Final Exam Flashcards

(52 cards)

1
Q

How does the body maintain fluid balance?

A

-Kidneys produce renin which interacts w/ renin-angiotensin-aldosterone-system (RAAS) to regulate fluid balance
-Input + production = utilization + output
-Vasopressin opens channels in kidney letting water follow NaCl into bloodstream which promotes reabsorption
-Atrial Natriuretic Factor (ANF) causes Na + H2O to be excreted via urine when fluid volume is too high
-Hormones influence permeability of nephrons controlling mvmt of Na & Cl back out into blood
-K+ secreted from bloodstream –> nephron –> urine

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2
Q

Describe what happens at different sections of the nephron

A

-Nephron: Functional unit of the kidney, filters ~48 gal. of blood daily & helps maintain homeostasis
-Renal corpuscle: Composed of the glomerulus & Bowman’s capsule; it’s the primary blood filtering unit
-Proximal convoluted tubule: Reabsorbs AAs, Na, bicarb, K, Ca & H2O; also secretes drugs and produces ammonium
-Loop of Henle: Concentrates urine and regulates fluid sent to collecting ducts & ureters
-Distal tubule: Reabsorbs 99% of filtrate into vasa recta and includes thick ascending limb which is regulated by vasopressin, PTH & calcitonin; macula densa senses Na & releases renin; maintains electrolyte balance
-Collecting duct: Principal cells reabsorb NaCl & secrete K+ and intercalated cells regulate acid-base balance by secreting H+ & bicarb

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3
Q

Describe how the body registers changes in fluid balance within the cardiovasculature and responds hormonally

A

-ADH: Enhances water reabsorption by increasing Na channels in kidney principal cells
-Angiotensin II: Stimulates ADH secretion, promoting H2O retention
-ANP: Decreases ADH secretion, helping regulate blood volume & pressure
-When responding to hemorrhage, BV reduction leads to lower mean arterial pressure (MAP)
-ADH & RAAS are activated to facilitate H2O retention and vasoconstriction to stabilize cardiovascular function

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4
Q

Describe the interaction of the specific hormones’ actions at the nephron including the medullary osmotic gradient

A

-Medullary osmotic gradient: Decreases osmolarity near cortex & increases near renal pelvis; also facilitates water reabsorption via osmosis
Water reabsorption breakdown:
-70% in the proximal tubule (passive, unregulated)
-20% in distal tubule (regulated by ADH)
-10% in the collecting ducts (influenced by ADH)
Role of ADH:
-Stimulates aquaporin-2 channels in distal tubule & collecting ducts; they increase H2O permeability, enhancing reabsorption into bloodstream
-ADH adjusts H2O permeability in distal tubules/collecting ducts while medullary osmotic gradient ensures H2O conservation & fluid balance

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5
Q

Describe the difference between how the respiratory system compensates for acidosis vs. how the renal system compensates

A

-Acidosis can result from increased CO2 (respiratory) or excess H+ (metabolic); blood pH < 7.35
-Respiratory system enhances ventilation rate, allowing more CO2 to be exhaled; this decreases CO2 in blood & helps to raise the pH
-Renal system excretes more H+ into urine & reabsorbs/synthesizes more bicarb to further buffer blood & restore pH balance
-Respiratory has quick response (within minutes-hours) & renal has slower response (hours-days)

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6
Q

How does hypertension cause kidney disease?

A

-HTN damages blood vessels (including those in kidneys) and causes vessel walls to thicken & narrow –> decreased blood supply
-Decreased blood supply impairs kidneys’ ability to filter waste & leads to buildup of waste/fluids in the body
-Uncontrolled HTN can lead to kidney failure, requiring dialysis/transplant
-Chronic high BP can worsen pre-existing kidney damage, accelerating decline in function

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7
Q

How does diabetes cause kidney disease?

A

-Diabetic nephropathy: Gradual loss of kidney function in people w/ DM caused by prolonged exposure to high BG which impairs waste filtration
-Early sign is glomerular hyperfiltration where excessive blood filtering strains nephrons
-Glomeruli become leaky forming advanced glycation end products (AGEs), which causes inflammation & scarring leading to impaired nephron function
-High BP (common in DM) worsens kidney damage

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8
Q

How is CKD classified?

A

Classification based on glomerular filtration rate (GFR), which measures how well kidneys are functioning

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9
Q

What is happening at CKD Stage 1?

A

-There’s kidney damage but GFR remains normal/increased (> 90 mL/min)
-Damage is minimal & often only detected through protein in urine or physical damage seen on imaging

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10
Q

What is happening at CKD Stage 2?

