Exam2 - Movement/Support + Perfusion

Question 1

Dorsal to ventral, what is the order of the spinal cord coverings?

Answer 1

Dura mater
Arachnoid mater
Pia mater

Question 2

How does spinal anaesthesia differ from epidural anaesthesia? How are they similar?

Answer 2

They are both analgesics (pain relief) and anaesthetics (numbing).

Epidural location is the fatty epidural space between dura and dorsal vertebrae. A catheter is threaded and it’s hooked up to a continuous drip.
Epidurals medicate afferent nerves. They do not enter the spinal fluid.

The spinal anaesthetic location is in the subarachnoid space. It is an injection (no drip) and wears off in two hours. It enters the space with spinal fluid.

Question 3

Which nerves are afferent and which are efferent? (Dorsal vs ventral)

Answer 3

Dorsal nerves are afferent (sensory relay to brain)

Ventral nerves are efferent (motor relay to body)

Question 4

What does RANK-L do? Who releases it? What initiates its release?

Answer 4

Rank ligand. Activates bone resorption by attaching to RANKL receptors on osteoclasts.

Released by osteoblasts.

When blood calcium levels decrease, parathyroid gland releases PTH, which tells the osteoblasts to release RANKL.

Question 5

What is OPG and what does it do? Who releases it? What initiates its release?

Answer 5

Osteoprotegrin.

It supports bone formation by attaching to RANKL so it can’t attach to osteoclasts. Prevents osteoclasts from resorbing and allows osteoblasts to build bone.

Released by osteoblasts.

Its release is initiated by testosterone, estrogen, and weight-bearing exercise.

Question 6

What effects do low blood calcium levels have on osteoblasts and/or osteoclasts?

Answer 6

Parathyroid gland releases PTH in response to low Ca++ levels.

PTH stimulates RANKL release by osteoclasts.

Osteoclasts resorption releases Ca++ into bloodstream.
(PTH release slows when Ca++ levels rise).

Question 7

What effect do high blood calcium levels have on osteoblasts and/or osteoclasts?

Answer 7

With high blood Ca++ levels, the thyroid releases Calcitonin, which tells osteoclasts to stop resorption activity.

(PTH release will also slow).

Question 8

What is RANK?

Answer 8

RANK is the receptor for RANKL (found on osteoclasts)

Question 9

What are the risk factors for osteoporosis?

Answer 9

**Post-menopause (low estrogen=low OPG release)
Insufficient dietary Ca++ before age 30
Poor Ca++ absorption
Vitamin D deficiency
Excess caffeine/nicotine/alcohol
Inadequate weight-bearing exercise
Endocrine disorders (like excess PTH)

Question 10

Where is osteoporosis most likely to occur?

Answer 10

In porous parts of bone, like the femoral neck of the trochanter, the wrist, and the thoracic and lumbar spine.

Question 11

What are the three types of fractures we talked about and any risks associated with them?

Answer 11

Closed fracture
Open fracture (broken skin = increased risk for infection)
Pathologic fracture

(Note: if any of the above are breaks fo the femur, there is a high risk for blood loss leading to hypovolemic shock).

Question 12

What is compartment syndrome and why does it happen?

Answer 12

Inflammatory response can lead to fluid increase/swelling, that puts pressure on arteries, veins, nerves, muscle in the compartment.

It can happen if a hard cast is put on a broken limb too soon, or inside the abdomen (unrelated to casting).

Question 13

What signs and symptoms are associated with compartment syndrome?

Answer 13

Swelling, skin color change (pallor), signs of occluded blood supply on other end of cast:

• decreased SpO2
• decreased cap refill
• decreased pulse strength
• decreased sensation (due to hypoxic cell injury)

Monitor circulation, motion and sensation.

Question 14

What are the types of spinal cord injuries we talked about that can lead to spinal shock? Are they primary or secondary neurologic injuries?

Answer 14

Concussion: (violent shaking of brain tissue or spinal cord tissue up against bone. From force of acceleration, deceleration, or rotation).

