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457 Cards in this Set

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  • Back
Describe the normal aging changes. What are the implications for these changes?
• skin-thinner, less subcutaneous fat, more friable, decreased elasticity, dryness
• hair-grey, drier, coarse, thinner
• changes in the number & function of taste buds
• less lean mm mass
• decreased peristalsis
• more body fat
• decreased glomerular filtration rate
• achlorhydria (production of gastric acid in stomach is absent or low)
• decreased blood flow to the liver
• gallbladder disease
• decrease in olfactory sensation
• decrease in hearing & vision
• decreased immune response
• slowed reflexes
• gait changes
• orthostatic hypotension
What is a functional assessment and how is it used (page 830 - see readings on ADLs and IADLs)?
• functional assessment is the basis for care planning, goal setting, and discharge planning.
• a functional assessment includes three domains: activities of daily living (ADLs), instrumental activities of daily living (IADLs) and mobility.
What are Activities of Daily Living (ADLs)?
• these are tasks necessary for self-care. (eating/feeding, bathing, grooming, dressing, toileting, walking, using stairs, and transferring)
What are Instrumental Activities of Daily Living (IADLs)?
• IADLs are the functional abilities necessary for independent community living (shopping, meal preparation, housekeeping, laundry, managing finances, taking medications, and using transportation)
Is depression a problem in the elderly population?
• it is not a problem if compared to other generations
• however depression is never wanted
• depression is not a normal syndrome of getting older
How can depression be assessed?
• use the geriatric depression scale (short form)
• ask the following questions
• have you been preoccupied with your own death?
• have you had unusual spells of crying or tearfulness?
• have you thought about harming yourself?
• if yes, do you have a plan?
How does dementia and delirium differ?
• delirium presents an acute change in cognition, affecting the domain of attention.
• dementia has alterations in word finding and naming objects in addition to memory problems.
What is polypharmacy?
the use of 5 or more medications consumed daily (prescription, herbs, OTC)
Why is polypharmacy important to assess in the elderly?
• elderly are more subjected to SE & ADRs
• therefore elderly will be more at risk for falls, toxicity, etc.
Describe innate vs. adaptive immunity.
innate (fast) immunity requires no previous exposure to effectively respond to an antigen. innate is made up of NK cells and phagocytic cells. adaptive (slower) immunity response more effectively the second time and are composed of t and b lymphocytes.
Discuss components of immune system.
the main components are as follows:
-skin and mucous membranes
-lymphoid system
-bone marrow
-leukocytes (WBC)
Where do t-cells mature?
Where do b-cells matures?
bone marrow
What occurs in the lymph nodes?
they house b-cells, t-cells, and other immune cells all waiting to attack foreign particles. the nodes act as filters or traps to catch the foreign particles.
What are primary vs. secondary organs in immune system?
the primary organs are the thymus and bone marrow. the secondary are the spleen, lymph nodes, tonsils, and peyers patches.
Discuss leukocytes: agranulocytes vs. granulocytes
granulocytes consist of neutrophils, eosinophils and basophils. agranulocytes consist of b-cells, t-cells, and natural killer. (monocytes)
Which are macrophages?
monocytes that migrate from the blood into tissues
Which are lymphocytes?
NK cells
What is required for a macrophage to engulf an offender?
DAMP and PAMP secreted from damaged cells is required for a macrophage to be called in to engulf an offender.
What are the primary effectors of the immune system?
WBC: Leukocytes
What do neutrophils primarily respond to?
they consist of 60-80% of all WBC. they are the first responders to injury and they travel in large amounts. they are phagocytes and engulf microorganisms. they are attracted to areas of inflammation.
What do eosinophils primarily respond to?
eosinophils are associated with and increase in numbers with an allergic reaction and infection by intestinal parasites.
