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NRS 232 Pathophysiology Final Exam Latest 2024- 2025 Exam 100% Accurate Fall-Spring Term, Exams of Pathophysiology

Oregon State University (OSU)Pathophysiology

A comprehensive review of key concepts in pathophysiology, focusing on the body's stress response, circulatory system, and the development of atherosclerosis. It includes detailed explanations of physiological processes, clinical implications, and potential treatment strategies. The document also features a series of questions and answers that test understanding of the material.

Typology: Exams

2024/2025

Available from 12/16/2024

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NRS 232 Pathophysiology Final Exam Latest 2024-
2025 Exam 100% Accurate Fall-Spring Term
What Does Stress SNS Activation Do?
-Increased epinephrine and norepinephrine
-Increased heart rate and blood pressure
-Increased cortisol release and blood sugar
-Pupils dilate
-Decreased gut motility
-Vasoconstriction to shunt blood to muscles, brain, and heart
-Increased muscle contractility
-Increased stomach acid
-Increased breathing rate
-Bronchodilation (increased airflow)
-Increased blood coagulability
-Dry mouth
-Water retention (edema)
-Increased growth hormone (developmental issues)
Epinephrine and Norepinephrine
-Released from adrenal medulla (inner part of adrenal gland)
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Download NRS 232 Pathophysiology Final Exam Latest 2024- 2025 Exam 100% Accurate Fall-Spring Term and more Exams Pathophysiology in PDF only on Docsity!

NRS 232 Pathophysiology Final Exam Latest 2024-

2025 Exam 100% Accurate Fall-Spring Term

What Does Stress SNS Activation Do?