Contusion: (bruising of neural tissue)

These are all primary neurologic injuries.

Laceration: (tearing of neural tissue)

Question 15

What is transection and why isn’t it associated with spinal shock?

Answer 15

Transection is a complete severing of the spinal cord. There will be total and irreversible loss of function below the level of the cord injury.

(Spinal shock is temporary)

Question 16

What is a secondary neurologic injury?

Answer 16

When spinal blood flow is obstructed due to an inflammatory response. The obstruction leads to ischemia and necrosis of neural tissue.

Question 17

What is spinal shock and why does it happen? Is it a primary or a secondary neurologic injury?

Answer 17

A temporary loss of function due to swelling around the nerves in the spinal cord. (Despite the word “shock,” has nothing to do with vascular supply).

Mast cells detect concussion/contusion/laceration and begin the inflammatory process.

Spinal shock is a secondary neurologic injury - it is due to swelling.

Question 18

What are dermatomes and what are some ways we use them?

Answer 18

Dermatomes mapped out sections of the body that correlate with spinal nerves.

We use them to test for sensation at different levels:

• C3/C4 on side of neck
• T6 at nipple line: critical level for neurogenic shock/failure of vital processes. Monitor for patients with an indwelling epidural cath. If loss of sensation rises to T8/T7, get a BVM an a provider.

Shingles: location of skin blisters tells you where in the nerve fibers varicella is acting up. Provider can give cortisone shots along the nerve route to treat.

Question 19

What is the most common cause of lower back pain?

Answer 19

Acute lumbar disc herniation due to poor body mechanics.

Herniation in towards the spinal cord puts pressure on the capillary beds there.

Local ischemia d/t occluded blood flow. Mast cells detect and send out chemotactic factors to initiate inflammatory response.

(Slide says most low back pain is idiopathic).

Question 20

What is degenerative joint disease?

Answer 20

Also called osteoarthritis. It occurs in load-bearing synovial joints. Excess wear and tear leads to degradation of cartilage. Bone rubs on bone, leading to inflammation. Sometimes associated with crepitus (crunching sound from bone fragments in joint)

Biggest risk factor is a BMI greater than 30.
Age also increases risk d/t decreased cartilage
Also, joint stress/trauma
genetic & environmental factors

Question 21

What is Rheumatoid Arthritis?

Answer 21

Autoimmune condition where your adaptive immune system attacks the synovial membrane, thinking its antigens are foreign invaders.

Chronic inflammatory process in joints leads to fibrotic scarring. Synovial membranes experience hyperplasia, developing nodules called “pannus” that are most visible on surface joints. Limit movement.

Question 22

Describe the immune process behind rheumatoid arthritis

Answer 22

Rheumatoid factor attaches to the synovial membrane cells, initiating the inflammatory response.

Neutrophils and Macrophages start to phagocytize damaged tissue.

Macrophages present the antigen to CD4 cells

CD4 cells connect with naive B cells and initiate their differentiation into plasma & memory B cells.

Lots of antibodies produced against synovial cells.

(A positive test for rheumatoid arthritis will reveal elevated levels of rheumatoid factor).

Question 23

What is the primary symptom of Gout? What causes it?

Answer 23

Red swelling, pain, and eventually a hard nodule called a “tophi” in the big toe.

Caused by uric acid crystals that form in the synovial fluid and slightly lower temps of the toe.

-Uric acid can accumulate because of hyperuricemia (elevated blood uric acid levels). Decreased kidney function, high purine diets, conditions with rapid cell turnover and repair (like burns) can increase risk.

Question 24

What gives cartilage its cushioning characteristics and why doesn’t it heal? What happens instead?

Answer 24

Cartilage attracts water, which helps to cushion loads.

• chondrocytes don’t proliferate
• don’t receive nutrients through a blood supply, but rather through diffusion.