Know about basophils, which become mast cells and HISTAMINE in granules.
basophils circulate in the vascular system and mast cells are found in connective tissue. when basophils are stimulated by cytokines they migrate to tissue which is where they become mast cells. the degranulation of mast cells and basophils begins the inflammatory response often seen in allergic reactions. mast cells and basophils contain histamine within the granules, platelet activating factor and vasoactive amines that are important mediators. both are also involved in wound healing and chronic inflammation.
What is the role of cytokines secreted by macrophages?
the cytokines secreted by macrophages induce inflammation and chemotaxis. the cytokines secreted by macrophages also stimulate growth and differentiation of other WBC types to continue fighting off the pathogen.
Discuss NK cells as lymphocytes: associated with innate immunity, can respond without prior exposure.
NK cells are part of the innate immunity and do not depend on the thymus for development. they fully mature in the bone marrow. they can effectively kill tumor cells and virally infected cells without previous exposure. NK cells differ because they can respond to a variety of antigens therefore they are not limited. NK cells recognize antibodies by the Fc receptors.
CD4+ t-cells (Th cells): what do they do?
the Th cell has a CD4+ protein thant interacts with a MHC II complex on a dendritic cell for example. when they connect the dendritic cell gives a piece of the gobbled antigen to the Th cell. this process activates the Th cell to attack. the Th cell proliferates into effector cells and memory cells. effector Th cells activate b-cells and release cytokines. the memory Th cells stay around for any 2nd time infections
CD8+ t-cells (CTL cells): how do they induce cell death?
the Tc has a CD8+ protein that wants to interact with MHC I complex on a cell that is infected. it automatically lysis and cells the cell. the Tc cell also proliferates into effector and memory cells.
Discuss epitope and Ag fitting together.
the b-cells receptors that are membrane bound antibodies are specific to the epitope on an antigen. the particular b-cell that attached starts to proliferate. when this binding happens the b-cell takes the protein antigen processes it and presents it to the t helper cells. the exposure to the antigen stimulates b-cells into mature b-cells (plasma cells) and memory cells. they create antibody factories that are capable of binding to the foreign particle. this is called opsonization. by doing this is signals to the macrophages to come gobble up the foreign particle. the epitope on an antigen is very particular to the receptor on a particular b-cell. not every b-cell will have this receptor and that is why once activated this particular b-cell begins to proliferate.
Complement cascade: why did mother nature design it this way?
mother nature was intelligent enough to say we need this to happen fast so we are going to take the alternate route to C3 instead of the classic route with C1.
Discuss complement:
-classical pathway
-alternative pathway
-MAC: how does it induce cell death?
-classical pathway is initiated by an adaptive response at C1that attaches to the Ag/Ab complex.
-alternative pathway is initiated by an innate response at C3
-MAC the C5b fragment combines with C6, C7, C8, and C9 to form pore-like structures called MAC on the lipid bi-layer. This attack causes a direct cytotoxic effect on the lipid bi-layer. This cause free movement of sodium and water to move into the cell causing it to lysis.
What is the purpose of inflammation? (3)
1. neutralize and destroy invading and harmful agents
2. limit spread of harmful agents to other tissue
3. prepare damaged tissue for repair
Discuss acute vs. chronic inflammation.
-acute inflammation is short only lasting less than two weeks.
-chronic inflammation extends over longer time. it may result in scar tissue formation of deformity.
What are the clinical signs of inflammation?
-loss of function
What is the role of vasodilation in inflammation? (page 198)
vasodilation allows more blood to travel to the injured areas and contributes to redness, pain, heat, and swelling of the inflammation.
What are the 3 players in healing (page 201)?
-fibroblasts who are stimulated to make collagen, proteoglycans, and fibronectin to enduce repair to damage. they facilitate orderly cellular growth.
-endothelial cells expand in new capillaries to bring more nutrients for tissue repair and wound healing. but sometimes new capillaries are leaky causing edema.
-myfibroblasts develop at the edge of a wound to induce wound contraction.
What are 4 kinds of exudates (page 201-202)?
-serous exudate is watery with low protein content. similar to fluid buildup under a blister and causes mild inflammation.