A

-Damage progresses, GFR mildly decreased (60-89 mL/min)
-Kidneys still function enough to prevent waste buildup
-Early detection at this stage is CRUCIAL for managing & slowing the progression of this disease

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11
Q

What is happening at CKD Stage 3?

A

-Stage 3a: Moderate decrease in GFR (45-59 mL/min) & Stage 3b: GFR of 30-44 mL/min
-Function continues to decrease & kidneys may no longer adequately filter waste leading to toxin buildup
-Symptoms include fatigue, fluid retention, changes in urination & discomfort in kidney area
-CKD often detected at this stage

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12
Q

What is happening at CKD Stage 4?

A

-Severe decrease in GFR (15-29 mL/min)
-Kidneys no longer filtering waste leading to more pronounced symptoms like anemia, decreased appetite, bone disease & abnormal levels of phos, K+ & other lytes
-Risk of CVD significantly increases

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13
Q

What is happening at CKD Stage 5?

A

-AKA kidney failure or ESRD
-GFR < 15 mL/min, kidneys lost almost all ability to function, significant buildup of waste products/lyte imbalances/fluid overload
-Dialysis or transplant needed for survival
-Symptoms include N/V, breathlessness, confusion & loss of appetite

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14
Q

Explain why people with CKD may get osteoporosis?

A

-Disruptions in Ca & bone metabolism
-PTH acts on both kidneys & bones by influencing synthesis of the active form of vitamin D (1,25-dihydroxycholecalciferol)
-As kidney function decreases, kidneys become less able to excrete phosphate & activate vitamin D which leads to elevated phos levels & decreased Ca absorption (both which stimulate parathyroid gland to release more PTH)
-When PTH above normal range, patients are at risk for secondary hyperparathyroidism which leads to increased Ca serum levels, excessive bone resorption & potential tissue calcification
-When GFR is <30 mL/min, kidneys lose ability to convert vitamin D in active form and places a greater burden on bones to release Ca leading to bones being broken down worsening risk of osteoporosis

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15
Q

Explain why patients with CKD often become anemic

A

-Erythropoietin (EPO) production is decreased and is a hormone that stimulates bone marrow to produce RBCs
-In CKD, decreased RBC production & shortened lifespan lead to anemia
-CKD can also lead to an iron deficiency because it interferes w/ body’s ability to absorb & use iron, which is essential for RBC production (iron loss in urine, decreased intake due to restrictions & inflammation associated)
-Dialysis also plays a role due to blood loss during and the use of heparin

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16
Q

What is a pre-renal AKI?

A

-When there’s an obstruction of blood flow to kidneys
-Results from decreased cardiac output, hypovolemia, vascular emboli, HF & LF or meds that affect blood supply
-Can be reversed within couple days when normal blood flow is restored
-But if underlying cause is not effectively treated, could lead to intra-renal

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17
Q

What is a intra-renal AKI?

A

-Involves damage to kidney cells themselves
-Can be caused by nephrotoxic agents, infections, or systemic diseases (lupus or sarcoidosis)
-Sepsis from pre-renal can trigger intra-renal
-More severe and likely alters nutritional requirements of the patient, where they will need careful monitoring & management

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18
Q

What is a post-renal AKI?

A

-Obstruction in flow of urine from kidneys
-From kidney stones, enlarged prostate, cervical cancer or other tumors
-Can often be reversed within a few days once the obstruction is cleared
-No change in nutrition but very important to focus on addressing obstruction to restore function

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19
Q

Explain why someone might want to ensure at least some nutrition is flowing through the gut, even if someone is receiving parenteral nutrition

A

-Preserves gut health by maintaining GI barrier function & mucosal integrity; also supports digestion & nutrient absorption
-Prevents infections by strengthening mucosal barrier, reducing bacterial translocation (bacteria/toxins entering bloodstream)
-Boosts immunity by enhancing systemic & local immune responses; stimulates epithelial cell metabolism, turnover & intestinal blood flow
-Promotes release of trophic hormones essential for gut health
-Supports gut tissue by preventing atrophy of Gut-Associated Lymphoid Tissue (GALT) & Mucosa-Associated Lymphoid Tissue (MALT)
-Combats malnutrition by addressing complications from impaired nutrient absorption & supports immune system function

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20
Q

What is at risk if we don’t confirm enteral tube placement before we begin tube feeding?

