Flashcards in Exam2 - Movement/Support + Perfusion Deck (117):
Dorsal to ventral, what is the order of the spinal cord coverings?
How does spinal anaesthesia differ from epidural anaesthesia? How are they similar?
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.
Which nerves are afferent and which are efferent? (Dorsal vs ventral)
Dorsal nerves are afferent (sensory relay to brain)
Ventral nerves are efferent (motor relay to body)
What does RANK-L do? Who releases it? What initiates its release?
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.
What is OPG and what does it do? Who releases it? What initiates its release?
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.
What effects do low blood calcium levels have on osteoblasts and/or osteoclasts?
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).
What effect do high blood calcium levels have on osteoblasts and/or osteoclasts?
With high blood Ca++ levels, the thyroid releases Calcitonin, which tells osteoclasts to stop resorption activity.
(PTH release will also slow).
What is RANK?
RANK is the receptor for RANKL (found on osteoclasts)
What are the risk factors for osteoporosis?
**Post-menopause (low estrogen=low OPG release)
Insufficient dietary Ca++ before age 30
Poor Ca++ absorption
Vitamin D deficiency
Inadequate weight-bearing exercise
Endocrine disorders (like excess PTH)
Where is osteoporosis most likely to occur?
In porous parts of bone, like the femoral neck of the trochanter, the wrist, and the thoracic and lumbar spine.
What are the three types of fractures we talked about and any risks associated with them?
Open fracture (broken skin = increased risk for infection)
(Note: if any of the above are breaks fo the femur, there is a high risk for blood loss leading to hypovolemic shock).
What is compartment syndrome and why does it happen?
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).
What signs and symptoms are associated with compartment syndrome?
Swelling, skin color change (pallor), signs of occluded blood supply on other end of cast:
-decreased cap refill
-decreased pulse strength
-decreased sensation (due to hypoxic cell injury)
Monitor circulation, motion and sensation.
What are the types of spinal cord injuries we talked about that can lead to spinal shock? Are they primary or secondary neurologic injuries?
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)
What is transection and why isn’t it associated with spinal shock?
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)
What is a secondary neurologic injury?
When spinal blood flow is obstructed due to an inflammatory response. The obstruction leads to ischemia and necrosis of neural tissue.
What is spinal shock and why does it happen? Is it a primary or a secondary neurologic injury?
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.
What are dermatomes and what are some ways we use them?
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.
What is the most common cause of lower back pain?
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).
What is degenerative joint disease?
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
What is Rheumatoid Arthritis?
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.
Describe the immune process behind rheumatoid arthritis
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).
What is the primary symptom of Gout? What causes it?
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.
What gives cartilage its cushioning characteristics and why doesn’t it heal? What happens instead?
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.
What can you do to promote bone repair/growth?
Change your diet:
-antioxidants to combat any inflammatory ROSs from damage.
Avoid: nicotine, excess caffeine, alcohol
Add weight-bearing exercise to increase OPG release.
What is a soft callus?
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)
What leads to scoliosis and why do people have surgery to correct it?
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.
What happens to sensory input once it arrives at the brain?
-Motor cortex (in cerebrum) interprets & determines response
-Sends message to thalamus
-Thalamus (sensory relay center) interprets both incoming and outgoing messages
What do we need to know about the basal ganglia?
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.
What do we need to know about the cerebellum?
Home of the Reticular Activating System (RAS) - a cluster of nerve cells that helps regulate movement.
Problems in which areas of the brain can lead to coordination and movement issues? What sort of problem might cause that?
Motor cortex (cerebellum)
Hemorrhagic stroke is one of the problems that can damage these areas.
What are some motor dysfunctions related to tone?
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.
How does muscle tone differ from strength?
Tone is observable in activities like sitting, turning, general ADLs.
Strength relates to the ability to push, pull, lift, etc.
What type of motor dysfunction is related to strength?
Paresis: muscle weakness but normal tone
What type of motor dysfunction is related to movement?
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).
What is the most common cause of hypotonia in infants?
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).
What is disuse syndrome and how does it relate to limited mobility?
Inability to move around leads to a deterioration of body function/systems.
What does nitric oxide do? What medication do we give for MIs that mimics its effects.
Nitric Oxide (NO) causes arteries to dilate, improving blood flow.