Cartilage is prone to calcification:

• calcified cartilage can’t properly diffuse nutrients
• this leads to swelling and death of chondrocytes
• eventually, bone will replace cartilage.

Question 25

What can you do to promote bone repair/growth?

Answer 25

Change your diet: - extra Ca++ - extra protein - vitamin D - antioxidants to combat any inflammatory ROSs from damage. Avoid: nicotine, excess caffeine, alcohol Add weight-bearing exercise to increase OPG release.

Question 26

What is a soft callus?

Answer 26

Forms when bone has been damaged and is in the process of regrowing (osteoblasts). Includes new blood vessels and collagen (thanks to macrophages). Weight-bearing in the first 2-3 weeks of bone repair can cause deformities. (The soft callus will become harder, but the bone won’t fully heal for about 4 months)

Question 27

What leads to scoliosis and why do people have surgery to correct it?

Answer 27

It’s due to genetic factors and occurs during rapid growth in adolescence. Surgery consists of the severing of all muscles, placing in traction, total spinal fusion, titanium rods and screws. Corrective surgery is because the curvature in the spine can put pressure on the lung tissue leading to shortness of breath, and pressure on the heart, leading to low cardiac output.

Question 28

What happens to sensory input once it arrives at the brain?

Answer 28

- Motor cortex (in cerebrum) interprets & determines response - Sends message to thalamus - Thalamus (sensory relay center) interprets both incoming and outgoing messages

Question 29

What do we need to know about the basal ganglia?

Answer 29

Cluster of cells in and around the thalamus that release dopamine. (Dopamine inhibits excess movement and smooths out good movements). These are the cells that atrophy in Parkinson’s, decreasing dopamine and resulting in a resting tremor and other movement control issues.

Question 30

What do we need to know about the cerebellum?

Answer 30

Home of the Reticular Activating System (RAS) - a cluster of nerve cells that helps regulate movement.

Question 31

Problems in which areas of the brain can lead to coordination and movement issues? What sort of problem might cause that?

Answer 31

Motor cortex (cerebellum) Thalamus Basal ganglia Cerebellum Hemorrhagic stroke is one of the problems that can damage these areas.

Question 32

What are some motor dysfunctions related to tone?

Answer 32

Hypertonia: too much muscle tone - leads to stiff, difficult to move muscles. (Can result from blocked efferent messages - muscles tighten due to disuse) Hypotonia: Low muscle tone, many times with reduced strength.

Question 33

How does muscle tone differ from strength?

Answer 33

Tone is observable in activities like sitting, turning, general ADLs. Strength relates to the ability to push, pull, lift, etc.

Question 34

What type of motor dysfunction is related to strength?

Answer 34

Paresis: muscle weakness but normal tone Plegia: paralysis

Question 35

What type of motor dysfunction is related to movement?

Answer 35

Hyperkinesia: increased muscular activity, resulting in excessive abnormal movements (like tremors in Parkinson’s) Hypokinesia: Abnormally decreased muscle movement (slow gait in Parkinson’s, or difficulty in initiating movement).

Question 36

What is the most common cause of hypotonia in infants?

Answer 36

Lack of oxygen to the brain in the birth process leads to hypoxic cell injury to the brain. Creates motor cortex problems (no motor output).

Question 37

What is disuse syndrome and how does it relate to limited mobility?

Answer 37

Inability to move around leads to a deterioration of body function/systems.

Question 38

What does nitric oxide do? What medication do we give for MIs that mimics its effects.

Answer 38

Nitric Oxide (NO) causes arteries to dilate, improving blood flow. We give Nitroglycerin during MIs because it has the same effect.

Question 39

What do free radicals have to do with NO (nitric oxide) production? How do we combat their effects?

Answer 39

The enzyme that produces NO gets highjacked by free radicals and changes it so it produces MORE free radicals. Due to free radical damage, arteries will stiffen and become dysfunctional - they won’t relax when they should. Large quantities of fruits and vegetables in our diet will use up the free radicals so they can’t hijack this enzyme.