A

-Tube can mistakenly go down the trachea into the lungs, EN could end up filling the lungs
-Can lead to aspiration pneumonia, where food/liquid enters the lungs rather than stomach and can cause infections & death
-Important to check placement through CT scan

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21
Q

In more highly concentrated enteral formulas, why is there a higher percentage of calories from fat?

A

-Fat is the most calorie-dense macronutrient and allows a significant amount of energy to be delivered in a smaller volume, especially for patients w/ fluid restrictions
-As formula concentration increases, the osmolarity of formula also increases
-By increasing %kcals from fat, the formula can deliver more kcals without exacerbating osmolarity-related issues

22
Q

Describe refeeding syndrome

A

-Series of metabolic & electrolyte disturbances that can occur when calories are reintroduced or increased after a period of significantly decreased or absent calorie intake
-Hallmarks include hypophosphatemia, hypokalemia & hypomagnesemia
-Can develop with reintroduction of kcals from any source shifting metabolism from fat to carb metabolism increasing insulin production and decreasing glucagon production
-Increased insulin production drives phos, K+, and Mg into cells, depleting already low reserves which exacerbates risk of dangerous imbalances

23
Q

Why does refeeding syndrome happen?

A

-During malnutrition, body relies on glycogenolysis (glycogen breakdown) & gluconeogenesis (glucose creation) for energy
-Liver glycogen depletes in 12-24 hours, shifting to ketones from fat oxidation
-Intracellular depletion of phos, K+ & Mg occurs to maintain balance
-Serum levels appear normal, masking growing intracellular deficits
-Insulin secretion increases with feeding, driving glucose & lytes (especially phos) into cells
-Rapid carb metabolism depletes Mg & thiamin
-Thiamin stores are naturally low with a half-life of 7-10 days, deficiency can lead to refeeding syndrome

24
Q

How is refeeding syndrome prevented?

A

-Involves starting caloric intake slowly & gradually increasing over several days
-Do this by monitoring and supplementing lytes & thiamin prior to and during refeeding
-Also regularly assess lab values & patient symptoms to address imbalances early