-fibrinous exudate is when more protein can get through the blood vessel wall. it is mostly sticky and thick. often this exudate has to be removed to prevent scar tissue and allow healing.
-purulent exudate is called pus and typically occurs in severe inflammation by bacterial infection. May be seen as an abscess and need to be drained for healing to happen.
-hemorrhagic exudate has a large amount of RBC and this exudate is present in the most severe inflammation. usually occurs with severe leakage of blood vessels or necrosis.
What is MHC and why is it important? (page 203)
MHC is a cluster of genes on chromosome 6. They are so important because they are individual for every person. They are proteins that are made by these genes to recognize their "self". this will allow great detection of foreign particles.
Know about b-cells/memory b-cells and role in specific immunity.
b-cells have membrane bound Ab. they can attach directly to the epitope of a Ag. b-cells gobble the antigen and present it to Th cells to begin attack. once the b-cells stimulate the Th cells the b-cells begin to proliferate into effector cells and memory cells. the effector cells are called plasma cells and the spit out antibodies at a fast rate to bind to anymore Ag's. once the Ab's bind to the Ag's this signals the macrophages to come eat them.
Antibodies: what do they do?
-precipitation/agglutination: allows Ag/Ab complex (insoluble) to leave body fluids. this allows for phagocytosis.
-neutralization: neutralizes the bacterial toxin. binds with toxin before it can interact with a cell.
-opsonization is when the Ab coats the Ag making it more recognizable to macrophages.
Discuss the 5 antibody classes and their general association (Page 210-212).
-IgG is the most common and accounts for 75-80%. they are found in the intravascular and interstitial compartment. long half life of 3 weeks. they are the smallest and can escape bloodstream easier to get to the tissues.
-IgM accounts for 10% and is mostly found in intravascular pool. it's large structure prevents it from traveling outside the capillary. it is the first immunoglobulin to be produced on exposure to antigens after immunizations and it is the major antibody found on b-cell surfaces. half life 10 days. works best to complement.
-IgD is found in trace amounts in serum and is on the surface of b-cells with IgM. little is known about IgD. half life 3 days.
-IgE is found by its Fc tail to receptors on the surface of basophils and mast cells. half life 2 days. immunity against helminthic parasites and is responsible for initiating allergic reactions.
-IgA is produced by plasma cells located in the tissue under the skin and mucous membranes. it is found in saliva, tears, tracheobroncial secretions, colostrum, breast milk, and GI and GU secretions. half life 6 days.
Discuss passive immunity vs. active immunity (page 215).
passive immunity is using the antibodies against a pathogen that it has never been exposed to. an example is a fetus receiving antibodies from the mother (breast milk). active immunity is when you are exposed to antigens through immunization or entry through the skin. you are exposed to antigens and your b-cells are triggered to make memory cells to remember the antigen in the future.
What is a macromolecule (typically foreign) that provokes an immune system response?
What are antimicrobial peptides produced by the skin's epithelium to kill a wide variety of bacteria and fungi?
What is a bacterial peptide produced by the intestinal epithelium that prevents bacteria from colonizing on the intestinal wall?
What are monocytes that migrate to the liver to become macrophages?
Kupffer cells
What are monocytes that migrate to the skin to become macrophages?
Langerhans cells
What cells are derived from the bone marrow and from the same cells that produce monocytes and macrophages. they are structurally and functionally similar to macrophages?
Dendritic cells
What are the first immune cells to encounter a pathogen?
What is it called when there is an increased neutrophil count in the blood?
What is it called when the inflammatory cytokines stimulate more immature neutrophils called bands from the bone marrow. it is an increased ratio of bands to mature neutrophils?
shift to the left
What is adhesion for "stick and roll". adhesion molecules?
What is secreted by basophils and mast cells during allergic reactions?
What is found in the cell wall and is triggered during every inflammation response. it generates prostaglandin, thromboxane, and leukotrienes?
arachidonic acid
What is a large family of transmembrane proteins that mediate adhesion of cells to the extracellular matrix. adhesion molecules?
