydration status 4. Plasma proteins (fibrinogen, albumin) -> minor contributor - **Factors that decrease viscosity**: - **Anemia**, **hemorrhage**, or **increased body temperature** → ↓ hematocrit → ↓ viscosity → ↓ BP

Answer 25

- **Peripheral resistance (PR)** is **directly proportional** to **total vessel length** → ↑ length → ↑ resistance → ↓ flow → ↑ BP (to maintain flow) - **Obesity increases total vessel length**: - ~**200 miles** of new vessels per **1 lb of fat** - ↑ adipose tissue → ↑ number of vessels → ↑ resistance → ↑ BP - Longer vessels increase **friction** against blood flow → heart must generate **higher pressure** to maintain circulation

Answer 26

- **Systolic BP** is **directly proportional** to **arterial blood volume** → ↑ volume → ↑ systolic pressure (due to greater stretch on vessel walls) - **Increased sodium intake** → ↑ blood osmolarity → **Water follows salt** → ↑ blood volume → ↑ BP - **Dehydration or hemorrhage** → ↓ blood volume → ↓ arterial pressure → ↓ systolic BP

Answer 27

- **Inverse relationship** with blood pressure → More compliance = **lower BP**, less compliance = **higher BP** - *High compliance* (young, healthy arteries) → Arteries stretch easily during systole → **dampen pressure surge** - *Low compliance* (aging, arteriosclerosis) → Arteries resist stretch → ↑ systolic pressure → ↑ pulse pressure

Answer 28

shock is defined as a sudden and severe drop in blood pressure that leads to inadequate tissue perfusion and cellular oxygenation -> it’s hypoperfusion tissues don’t get enough oxygen/nutrients 1. **Cardiogenic shock** → Pump failure (e.g., myocardial infarction) 2. **Low venous return (LVR) shock** → ↓ preload not enough blood returning to heart --- **Types of Low Venous Return Shock** 1. **Hypovolemic shock**:↓ blood volume from trauma, dehydration, hemorrhage, orextensive burns (loss of skin barrier → can't retain water) 2. **Obstructed venous return shock**: Tumor or aneurysm compresses a vein → ↓ return to heart 3. **Venous pooling (vascular) shock**: Blood pools in limbs (e.g., long standing or widespread vasodilation) 4. **Neurogenic shock**: loss of **sympathetic tone** → systemic vasodilation 5. **Septic shock**: bacterial toxins → **vasodilation** + ↑ **capillary permeability** 6. **Anaphylactic shock**: severe allergic response → **histamine** release → vasodilation + permeability

Answer 29

- *Definition*: Inadequate cardiac output → insufficient **tissue perfusion** - *Two main categories*: 1. **Cardiogenic shock** → *Pump failure* (e.g., **myocardial infarction**) 2. **Low venous return (LVR) shock** → *↓ preload*, not enough blood returning to heart --- **Types of Low Venous Return Shock** 1. **Hypovolemic shock** - *Cause*: ↓ blood volume from trauma, dehydration, hemorrhage, or **extensive burns** - *Burns*: loss of skin barrier → can't retain water 2. **Obstructed venous return shock** - *Cause*: Tumor or aneurysm compresses a vein → ↓ return to heart 3. **Venous pooling (vascular) shock** - *Cause*: Blood pools in limbs (e.g., long standing or widespread vasodilation) - Subtypes: - **Neurogenic shock**: loss of **sympathetic tone** → systemic vasodilation - **Septic shock**: bacterial toxins → **vasodilation** + ↑ **capillary permeability** - **Anaphylactic shock**: severe allergic response → **histamine** release → vasodilation + permeability

Answer 30

1. **Compensated shock**: Homeostatic mechanisms restore perfusion. E.g., fainting → lying flat lets gravity restore cerebral blood flow 2. **Decompensated shock**: Fails to correct itself → **positive feedback loops**/ ↓ perfusion → Myocardial infarction → ↓ CO → tissue death. - Risk of **Disseminated Intravascular Coagulation**: coagulation due to undiluted fibrinogen/thrombin which results from slow blood flow -

Answer 31

*Blood Changes* - ↓ **Hematocrit** → ↓ **viscosity** - ↑ Risk of **thrombi** and **emboli** formation - **Venous pooling** in legs due to reduced venous return *Heart Changes* - ↓ **Efficiency** and **elasticity** of myocardium - Formation of **scar tissue** - ↑ Risk of **coronary atherosclerosis** → *Note*: **Estrogen** is protective against **LDL**, so risk ↑ post-menopause *Blood Vessel Changes* - ↓ **Elasticity** → stiffer vessels - **Calcium deposits** damage vessel walls → contribute to arterial stiffness

Answer 32

- Growth of **plaque deposits** (lipids, foam cells, calcium) inside **arterial walls** → narrows lumen → ↑ vascular resistance - Triggered by **endothelial injury** (e.g., hypertension, smoking, oxidized LDL) → LDL enters intima → engulfed by macrophages → foam cells accumulate - Plaques create a **positive feedback loop**: narrowed vessels → ↑ BP → more endothelial damage → more plaque - ↓ Perfusion to downstream tissues → ↑ risk of **ischemia**, **infarction**, **stroke** **Risk Factors and Complications** - Risk factors: **diabetes**, **hyperlipidemia**, **hypertension**, **smoking**, **postmenopausal estrogen loss** - Complications: - **Coronary artery disease** → angina, **myocardial infarction** - **Carotid atherosclerosis** → **stroke**, **transient ischemic attacks** - **Peripheral artery disease** → claudication, ulceration - **Renal artery stenosis** → ↓ GFR, activation of RAAS → worsens hypertension - **Aneurysm formation** (especially abdominal aorta) due to weakened vessel wall

Blood Vessels - Class Flashcards

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