25
When we say hydration is not a "set it and forget it" scenario, what do we mean and why could it happen?
-Managing fluids is an ongoing process that requires close monitoring & adjustments, fluid overload can happen if we're not careful -That's why labs are always being checked to see what the patient needs & adjusting fluids accordingly -Na is the most osmotically active lyte, so Na levels are monitored to understand how fluids are shifting in the body -Isotonic fluids: Stay in extracellular space & increases overall FV -Hypotonic fluids: Draw water out of cells into extracellular space
26
What is the major consideration for whether or not we can feed through peripheral PN vs. central PN?
-Comes down to osmolarity of solution & duration of use -Central PN is preferred because solutions tends to be hypertonic & can't be safely administered peripherally -For peripheral PN, max osmolarity that the vein can tolerate is 800 mOsm/L -Another issue is that venous access needs to be changed frequently to keep vein open & irritation limits the use of peripheral fluids to 2x/week -Peripheral is typically reserves for patients not on fluid restriction, since you can increase volume to provide more kcals & protein but it's not always practical for long-term and increased nutrient needs
27
Describe the differences of cancer risk by sex and race
-Men have higher rates than women and most common cancer is prostate, then lung, followed by colorectal cancer -Most common cancers for women are breast, lung, and colorectal cancer -Black men face the highest rates and Asian American & Pacific Islanders have the lowest rates -Black people have lowest survival rates often due to a later diagnosis & limited access to quality care
28
You are teaching a patient with a strong family history of cancer about modifiable & non-modifiable risk factors for cancer, how do you inspire them towards better behavior?
-Encourage them by explaining the difference between the two while empowering them with hope & practical steps they can take -Non-modifiable: Genetics, hormones, immune factors -Modifiable: Smoking, weight, drinking, sun exposure, physical activity, healthy diet -It can feel overwhelming but every small step counts, think of it as investing in your health & future one day at a time
29
What is cancer cachexia?
-Continuous loss of skeletal muscle with or without fat loss & doesn't fully respond to nutritional support -Shows up in ~1/2 of cancer patients & in up to 80% of those with advanced cancer -Early sign of illness with symptoms like anorexia & weight loss -Associated with a poor prognosis since fat & muscle loss happen when patients start eating less
30
Explain 2 mechanisms that create cancer cachexia
-Brain-related anorexia: Change in hypothalamic signals reduce appetite, along with diminished senses of taste & smell -Lipolysis: When fat tissue breaks down, FAs are released and making the body inefficient
31
Explain cancer through the lens of natural selection and survival of the fittest from the viewpoint of the cancer cell
-Increased proliferation speeds up evolution, allowing only the strongest cells to survive; advantage typically comes from a specific set of mutations that occur in successive clonal generations -Tumors are genetically diverse populations of cancer cells, offering advantage in resisting the body's defense mechanisms; cancer cells evolve resistance to therapies over time, reducing effectiveness of treatment -Tumor microenvironment supports cancer evolution by inducing genetic instability, which fosters therapy-resistant cells and releases pro-inflammatory signals that aid tissue repair creating a supportive stroma around tumor -Continued mutation & evolution in tumor increases cell diversity and aggressiveness; some cells acquire metastatic abilities allowing them to spread -Cancer behaves like an evolving system with cells mutating, adapting & competing, viewing cancer through this lens can help develop more effective treatments
32
Explain the pathophysiology of GERD
-Condition which stomach contents flow back into the esophagus, often causing discomfort & damage -Happens due to dysfunction in the lower esophageal sphincter (LES), a muscle barrier that normally separates the stomach from the esophagus -LES maintains pressure difference between the 2 areas to prevent reflux, but when it relaxes too frequently or for too long, it can be ineffective -Acidic contents (gastric acid & pepsin) can be moved upward into the esophagus
33
How do you minimize GERD symptoms?
-Goals are to enhance the competence of the LES, decreasing acid secretion & protecting the esophageal lining -Antacids & histamine blockers can be helpful in neutralizing stomach acid and decreasing its production -Addressing lifestyle factors like quitting smoking, managing, weight & reviewing meds that might aggravate symptoms can be crucial -Surgical options like Nissen fundoplication (where part of stomach is wrapped around LES to strengthen it), partial fundoplication, or Roux-en-Y bypass might be considered -Nutritionally, focus on decreasing gastric acidity and avoiding meals that can relax the LES -Peppermint, chocolate, fried or fatty foods, alcohol & coffee can decrease LES pressure and coffee, alcohol, and pepper can increase gastric secretion -Also consuming smaller, more frequent meals and conducting a dietary trial to identify & exclude foods that may trigger symptoms
34
Describe pathophysiology of dumping syndrome
-When rapid movement of stomach contents into SI due to increase in osmolar load entering SI too quickly, often due to alteration in gastric function -When stomach is removed, bypassed & otherwise impaired, gastric emptying becomes significantly accelerated -Partially digested food (chyme) enter SI and is hyperosmolar, causing fluid shift from bloodstream into SI to dilute contents -Fluid shift can leads to cramping, abdominal pain, increased intestinal movement & diarrhea; can also affect vascular compartment, causing dizziness, weakness & increased heart rate (tachycardia) -When food moves to colon, fermentation process is carried out by intestinal microflora which can produce gas contributing to abdominal discomfort, cramping & diarrhea -"Late dumping syndrome" occurs 1-3 hours after eating, especially after consuming simple carbs; it is triggered by rapid absorption of glucose in SI leading to surge in insulin release -Insulin causes BG levels to decrease rapidly as it promotes cellular uptake leading to hypoglycemia where one can experience shakiness, sweating & confusion