What is the site on the surface of an antigen that is specifically recognized by an immune cell which in turns creates an immune response?
What are the cells that secrete antibodies at a rate of 2000 per second after an infection and only live for a few days?
plasma cells
What are small polypeptides that cause powerful vasodilation?
kinins (page 195)
What is it called when blood is escaping the blood vessel?
What is the coating of a pathogen (antigen) by antibodies so macrophages will phagocytosis the pathogen?
What is an accumulation and adhesion of leukocytes to the epithelial cells of blood vessel walls at the site of injury in the early stages of inflammation?
What are the movement of cells according to chemical gradients that attract them?
What maintains the harmony of input & output?
-thirst drive from hypothalamus
-output of urine by kidneys
What are the (3) compartments that water moves through?
-intracellular (in body cells) 60%
-extracellular (in-between cells/in BV) (interstitial & intravascular)
-transcellular (saliva, CSF, synovial)
What is a solute?
substance that is dissolved in another substance
Name some solutes found in the body?
What is a solvent?
a liquid, solid or gas that dissolves the other liquid, solid or gas
What is the major solvent in the body?
What are the functions of water?
-carrier vehicle for wastes (urine, feces, lungs, skin)
-cushion for protection
-temperature regulation
What is diffusion?
free movement of particles down a concentration gradient (high to low concentration) until equilibrium is reached.
What is osmosis?
movement of water molecules across a membrane (water follows salt)
What is osmolarity?
measure of degree of concentration (number of particles per kilogram of solvent)
What hormone regulates osmolarity?
ADH. this hormone is secreted by hypothalamus & promotes water retention (water-saving)
What happens to water when osmolarity in the ECF>ICF?
water flows out of the cells to maintain balance
What happens to water when osmolarity in the ECF<ICF?
water flows into the cell to maintain balance
What happens to water when osmolarity in the ECF=ICF?
no movement takes place since osmolarity is balanced
What are osmoreceptors?
receptors in the CNS that responds to change in osmolarity of the plasma. when activated they signal hypothalamus to increase release of ADH.
What is the renal role in fluid retention?
-very important in regulating water balance
-ADH is released to increase the permeability of the renal collecting ducts which allows water to be reabsorbed into the plasma
-Renin secreted by kidneys cause Na+ retention therefore retaining more water
What happens to water movement when isotonic IV solution is infused?
there is no movement in water
What happens to water movement when hypotonic IV solution is infused?
water will move into the cells
What happens to water movement when hypertonic IV solution is infused?
water will move out of the cells
What is the main regulator of ECF osmolarity?
What is the main regulator of ICF osmolarity?
What is hydrostatic pressure?
-pressure exerted by a liquid
-pushing pressure for water
-generated by BP
-pushing fluids into interstitial spaces
What is oncotic pressure (colloid osmotic pressure)?
-pressure produced by passage of fluid from less concentration to higher concentration
-pulling pressure for water
-generated by proteins (typically albumin)
What helps maintain oncotic pressure?
plasma proteins
Why is hydrostatic pressure > oncotic pressure in arterioles?
-hydrostatic pressure is greater bc arteries are delivering nutrients to tissues (pushing out)
Why is oncotic pressure > hydrostatic pressure in veins/venules?
-oncotic pressure is greater bc it is pulling in fluid from interstitial space to return to the circulation
What picks up the leftover fluid in the interstitial space?
What is edema?
excess fluid in the interstitial compartment
What is ascites?
abnormal accumulation of fluid in peritoneal cavity. typically problem with oncotic pressure related to lack of albumin. fluid stays in abdomen.
Why might a pt in liver failure have edema?
-lack of albumin
-albumin is protein in vessel that pulls fluid back into vessel
What are the (4) mechanisms that cause edema?
-increased capillary pressure (HF, pregnancy)
-decreased colloid osmotic pressure (liver failure)
-increased capillary permeability (burns, allergic reactions)
-lymphatic obstruction (inflammation, removal of lymph)
What is isotonic dehydration?
loss of both ECF fluid and solute is proportionate
What is the most common type of dehydration?
isotonic dehydration
What are the causes of isotonic dehydration?