We give Nitroglycerin during MIs because it has the same effect.
What do free radicals have to do with NO (nitric oxide) production? How do we combat their effects?
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.
How do Aortic & Carotid Baroreceptors participate in heart rate regulation.
What is the response?
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.
A patient has broken his wrist. Which cells will the mast cells summon during degranulation?
Phagocytes: neutrophils and monocytes/macrophages.
Your patient with the broken wrist has mast cells that will synthesize platelet-activating-factor. How is this going to help repair his bone?
It signals the liver to release clotting factors - both fibrinogen and platelets are activated for response.
Which WBC promotes angiogenesis?
What are 3 ways that macrophages help to repair broken bone?
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.
A fibrin mesh is being laid down at a broken bone injury site. How did the clotting cascade get started?
Mast cells synthesized platelet activating factor.
This signaled the liver to release clotting factors and fibrinogen.
What should you tell your broken-bone patient about diet and activity?
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.
What scenarios are going to create excess preload?
Na+/H2O Retention in cases of excess aldosterone
Which scenarios will cause increased afterload?
Hypertension (systemic vascular resistance)
Aortic valve stenosis (narrowing of aorta)
What condition (preload or afterload) will ventricular hypertrophy increase?
What condition - preload or afterload - would excess aldosterone production increase?
(Excess aldosterone leads to excess water retention, which would lead to hypervolemia)
Valve regurgitation is going to increase what - preload or afterload?
A patient is presenting with shortness of breath (especially when lying down), crackles in lungs, dependent edema and JVD. What are these symptoms of?
What is the main physiological change that will occur with chronic increased afterload?.
L. Ventricular hypertrophy.
What can a patient do for himself to decrease preload?
Decrease sodium in diet (decrease fluid volume)
What can a patient do to help decrease his afterload?
Support thermoregulation (assuming this is for adequate warmth) to promote vasodilation
Work on fluid balance.
Will elevated PTH decrease or increase OPG levels?
It will decrease OPG production.
Will elevated TNF (tumor necrosis factor) increase or decrease RANKL levels?
TNF increase will increase RANKL levels.
What effect does estrogen have on RANKL production?
RANKL isn’t produced as much when estrogen levels rise. (Additionally, OPG is produced more).
What does TNF (tumor necrosis factor) have to do with osteoporosis?
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.)
Which bones are at highest risk for fracture secondary to osteoporosis (ie, pathological fracture)?
Trochanter of hip
Is aldosterone fat-soluble or water-soluble?
Is ADH fat-soluble or water soluble?
What organ does aldosterone come from, and what activates its release?
Adrenal gland. Activated by Angio II.
What organ does ADH come from
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)
What response does Aldosterone produce in its target cells?
-Causes cells in nephron to retain sodium (from urine filtrate) and excrete potassium.
(This causes water to follow sodium, retaining water.
What response does ADH create in its target cells?
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.
What is the overall effect of aldosterone on the body?
Sodium retention —> water retention
INCREASED VASCULAR VOLUME, which should raise BP.
What is the overall effect of ADH on the body.
Vasoconstriction increases BP
Water retention increases BP (due to increased volume)
What type of patient situation would cause the body to release aldosterone?
Drop in BP - sensed at the kidneys as a decrease in renal perfusion.
What causes the body to release ADH
Dehydration and/or low perfusion pressure around the hypothalamus.
Stimulation of the SNS
Drop in BP at the kidneys.
What is the job of the RAAS? What are its two triggers?
-regulate fluid balance
-regulate arterial blood pressure.
-increase in SNS activity
-Decrease in blood pressure (specifically MAP) at the JGA cells - presents to kidney as a decrease in renal perfusion.
How does Renin become Angio II?
Renin + Angiotensin (Liver) = Angio 1 + A.C.E (lungs) = Angio II.
What four things does Angio II stimulate?
Endothelial cells (AT2 receptors): Vasoconstrict
Posterior Pituitary: Release ADH
Kidneys: Resorb sodium and potassium
Adrenals: release aldosterone.
How does Angio II’s effects on the kidneys differ from Aldosterone’s effects on the kidneys.
It doesn’t. Both tell the kidneys to resorb water and release potassium.