Question 40

How do Aortic & Carotid Baroreceptors participate in heart rate regulation. What is the response?

Answer 40

Stretch receptors that detect a pressure change in the arteries (based on the amount of stretch). Send signals via connected nerves to the medulla oblongata. Cardiac Control Center in oblongata has a “set point” for blood pressure. It interprets message and sends signals along efferent nerve to bring it back to set point. If BP is too high, efferent vagus nerve (PNS fibers) to SA node, releases ACH and inhibits/slows heart rate. (Notes also say systemic dilation of arterioles and veins). If BP is too low, efferent cardiac nerve (SNS fibers) - releases Norepinephrine and increases heart rate.

Question 41

A patient has broken his wrist. Which cells will the mast cells summon during degranulation?

Answer 41

Phagocytes: neutrophils and monocytes/macrophages.

Question 42

Your patient with the broken wrist has mast cells that will synthesize platelet-activating-factor. How is this going to help repair his bone?

Answer 42

It signals the liver to release clotting factors - both fibrinogen and platelets are activated for response.

Question 43

Which WBC promotes angiogenesis?

Answer 43

Macrophages

Question 44

What are 3 ways that macrophages help to repair broken bone?

Answer 44

1. Clean up debris at site (phagocytosis). Stay a while because it can replicate. 2. Grow a new blood supply so area can heal. 3. Release cytokines - promote collagen and callus growth.

Question 45

A fibrin mesh is being laid down at a broken bone injury site. How did the clotting cascade get started?

Answer 45

Mast cells synthesized platelet activating factor. This signaled the liver to release clotting factors and fibrinogen.

Question 46

What should you tell your broken-bone patient about diet and activity?

Answer 46

1. DO eat calcium, vitamin D and protein. 2. Avoid OPG inhibitors like caffeine, alcohol and nicotine. 3. Avoid weight bearing exercise during soft-callus formation.

Question 47

What scenarios are going to create excess preload?

Answer 47

Hypervolemia Valve regurgitation Ventricular hypertrophy Na+/H2O Retention in cases of excess aldosterone

Question 48

Which scenarios will cause increased afterload?

Answer 48

Hypertension (systemic vascular resistance) Aortic rigidity Aortic valve stenosis (narrowing of aorta)

Question 49

What condition (preload or afterload) will ventricular hypertrophy increase?

Answer 49

Increased preload

Question 50

What condition - preload or afterload - would excess aldosterone production increase?

Answer 50

Preload | Excess aldosterone leads to excess water retention, which would lead to hypervolemia

Question 51

Valve regurgitation is going to increase what - preload or afterload?

Answer 51

Preload

Question 52

A patient is presenting with shortness of breath (especially when lying down), crackles in lungs, dependent edema and JVD. What are these symptoms of?

Answer 52

Increased preload.

Question 53

What is the main physiological change that will occur with chronic increased afterload?.

Answer 53

L. Ventricular hypertrophy.

Question 54

What can a patient do for himself to decrease preload?

Answer 54

Decrease sodium in diet (decrease fluid volume) Daily weights Fluid restrictions

Question 55

What can a patient do to help decrease his afterload?

Answer 55

Reduce stress Support thermoregulation (assuming this is for adequate warmth) to promote vasodilation Work on fluid balance.

Question 56

Will elevated PTH decrease or increase OPG levels?

Answer 56

It will decrease OPG production.

Question 57

Will elevated TNF (tumor necrosis factor) increase or decrease RANKL levels?

Answer 57

TNF increase will increase RANKL levels.

Question 58

What effect does estrogen have on RANKL production?

Answer 58

RANKL isn’t produced as much when estrogen levels rise. (Additionally, OPG is produced more).

Question 59

What does TNF (tumor necrosis factor) have to do with osteoporosis?

Answer 59

An increase in osteoclasts activity activates cytokines which actually leads to inflammatory responses. TNF is activated in the process. TNF will further enhance osteoclasts activity. (If this is happening while OPG levels are decreasing/decreased, you have an imbalance of homeostasis and you will get more bone loss.)