-NPO status
-poor PO intake
What is the "3rd spacing" of fluid?
movement of fluid into the interstitial space (pleural, peritoneal, cardiac)
What are the clinical manifestations of isotonic dehydration?
-sudden weight loss
-decreased BP
-skin tenting
What will a clinician see in labs of someone with isotonic dehydration?
-decreased BP
-increased Hct (increased concentration)
-increased plasma protein levels
What treatment will be done for someone with isotonic dehydration?
-isotonic fluid replacement
-fluid replacement
What is the second most common type of dehydration?
hypertonic dehydration
What is hypertonic dehydration?
-cellular dehydration
-more water loss in ICF than ECF
-more solute in ECF (water follows salt)
-cells shrink
What are the causes of hypertonic dehydration?
-excessive perspiration
-severe hyperglycemia
-hypertonic fluid replacement (TPN)
What are the clinical manifestations of hypertonic dehydration?
-hypernatremia (high Na+ in ECF)
-intense thirst
What is the least common type of dehydration?
hypotonic dehydration
What is hypotonic dehydration?
-cellular swelling
-more solute in ICF (water follows salt)
-solutes leave ECF (Na+ & K+)
-cells swell
What is the most likely cause of hypotonic dehydration?
renal failure
What is the worst problem with hypotonic dehydration?
-not enough solute in ECF
-water moves to ICF
-causes cerebral edema
In a pt with a brain injury, why is it so important to infuse an appropriate IV fluid?
you do not want to create more swelling
What would happen if a hypertonic solution was infused to a pt. with a brain injury?
-decreased cellular swelling
-water will be pulled out of cells
-decrease pressure on the brain
What would happen if a hypotonic solution was infused to a pt. with a brain injury?
-increased cellular swelling
-creating more pressure on the brain
Why is 0.9% a good first line choice of IV fluid for restoration/maintenance of fluid balance?
-this will not create any change in fluid movement
-safe way to go until sure of diagnosis
What is the importance of Na+ (sodium balance)?
-determines plasma osmolality
-maintains membrane potential
-maintains neural conductance
The regulation of plasma sodium is mainly achieved by what?
What are the potential causes of hyponatremia?
-excessive sweating
-excessive hypotonic fluid (0.45% NaCl)
-diuretic therapy
What are the clinical manifestations of hyponatremia?
-cerebral edema (confusion, HA)
-cellular swelling
-peripheral/pulmonary edema
-mm weakness
What are the potential causes of hypernatremia?
-decreased ADH secretion
-excessive Na+ diet
-renal failure
What are the clinical manifestations of hypernatremia?
-cellular shrinking
-increased thirst
-mental status change
-mm twitching
What is the importance of K+ (potassium balance)?
-cardiac excitability
-neuronal excitability
-mm excitability
-ICF osmotic pressure
What are the potential causes of hypokalemia?
-decreased intake
-K+ depleting drugs
What acid-base imbalance is associated with hypokalemia?
What are the clinical manifestations of hypokalemia?
-mm cramping
-fatigue/weakness (respiratory mm)
-cardiac irritability (dysrythmias)
-paralytic ileus
What is treatment for hypokalemia?
-replace K+
-must be diluted in IVF's
What are the potential causes of hyperkalemia?
-renal failure
-excessive drugs that preserve K+
What acid-base imbalance is associated with hyperkalemia?
acidosis: drop in pH causes K+ to move out of cells into vascular space.
What are the clinical manifestations of hyperkalemia?
-cardiac depression
-cardiac dysrhythmias
-cardiac arrest
-mm weakness
What is the importance of Ca++ (calcium balance)?
-cell membrane permeability
-nerve impulse transmission
-blood coagulation
What (2) forms of Ca++ must we consider as nurses?