How does Angio II’s effects on the kidney differ from ADH’s effects on the kidney?
Angio II makes kidney cells resorb sodium and release potassium.
ADH makes kidney cells open aquaporins and absorb water.
What is the normal MAP range? How do you calculate it?
Calculate it by: (Systolic-Diastolic)/3= pulse pressure.
THEN, pulse pressure + diastolic = MAP.
What is the definition of preload? Where does it come from?
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)
What effect is excess preload going to have on the entering blood vessels?
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.
What is afterload? What is it determined by?
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.
What are two potential causes of increased afterload to the Right Ventricle? (One acute, one chronic?). What is the resulting damage/effect?
-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.
What is a cause of increased afterload to the L. Ventricle? What is the effect?
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.
What pressures are involved in perfusion homeostasis?
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.
What cellular problems might come about from insufficient systolic pressure (decreased CO)? What are the signs/symptoms?
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
#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?)
What can cause a decrease in oncotic pressure? What happens if it’s local? Systemic?
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).
What is the definition of Shock? (Anything but spinal shock, that is).
Circulatory system fails to meet the perfusion demands of cells, tissues and organs. In other words, severe HYPOPERFUSION.
Causes cellular hypoxia.
Why would shock cause a vicious cycle of “worsening” shock?
Hypoperfusion leads to cellular injury.
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.
What are the body’s compensatory responses to shock?
-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).
Are body’s compensatory measures to shock long-lasting? What effects will they have?
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.
What do you suspect for a patient exhibiting a change in level of consciousness.
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.)
Why do we NOT do Trendelenburg for shock victims?
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.
Why are catecholamines, growth hormone and cortisol released when the body is in hypoperfusion? What is the ultimate effect?
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.
How does acidosis affect Hemoglobin?
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).
What is cardiogenic shock? What is the primary cause?
-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.
What is a normal stroke volume?
How will cardiogenic shock present?
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
What is obstructive shock? What is the primary cause?
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.
How does obstructive shock d/t pulmonary embolism present?
Sudden onset chest pain
Gasping for air
Hemoptisis (coughing up blood)
What is hypovolemic shock? What things are most likely to cause it?
Severe hypoperfusion due to loss of blood/fluid (15% or 900+mL).
Most likely from hemorrhage or excessive dehydration.
How does the body compensate for hypovolemic shock?
Activates the RAAS.
What will hypovolemic shock present as?
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).
What is neurogenic shock? What causes it?
A loss in blood vessel tone due to overstimulation of PNS or understimulation of SNS
(Blood will pool in extremities - no venous return).
What are the cardinal signs of neurogenic shock?
Warm, dry skin
What is anaphylactic shock? What causes it?
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).
What are the signs of anaphylactic shock? How do you treat it?
-Laryngeal edema (swelling of the airway) leads to bronchospasm: difficulty breathing.
-Decrease in BP
-weak, thready pulse
Can start as:
-warm, burning skin
-respiratory distress (coughing, wheezing, choking)
Tx: epinephrine causes systemic vasoconstriction and bronchiole relaxation.
What is septic shock? What causes it?
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.
How will septic shock present? How can you test for it? How can you prevent it?
Warm, flushed skin
Prevention: Catheter care - meatus and away from it, cleaning colonization of bacteria from tube.
Test: Serum Lactate, CRP (opsonins), Procalcitonin (bacteria)
What are atrial stretch receptors for?
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.
What are the two main reasons for DVT (deep vein thrombosis). How can you help prevent it?
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.
What is the difference between primary hypertension and secondary hypertension?
Primary: genetic cause (90-95% of HTN). Cells don’t make enough NO, which usually causes vasodilation.
Secondary: due to a 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).
What is isolated systolic hypertension
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.
What is an aneurysm
Weakness in an artery due to too much hydrostatic pressure over time.
Rupture of an aneurysm —> hemorrhagic stroke.
What is raynaud’s
Vasoconstriction in periphery
Brought on by cold, stress
What is thrombocytopenia
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.
What do our notes say about platelet dysfunction?
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.
What does ‘coagulation dysfunction’ refer to?
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.
What is ACTH and when does our body make it?
Adrenocortotropic hormone: part of the SNS response. Tells the adrenals to release epinephrine and norepinephrine.