Question 60

Which bones are at highest risk for fracture secondary to osteoporosis (ie, pathological fracture)?

Answer 60

Wrist Vertebrae Trochanter of hip

Question 61

Is aldosterone fat-soluble or water-soluble?

Answer 61

Fat-soluble. (-osterone)

Question 62

Is ADH fat-soluble or water soluble?

Answer 62

Water-soluble

Question 63

What organ does aldosterone come from, and what activates its release?

Answer 63

Adrenal gland. Activated by Angio II.

Question 64

What organ does ADH come from

Answer 64

Posterior pituitary gland - activated by 3 different things: 1. Angio II tells the posterior pituitary to release. 2. SNS response (fight or flight response) 3. Dehydration (sensed by hypothalamus, tells the post-pit to release)

Question 65

What response does Aldosterone produce in its target cells?

Answer 65

-Causes cells in nephron to retain sodium (from urine filtrate) and excrete potassium. (This causes water to follow sodium, retaining water.

Question 66

What response does ADH create in its target cells?

Answer 66

It causes endothelial cells in periphery to vasoconstrict It causes cells in nephron to reabsorb water (opens aquaporins) to it can go back to bloodstream.

Question 67

What is the overall effect of aldosterone on the body?

Answer 67

Sodium retention —> water retention Potassium excretion INCREASED VASCULAR VOLUME, which should raise BP.

Question 68

What is the overall effect of ADH on the body.

Answer 68

Vasoconstriction increases BP | Water retention increases BP (due to increased volume)

Question 69

What type of patient situation would cause the body to release aldosterone?

Answer 69

Drop in BP - sensed at the kidneys as a decrease in renal perfusion.

Question 70

What causes the body to release ADH

Answer 70

Dehydration and/or low perfusion pressure around the hypothalamus. Stimulation of the SNS Drop in BP at the kidneys.

Question 71

What is the job of the RAAS? What are its two triggers?

Answer 71

Jobs: - regulate fluid balance - regulate arterial blood pressure. Triggers: - increase in SNS activity - Decrease in blood pressure (specifically MAP) at the JGA cells - presents to kidney as a decrease in renal perfusion.

Question 72

How does Renin become Angio II?

Answer 72

Renin + Angiotensin (Liver) = Angio 1 + A.C.E (lungs) = Angio II.

Question 73

What four things does Angio II stimulate?

Answer 73

Endothelial cells (AT2 receptors): Vasoconstrict Posterior Pituitary: Release ADH Kidneys: Resorb sodium and potassium Adrenals: release aldosterone.

Question 74

How does Angio II’s effects on the kidneys differ from Aldosterone’s effects on the kidneys.

Answer 74

It doesn’t. Both tell the kidneys to resorb water and release potassium.

Question 75

How does Angio II’s effects on the kidney differ from ADH’s effects on the kidney?

Answer 75

Angio II makes kidney cells resorb sodium and release potassium. ADH makes kidney cells open aquaporins and absorb water.

Question 76

What is the normal MAP range? How do you calculate it?

Answer 76

Normal: 65-110 Calculate it by: (Systolic-Diastolic)/3= pulse pressure. THEN, pulse pressure + diastolic = MAP.

Question 77

What is the definition of preload? Where does it come from?

Answer 77

The load on the heart before a contraction begins Comes from the combined volume of: - the ejection fraction (amt of blood remaining in ventricles at diastole/relaxation) - the amt of blood entering ventricles (vena cava for R. Ventricle and Pulmonary vein for L. Ventricle)

Question 78

What effect is excess preload going to have on the entering blood vessels? R. Ventricle? L. Ventricle?

Answer 78

It will cause overflow. R. Ventricle: into the vena cava leads to JVD and edema in peripheral tissues (especially the ankles and sacrum). L. Ventricle: into the lungs via the pulmonary vein. Leads to fluid in the lungs (crackling) and cough + difficulty breathing while lying down.