35
I am just getting finished with intractable vomiting and nausea. What is the general plan to get from liquid back to solids?
-Once vomiting has stopped, slowly sip clear fluids like water, apple juice, warm/cold tea, or lemonade -Reintroduce liquids gradually, doubling amount every hour, depending on tolerance -After 8 hours without solids, start slowly by adding one type of food at a time in small amounts to see how body handles it -Avoid foods high in fiber or fat because it can be hard to digest & can produce strong odors/gas -Dry toast, crackers & pretzels and soft proteins like yogurt, baked chicken or eggs
36
Compare and contrast differences between IBS, Crohn's disease, UC, and Diverticulitis
-All impact the digestive system but differentiates in causes, symptoms & treatment -IBS is more about managing symptoms since it doesn't cause any structural damage -Crohn's & UC are inflammatory and can cause real damage to the intestines -Crohn's can affect different parts of the GI tract with deeper inflammation, while UC is confined to the colon & its surface layers -Diverticulitis is a more acute issue with inflamed pouches in colon, often due to dietary & lifestyle factors
37
What is Irritable Bowel Syndrome and how do you treat it?
-Functional disorder where people experience abdominal pain linked to bowel movement or changes in bowel habits at least once a week -Common, affects 12% of people in North America -Doesn't cause structural damage in gut but symptoms like stomach pain, bloating, gas & D/C can be disruptive -Genetics, an overactive immune response to certain foods, changes in gut bacteria & issues with serotonin regulation can make the gut more sensitive -Treatment includes managing symptoms through diet changes like low-FODMAP, finding foods triggers & managing stress
38
What is Crohn's disease and how do you treat it?
-Type of IBD and can pop up anywhere in the digestive tract but often show up in the SI/colon -It is more intense because it is chronic inflammation that can go deep into layers of intestinal walls, causing things like fistulas, strictures or blockages -Skip lesions can affect patches of gut while leaving other areas untouched -Stomach pain, weight loss, fatigue & malnutrition can occur due to nutrient absorption issues -Causes include genetic predisposition paired with triggers that set off an overactive immune response -Treatment includes meds to decrease inflammation and sometimes surgery to remove damaged parts of the bowel, nutrition support is also key since patients can become malnourished
39
What is Ulcerative Colitis and how do you treat it?
-Type of IBD but more contained than Crohn's, only affects colon and rectum & sticks to surface layers of colon -Symptoms include bloody diarrhea, stomach cramps & constant feeling of having to go to bathroom -Due to an overactive immune response but limited to the colon -Treatment includes meds to decrease inflammation and sometimes surgery is an option especially since removing the colon can essentially "cure" UC
40
What is Diverticulitis and how do you treat it?
-Little pouches (diverticula) form in the colon walls which can get inflamed or infected -Isn't chronic but can come on suddenly with intense symptoms like pain on lower left side of abdomen, fever & nausea -Often linked to a low-fiber diet & constipation, which increases pressure in colon -Risk factors include being overweight, not moving enough & smoking -Treatment includes starting with bowel rest & gradually adding clear liquids before moving to a high fiber diet to prevent future flare-ups; sometimes surgery is needed
41
Why does a patient with Celiac disease have malabsorption and what's the cure?
-Complex autoimmune condition that occurs in genetically predisposed individuals who are intolerant to gluten -The body mistakenly reacts to gluten leading to SI damage which disrupts nutrient absorption -Condition linked to maldigestion and malabsorption of essential nutrients, vitamins & minerals; patients present with significant weight loss, anemia or clear signs of vitamin/mineral deficiencies -Malabsorption usually affects nutrients absorbed in upper part of SI (iron, folate & calcium); as disease progresses further along intestine, it leads to malabsorption of carbs, fats & fat-soluble vitamins (A, D, E, K) + other micronutrients -There is not cure but adhering to a strict gluten-free diet is crucial in management -Eliminating all sources of gluten, including foods containing wheat, rye & barley; also look out for hidden gluten like hydrolyzed vegetable protein in processed foods & oats are GF but can easily be contaminated in processing
42
Describe the difference between the liver and the gallbladder's relationship with bile
-Liver, specifically in its lobules, produces bile through hepatocytes -Bile: Essential for emulsifying fats & facilitating their absorption in SI, primarily through the formation of micelles -Gallbladder functions as a store & concentration site for bile -It removes water & lytes to increase the bile's concentration, stores it until needed, and regulates its delivery to the duodenum in the form of Na & K salts to aid digestion
43
Explain how problems in the gallbladder could create a problem in the pancreas
-Shared anatomical pathways -Bile is transported through the cystic duct which merges with the common hepatic duct to form the common bile duct -Common bile duct joins the pancreatic duct, which carries digestive enzymes -If cholestasis occurs, where bile secretion is decreased or its flow into the digestive tract is obstructed, it can create a blockage into the bile & pancreatic duct -This obstruction could cause a backup of pancreatic secretions, potentially leading to inflammation of the pancreas (pancreatitis)