  • Increased epinephrine and norepinephrine
  • Increased heart rate and blood pressure
  • Increased cortisol release and blood sugar
  • Pupils dilate
  • Decreased gut motility
  • Vasoconstriction to shunt blood to muscles, brain, and heart
  • Increased muscle contractility
  • Increased stomach acid
  • Increased breathing rate
  • Bronchodilation (increased airflow)
  • Increased blood coagulability
  • Dry mouth
  • Water retention (edema)
  • Increased growth hormone (developmental issues) Epinephrine and Norepinephrine
  • Released from adrenal medulla (inner part of adrenal gland)
  • Release is stimulated by SNS activation
  • Limbic system (portions of the brain that regulate emotions) detects fear and signals the hypothalamus to release corticotropin-releasing factor (CRF). CRF triggers the locus coeruleus (located in brainstem) to activate SNS.
  • SNS signals the release of epinephrine and norepinephrine
  • Approximately 80% epinephrine and 20% norepinephrine released from adrenal medulla
  • Increases heart rate and blood pressure, vasoconstriction, respiratory rate, bronchodilation (increased airflow), and other symptoms related to SNS activation Cortisol
  • Limbic system activates hypothalamus to release corticotropin-releasing factor (CRF), which signals the anterior pituitary gland to release adrenocorticotropic hormone (ACTH). ACTH acts on the adrenal cortex to release cortisol. This is regulated by a negative feedback loop (more cortisol disrupts CRF release).
  • Cortisol increases blood sugar, fat, and protein for body use
  • Cortisol suppresses the immune system Reticular Activating System (RAS)
  • Difficulty regulating emotions (labile emotions)
  • Increased epinephrine and norepinephrine leads to hypertension, endothelial cell dysfunction, vasoconstriction, and tachycardia. All of this increases the risk of coronary artery disease, myocardial infarction, kidney disease. and stroke.
  • Constant activation of the reticular activating system (RAS) causes prolonged muscle tension and soreness. Muscle soreness is a stressor as well, so it amplifies the body's stress response How to Treat Patient Stress After Experiencing a Traumatic Event
  • Provide insulin to lower blood sugar and risk of infection
  • Address increased stomach acid by providing a proton pump inhibitor, which will help lower the risk of stomach ulcers
  • Monitor and intervene for constipation, increased blood pressure, and increased heart rate Stretch Reflex
  • Also called myotatic reflex
  • Muscle spindles detect stretch of a muscle, and afferent sensory neurons conduct action potentials to the spinal cord. Afferent neurons synapse with alpha motor neurons at the spinal cord. Alpha motor neurons carry action potentials back to the muscle to cause contraction and to prevent further stretching.
  • The reticular activating system (RAS) also prevents stretch by sending signals to gamma motor neurons. Gamma motor neurons conduct signals from the spinal cord to the muscle fibers and help regulate muscle tension involuntarily. This causes increased contractility of the muscle. What causes you to suddenly become wide awake and oriented when being woken up from an alarm? The reticular activating system (RAS), which is aroused by the limbic system in response to the alarm What are some additional responses to stress?
  • Increased ADH and aldosterone, which can lead to ECV excess and edema
  • Increased growth hormone can interfere with development by causing overgrowth of bones and other issues Can the effects of stress be passed on to offspring? Yes! Chronic stress alters the expression of multiple genes in the HPA axis, and can lead to epigenetic changes (changing how genes are expressed) that are passed onto offspring.
  • More fluids and proteins accumulate in tissues (increased oncotic pressure from increased proteins drives more fluid into interstitial space, and less fluid is brought back into circulation) Virchow's Triad
  • Factors that increase risk of thrombus formation in arteries, veins, and within heart chambers:
  1. Stasis (pooling) of blood
  2. Endothelial injury (this can lead to atherosclerosis)
  3. Hypercoagulability Arteriosclerosis versus Atherosclerosis
  • Arteriosclerosis is hardening of the arteries that can occur through many different physiological processes
  • Atherosclerosis is a specific pathophysiological process involving large and medium- sized arteries. It leads to obstructed arterial flow, which can cause ischemia and eventual necrosis. Normal Endothelial Function
  • Lines arteries and secretes nitric oxide (NO)
  • NO acts as a vasodilator to relax smooth muscles. NO also calms White Blood Cells and makes them "less sticky" and inhibits platelet aggregation/secretion Endothelial Dysfunction
  • Endothelial dysfunction is a key contributor to atherosclerosis, which is a high risk factor for heart attack and stroke.
  • Endothelial damage may be caused by chronic conditions such as hypertension and diabetes. Exercise is a protective factor against endothelial damage since it increases nitric oxide (NO) production of endothelial cells over time.
  • When damaged, endothelial cells produce less NO, which causes:
  1. Decreased dilation of blood vessel...decreased space for blood to flow. 2.Increased stickiness of endothelium...endothelium becomes more permeable to LDL cholesterol, which moves from the arterial space into the tunica intima. The endothelium also allows more White Blood Cells to adhere and transmigrate from blood into the tunica intima.
  2. LDL is engulfed by resident macrophages within the tunica intima, which signal an alarm by sending cytokines and other proinflammatory mediators. These mediators cause upregulation of selectin and integrin on the endothelium, which captures monocytes in the blood and causes them to roll, adhere, and transmigrate into the tunica intima.
  3. Monocytes become macrophages within the tunica intima and engulf more LDL. As they engulf more LDL, they become foam cells and form fatty streaks.
  • Layers of blood vessels from inner (exposed to blood) to outer:
  1. Endothelium
  2. Tunica intima
  3. Tunica media
  4. Tunica externa Chronic Arterial Insufficiency
  • Intermittent claudication; Pain while walking that resides when resting
  • Ischemia (lack of blood flow) which causes decreased/absent pulses, cool skin, pale skin, and muscle atrophy
  • No edema
  • Skin appears shiny and hairless
  • Thick nails
  • Ulcers and gangrene development Chronic Venous Insufficiency
  • Often painful, even at rest
  • Swelling and edema due to increased venous congestion and hydrostatic pressure of veins
  • Brown pigmentation of skin
  • Pulses present and normal
  • Normal temperature of skin Chronic Ischemia Vs. Acute Ischemia in Legs
  • Chronic arterial insufficiency happens over time and can be accompanied by intermittent claudication (pain while walking). Other symptoms include muscle atrophy, pale/shiny/cool skin, thick nails, lack of hair growth, and reduced pulses
  • Acute arterial occlusion occurs suddenly and can be followed by sudden acute pain. Other symptoms include pale/cool skin, no pulse, muscle weakness, and paresthesia (tingling/numbing sensation). Atrophy does not occur at this stage since that is a chronic sign of ischemia. Superficial Vs. Deep Vein Thrombosis (DVT)
  • Superficial vein thrombosis may occur in varicose veins or other superficial veins. Symptoms include visible redness along the vein, heat, tenderness, and aching
  • It is important to remember that artery narrowing can be clinically silent for years, so it is important to address modifiable behaviors as soon as possible! What can cause hypercoagulability?
  • Exogenous hormones (e.g., estrogen)
  • Polycythemia (too many RBCs in blood)
  • Pregnancy Consequences of ischemia
  • Acute ischemia can be reversed if intervention given in time, but chronic thrombus formation can lead to irreversible cell death and necrosis
  • Over time, the body will attempt to compensate for chronic ischemia by forming new blood vessels What is the risk if a thrombus forms in the venous system?
  • Thrombus can break off and become an embolus that travels to the lungs, which causes a pulmonary embolism (e.g., DVT from leg)
  • Pulmonary embolism is life-threatening!
  • Venous obstruction can also cause edema and pain due to increased hydrostatic pressure What are the risks if a thrombus forms in the arteries?
  • Myocardial infarction
  • Stroke
  • Peripheral arterial disease (PAD)
  • Organ damage (kidneys, eyes, etc.) What can possible be happening if a patient reports pain when walking and cold feet?
  • Arterial occlusion is likely since the patient reports intermittent claudication (pain that resides when resting) and cold feet What can cause stasis of blood?
  • Atrial fibrillation
  • Immobility
  • Most common in arteries within cerebral circulation and the thoracic/abdominal aorta
  • Causes pressure on adjacent structures possible leading to pain, hoarseness (due to pressure on laryngeal nerve), and venous congestion
  • Usually asymptomatic in the abdomen, and found mostly by chance imaging
  • May cause stasis of blood and thrombus/embolus formation.
  • Aneurysms can potentially rupture, leading to sharp pain and shock due to sudden lack of blood flow to the area...medical emergency! Systemic Vascular Resistance
  • Force exerted by vessels
  • How hard blood vessels need to squeeze down to counteract blood pressure
  • Determined by radius of arteries (arteries with atherosclerosis have greater systemic vascular resistance) Mean Arterial Pressure (MAP)
  • Average pressure in arterial system during one cardiac cycle
  • If MAP is greater than 70, you can assume that there is adequate perfusion to all tissues and organs
  • If MAP is less than 70, there is inadequate perfusion and risk of circulatory shock (cellular hypoxia, anaerobic metabolism, reversible cell swelling, and cell death)
  • At rest, MAP=2/3(DP)+1/3(SP)
  • Tachycardia, MAP=(DP+SP)1/ Orthostatic Hypotension
  • Normally, there is a slight decrease in systolic blood pressure and increase in heart rate when standing up from a supine position
  • During orthostatic hypotension, there is a significant change of systolic blood pressure (decreases by more than 20mmHg) within 3 minutes of standing
  • Can be caused by dehydration (ECV deficit), increased age, autonomic neuropathy (caused by diabetes), and some medications
  • Places individuals at greater risk of falls since individuals may become dizzy when standing Hypertension