Question 79

What is afterload? What is it determined by?

Answer 79

The amount of force the ventricles need to exert to move blood into the aorta and into the lungs. Determined by the amount of resistance in the arteries and/or the lungs.

Question 80

What are two potential causes of increased afterload to the Right Ventricle? (One acute, one chronic?). What is the resulting damage/effect?

Answer 80

- Pulmonary embolism (acute): Blood clot in the lungs. (Probably originating from DVT). Damage to the R. Ventricle, which keeps pumping, trying to overcome pressure. - Lung Tumor or COPD (chronic): Chronic increased afterload (Resistance) to the right ventricle results in a hypertrophy of right ventricular muscles, which leads to a decreased intraventricular radius and decreased preload.

Question 81

What is a cause of increased afterload to the L. Ventricle? What is the effect?

Answer 81

Atherosclerosis: plaque buildup in blood vessels will create resistance as the L. Ventricle tries to pump throughout the body. L. Ventricular hypertrophy, decreased interior size, decreased cardiac output.

Question 82

What pressures are involved in perfusion homeostasis?

Answer 82

Hydrostatic pressure: Pushing pressure from the systolic - force fluid generates while pushing against the capillary wall. Oncotic pressure: Pulling pressure on the venous end from serum albumin. Retrieves fluid from the tissues in the capillary bed.

Question 83

What cellular problems might come about from insufficient systolic pressure (decreased CO)? What are the signs/symptoms?

Answer 83

Insufficient pressure means: - decreased nutrients to tissues (O2 and glucose) - decreased ATP production (pump failure) - sodium accumulation in cell and hydropic swelling - cell lysis/hypoxic cell injury - acidosis. #1 sign: change in mental status due to metabolic acidosis - cardiac dysrhythmias (d/t hyperkalemia?) - increased respiratory rate (d/t acidosis) - increased temp (d/t inflammatory response?)

Question 84

What can cause a decrease in oncotic pressure? What happens if it’s local? Systemic?

Answer 84

Can be caused by: -Histamine release as part of the inflammatory process (antigen presence). This releases albumin from the vascular space into the tissues: not enough pull back into the bloodstream. If localized - yay! Fibrinogen/clotting platelets will block off area. If systemic - Decrease in blood volume = SHOCK (septic shock or anaphylactic shock).

Question 85

What is the definition of Shock? (Anything but spinal shock, that is).

Answer 85

Circulatory system fails to meet the perfusion demands of cells, tissues and organs. In other words, severe HYPOPERFUSION. Causes cellular hypoxia.

Question 86

Why would shock cause a vicious cycle of “worsening” shock?

Answer 86

Hypoperfusion leads to cellular injury. Inflammatory response. Vasodilation and endothelial cell retraction. Decreases oncotic pressure to draw blood back in to vascular system. Further decreases BP/volume/perfusion Further decreases ATP production, cellular injury. Acidosis.

Question 87

What are the body’s compensatory responses to shock?

Answer 87

SNS: - Increase in heart rate (cardiac center responds to decreased baroreceptor stretch in SA node) - Constriction of blood vessels (epinephrine and norepinephrine) to increase venous return for vital organs. Renin Release (with purpose of increasing blood volume, and therefore Blood pressure - measureable by urine output).

Question 88

Are body’s compensatory measures to shock long-lasting? What effects will they have?

Answer 88

No. Eventually they will decrease tissue perfusion and O2 supply. Ultimately, you’ll have cell injury (ATP pump failure, hydropic swelling and lysis, free radical formation). This creates systemic acidosis, hyperkalemia, and widespread inflammatory response. Multiple organ failure can result.

Question 89

What do you suspect for a patient exhibiting a change in level of consciousness.

Answer 89

Suspect shock (resulting acidosis changes LOC). Elevate legs, turn head to side, put blanket on them. (Legs up assists with blood to vital organs) (Blanket assists with hemoglobin release of O2.)