44
You are told a patient has chronic pancreatitis with a history of not complying with meds/PERT regimen. Pt reports having trouble driving at night because vision is impaired in low light and notices skin is flaking off in weird places. What is causing this and why?
-Chronic pancreatitis: Characterized by irreversible inflammation, fibrosis & tissue calcification in pancreas, leading to chronic abdominal pain, diabetes and steatorhhea -Vitamin A deficiency is common due to fat malabsorption as pancreas often produces insufficient enzymes to absorb fat-soluble vitamins -Vitamin A is essential for night vision and maintaining healthy skin as it supports cell turnover -Pt's non-compliance with her Pancreatic Enzyme Replacement Therapy (PERT) regimen likely exacerbates issue preventing adequate absorption of fat-soluble vitamins from diet and contributing to deficiency
45
Patient has a big gallstone that is not being treated. Last night he ate a high-fat meal and felt excruciating pain in right upper abdominal quadrant (under liver) that lasted for over an hour. What is happening?
-Gallstones form due to prolonged intake of increased dietary fat and low fiber, which increases demand for cholesterol production to synthesize bile for fat digestion -After eating high fat meal, pt experienced pain because gallstones likely blocked bile flow from gallbladder -Fatty meals stimulate gallbladder to contract & release bile for digestion but if a stone becomes lodged in duct, it obstructs flow and causes severe pain during digestion, which lasts for over an hour
46
What is happening in ascites and why?
-Ascites: Accumulation of fluid in peritoneal cavity commonly caused by liver cirrhosis -Arises from inadequate synthesis of serum proteins & increased sodium retention -Decreased serum protein levels and decreased oncotic pressure lead to fluid shifting in bloodstream into "3rd spaces" causing edema -As BV decreases, urine excretion also decreases, contributing fluid & Na retention -Cirrhosis causes elevated BP in hepatic portal vein and portal HTN forces fluid out of blood vessels into abdominal cavity, culminating in development of ascites
47
What causes the acute phase response (ARP)?
-Triggered by infection/injury to tissue -Key features are fever, altered vascular permeability and biosynthetic & metabolic shifts across organs -Primary initiators are macrophages at the site of infection/injury & monocytes in the bloodstream -These cells release IL-1 & tumor necrosis factor-a (TNF-a) which act as chemical messengers to coordinate inflammatory response -IL-6 regulates inflammatory response & chemokines (MCP-1 & IL-8) attract immune cells to site of injury -These initiate inflammatory cell infiltration and these mediators exert chemotactic & other systemic effects, setting off full-blown APR
48
What can we expect to see in the ebb phase of ARP?
-Attempts to restore BP & increase cardiac performance and maximum venous return -Lasts 12-24 hours if initial injury is under control -Tissue & gut hypoperfusion lead to decreased BP and gastric intolerance -Body increases catecholamines (norepinephrine) to regain hemodynamic stability to increase BP -Norepinephrine causes increased contractibility of HR & vasoconstriction -Increased sympathetic nervous system activity and release of norepinephrine & gluconeogenesis -Depending on injury severity, there may be hyperglycemia & also find decreased REE
49
What can we expect to see in the flow phase of ARP?
-Peaks at days 3-5 & resolves at days 7-10 -Starts with increased cardiac output to restore oxygen & nutrients -Then catabolism occurs, breaking down tissues for energy & immune needs -Insulin release increases with catecholamines, glucagon & cortisol -Anabolism causes AAs & FFAs to mobilize from muscle & fat stores; used to support energy and immunoglobulin production -Outcomes include a negative nitrogen balance (protein loss), decreased fat stores & changes in body composition - Changes include losses of protein, carbs & fat stores, accompanied by enlarged extracellular water compartments -This is where most ICU feeding will occur
50
Explain nitrogen balance. Why is it less informative in the ICU?
-Nitrogen balance: Difference between amount of nitrogen consumed through diet (mainly from protein) & amount of nitrogen excreted from the body through urine and feces -It's a steady state technique meant to be given under stable physiologic conditions where amount of protein given has been stable for over a week (none of these criteria are met in the ICU) -In the ICU, all it can tell you is how catabolic you are, not whether you're making use of the protein being fed -Completely invalid statistic in critical care
51
In starvation, lean muscle wasting stops when we begin feeding. Why does this not happen when we feed during APR?
-In starvation state, body prioritizes energy conservation & adaptation occurs when body lowers BMR -Energy shifts to using fat stores for fuel, sparing lean muscle mass & feeding during starvation halts muscle wasting because body no longer needs to breakdown protein for glucose production (gluconeogenesis) -APR is triggered by inflammation or severe injury/illness (sepsis/trauma) and doesn't halt muscle wasting because inflammatory state overrides anabolic signals from feeding -Protein is still broken down to support immune response, wound healing, acute phase protein synthesis & body remains in a catabolic state despite nutrient provision -Starvation is an adaptive process to conserve muscle mass which is reversible by feeding & ARP is a hypercatabolic process driven by inflammation where feeding can't fully counteract muscle loss due to ongoing cytokine activity
52
If we are having trouble weaning someone from mechanical ventilation and nothing is working, why might we try decreasing their caloric intake for a while?
-Overfeeding in any respiratory distress will increase the burden on the lungs & may result in delayed weaning from mechanical ventilation -Decreased caloric intake decreases CO2 production, easing the workload on the respiratory muscles