Circulatory Shock

  • Can be caused by hypovolemia, heart pump failure, vasodilation of vessels, and any factors that decrease cardiac output
  • Decreased cardiac output leads to cellular hypoxia, sodium/potassium pump failure, reversible cell swelling, and eventual cell death
  • Circulatory shock promotes anaerobic metabolism, which creates lactic acid buildup that can be measured by labs
  • With sepsis (systemic inflammatory response system plus infection), capillaries become leaky. This causes loss of fluid from vessels, which can lead to septic shock
  • Clinical manifestations include tachycardia, hypotension (this indicates severe shock since compensatory mechanisms have failed), decreased urine output (blood is being shunted mainly to heart and brain and not to kidneys or GI system), nausea, increased respiratory rate due to increased acid buildup, and cool/clammy skin due to SNS activation Septic Shock
  • Sepsis=SIRS (systemic inflammatory response syndrome plus infection)
  • In sepsis, capillaries become leaky and fluid is lost. This leads to septic shock
  • Clinical signs include increased heart rate and respiratory rate, hypotension, cool/clammy skin, nausea, and decreased urine output Compensatory Mechanisms to Restore Blood Pressure
  • RAAS activation to retain fluid and activate SNS. This causes increased preload (increases cardiac output) and vasoconstriction (increases systemic vascular resistance). Overall, RAAS increases blood pressure
  • Baroreceptors in the aortic arch and carotid arteries detect pressure change and activate SNS. This stimulates release or epinephrine and norepinephrine from the adrenal medullar, which causes increased heart rate and contractility of the heart. This causes increased cardiac output and blood pressure Complications of Shock
  • Oliguria (decreased urine output)
  • Acute respiratory distress syndrome (ARDS)
  • Edema and hypotension (edema due to leaky capillaries from sepsis or anaphylaxis)
  • Multiple organ failure
  • Decreased level of consciousness