Question 90

Why do we NOT do Trendelenburg for shock victims?

Answer 90

It increases vascular pressure at the heart, stimulating a PNS response (via CNX10) to release ACH, which will tell SA node to further decrease heart rate.

Question 91

Why are catecholamines, growth hormone and cortisol released when the body is in hypoperfusion? What is the ultimate effect?

Answer 91

They’re a result of SNS stimulation - they increase heart rate, increase vasoconstriction and strengthen contractility to compensate. But, they decrease glucose uptake by the cells. This leads to gluconeogenesis, glycogenolysis and lipolysis. These process not only require energy, but the result in lactic acid buildup, which contributes to acidosis.

Question 92

How does acidosis affect Hemoglobin?

Answer 92

The lower the pH, the more tightly the O2 will bind to the Hb molecule (The less likely it is to release it for cells).

Question 93

What is cardiogenic shock? What is the primary cause?

Answer 93

- Heart muscle can’t output enough blood to supply tissues. - #1 cause: myocardial infarction (blocked coronary artery, usually due to atherosclerosis). The blocked artery will prevent delivery of O2/glucose to a portion of the heart and damage/kill heart muscle. Damaged muscle means decreased inotropic function (strength of contractions). Decreased inotropic function means decreased stroke volume (30-40ml). Blood accumulates as end systolic volume, increases PRELOAD.

Question 94

What is a normal stroke volume?

Answer 94

60-80 mL

Question 95

How will cardiogenic shock present?

Answer 95

JVD distention and pulmonary edema from preload backup. - Pain in chest, radiates down arm. - Decrease in MAP - Decrease in systolic pressure w/ normal diastolic - Decrease in urine output (compensatory) - Change in LOC

Question 96

What is obstructive shock? What is the primary cause?

Answer 96

Something blocks the flow of blood - most commonly in lungs, where it reduces the return of oxygenated blood to the left ventricle. Not enough blood in left ventricle means not enough blood to pump to body. Right ventricle continues to pump despite resistance - gets a backup of blood. #1 cause - pulmonary embolism (Clot from DVT travels to lungs and occludes arteriole and nutrient supply to lung tissue.

Question 97

How does obstructive shock d/t pulmonary embolism present?

Answer 97

Sudden onset chest pain Gasping for air Hemoptisis (coughing up blood)

Question 98

What is hypovolemic shock? What things are most likely to cause it?

Answer 98

Severe hypoperfusion due to loss of blood/fluid (15% or 900+mL). Most likely from hemorrhage or excessive dehydration.

Question 99

How does the body compensate for hypovolemic shock?

Answer 99

Activates the RAAS.

Question 100

What will hypovolemic shock present as?

Answer 100

Decreased MAP & BP Increase in HR Cool, clammy skin (due to vasoconstriction) Decreased urine output (due to RAAS activation) Change in level of consciousness (often beginning as apprehension, agitation, and restlessness, then later decreased arousal, then loss of consciousness). (Due to acidosis).

Question 101

What is neurogenic shock? What causes it?

Answer 101

A loss in blood vessel tone due to overstimulation of PNS or understimulation of SNS (Blood will pool in extremities - no venous return).

Question 102

What are the cardinal signs of neurogenic shock?

Answer 102

bradycardia | Warm, dry skin

Question 103

What is anaphylactic shock? What causes it?

Answer 103

Widespread vasodilation and endothelial cell retraction causes loss of vascular volume into interstitial spaces. Due to an immune-mediated allergic response (systemic mast cell degranulation releases histamine everywhere).

Question 104

What are the signs of anaphylactic shock? How do you treat it?

Answer 104

- Laryngeal edema (swelling of the airway) leads to bronchospasm: difficulty breathing. - circulatory collapse - Decrease in BP - weak, thready pulse Can start as: - abdominal cramps - apprehension - warm, burning skin - itching, hives - respiratory distress (coughing, wheezing, choking) Tx: epinephrine causes systemic vasoconstriction and bronchiole relaxation.

Question 105

What is septic shock? What causes it?

Answer 105

Loss of blood volume to interstitial spaces due to systemic immune response (mast cell degranulation & histamine release) to a severe infection (often in the bloodstream). Commonly, e.coli or other bacterial endotoxins cause it. An indwelling catheter (esp in women) can frequently cause it.

Question 106

How will septic shock present? How can you test for it? How can you prevent it?

Answer 106

Presents as: Hypotension Warm, flushed skin Prevention: Catheter care - meatus and away from it, cleaning colonization of bacteria from tube. Test: Serum Lactate, CRP (opsonins), Procalcitonin (bacteria)

Question 107

What are atrial stretch receptors for?

Answer 107

Sense stretch due to increased venous return (increased atrial preload). They send message to brain to DECREASE pituitary production of ADH (don’t retain any more water) And they release their own ANP (atrial naturatic peptide) that causes the kidneys to excrete sodium, making you excrete more water, too.

Question 108

What are the two main reasons for DVT (deep vein thrombosis). How can you help prevent it?

Answer 108

Decreased mobility (blood pooling in legs, decreased venous return) Increased hematocrit (blood is too viscous to return). (Norm values 35-50%). ROM exercises for immobile patients.

Question 109

What is the difference between primary hypertension and secondary hypertension?

Answer 109

Primary: genetic cause (90-95% of HTN). Cells don’t make enough NO, which usually causes vasodilation. Secondary: due to a disease - renal disease - adrenal gland tumors (increased epinephrine, norepinephrine, and cortisol -which acts like glucose) - diabetes (AGES - glucose molecules permanently bind to proteins so endothelial cells can’t make NO).

Question 110

What is isolated systolic hypertension

Answer 110

High Systolic, normal diastolic, high pulse pressure. Due to age: worn-out endothelial cells (especially in aortic arch) don’t produce enough nitric oxide. Resistance in aortic arch gets transferred throughout entire cardiovascular system.

Question 111

What is an aneurysm

Answer 111

Weakness in an artery due to too much hydrostatic pressure over time. Rupture of an aneurysm —> hemorrhagic stroke.

Question 112

What is raynaud’s

Answer 112

Vasoconstriction in periphery | Brought on by cold, stress

Question 113

What is thrombocytopenia

Answer 113

Platelet deficiency - less than 100k. Leads to an increased bleeding risk. If count is less than 20k, spontaneous bleeding will result - you’ll need a platelet transfusion. Caused by bone marrow dysfunction, cancer (or treatments), anticoagulants.

Question 114

What do our notes say about platelet dysfunction?

Answer 114

Platelets lose the ability to aggregate properly. Can be due to medications (antibiotics, NSAIDS, antihypertensives) NSAIDS will interrupt the production of arachidonic acid to prostaglandin.

Question 115

What does ‘coagulation dysfunction’ refer to?

Answer 115

Body has enough platelets, but something is preventing them from clotting or promotes abnormally increased clotting. Hemophilia (congenital): carried on the Y chromosome. Liver doesn’t produce clotting factors 8 and 12. Acquired: Liver disease or vitamin K deficiency. DIC (disseminated intravascular coagulopathy): -triggered by SEPTIC SHOCK Widespread activation of mast cells - permeability - all platelets get used up! Causes spontaneous bleeding at eyes, nose, movement of joints.

Question 116

What is ACTH and when does our body make it?

Answer 116

Adrenocortotropic hormone: part of the SNS response. Tells the adrenals to release epinephrine and norepinephrine.

Question 117

What does epinephrine do? Norepinephrine?

Answer 117

Epinephrine: increases Heart rate (chronotropic) and strength of contractions (inotropic), for an increased cardiac output. Vasodilates the airways. Beta receptors. Norepinephrine: attaches to AT1 receptors in endothelial cells - leads to peripheral vasoconstriction. Alpha receptors.