-Ionizied Ca2+: controls neuromuscular function, cardiac controlled neuron impulses
-Non-ionized calcium: bound to albumin (extracellular)
What are the potential causes of hypocalcemia?
-acute pancreatitis
-inadequate diet (vitamin D or Ca++)
What are the clinical manifestations of hypocalcemia?
-hyperexcitable neurons (cramping, seizures)
-cardiac changes
-Trousseau (facial nerve twitches)
What are the potential causes of hypercalcemia?
-renal insufficiency
What are the clinical manifestations of hypercalcemia?
-hypoexcitable neurons (mm weakness)
-renal stones
-CNS depression
-cardiac changes (bradycardia)
-fracture risk
What is pH?
It is the power of hydrogen
Why do we care about pH?
-it represents the activity of H+ ions.
-pH decreases-H+ increases
-pH increases-H+ decreases
As H+ ion concentration increases, pH_____________
What are the types of acids produced by cellular metabolism?
-carbonic acid (H2CO3)
-metabolic acids (phosphoric acid H3PO4) & (sulfuric acid H2SO4)
pH of systemic arterial blood is normally slightly___________________
What is the normal pH?
What are the 3 systems involved in acid‐base balance?
-bicarbonate buffer system
-respiratory system
-renal system
The bicarbonate buffer system, respiratory system, and renal system work together all the time to balance what?
What is the function of an acid in maintaining acid‐base balance?
-fluid is alkaline
-acid releases H+
What is the function of a base in maintaining acid‐base balance?
-fluid is acidic
-base takes up H+
What is the most important system in maintaining pH?
bicarbonate buffer system
What are the main players in the bicarbonate buffer system?
-bicarbonate acid
-carbonic acid
What is the normal ratio of bicarbonate acid & carbonic acid required to maintain balance?
20:1 (HCO₃:H₂CO₃)
What systems are in place to excrete acid?
-respiratory system
-renal system
What is the respiratory contribution to acid-base balance? How fast does this happen?
-the lungs expire CO₂ and H₂O which is broken down from carbonic acid
-only takes seconds/minutes to respond
The lungs can only secrete which acid?
carbonic acid
Which receptors control the respiratory contribution to acid-base balance?
Baroreceptors sense the change in what?
-sense change in pressure
Chemoreceptors control what?
-rate & rhythm of respiration
How do chemoreceptors sense the pH?
through PaCO2 in the blood
The chemoreceptors sense changes in what?
The osmoreceptors sense the change in what?
osmolality (concentration)
What is the best indicator of the lung's effectiveness in correcting carbonic acid (H₂CO₃) levels (ABG)?
What does it mean to say that H₂O and CO₂ are volatile acids?
-carbonic acid must break down into H₂O & CO₂
-they are broken into gases and then excreted by the lungs
When PaCO₂ goes up, what happens to pH?
pH decreases
When PaCO₂ goes up, what happens to PaO₂?
PaO₂ decreases
What is the renal contribution to acid base balance? How quickly can it work?
-kidneys can excrete any acid but carbonic acid
-slow response (3-5 days)
What type of acids can the kidneys excrete?
metabolic acids
How does the kidney secrete acid?
-directly excrete metabolic acids
-reabsorption of filtered HCO₃ as H+ secreted into renal tubular filtrate
-formation of titratable acid
excretion of NH₄ in urine
As H+ is secreted into the renal tubular filtration, ________ is reabsorbed?
Why can't H+ be secreted in its free form within urine?
it would damage the renal tubular cells of the kidneys. instead it is excreted in a buffer form attached to NH₃.
How is H+ secreted in the renal system?
-HCO₃ moves through nephron
-H+ is secreted
-H+ is only secreted after HCO₃ is reabsorbed
-H+ is buffered with NH₃
Why is NH₄ guaranteed to be excreted within urine?
it is lipid soluble and will not go back into kidney tubules easily.
What is the best indicator of the kidney's effectiveness for excretion of metabolic acids (ABG report)?
What is the response of the Buffer System to maintain acid-base balance?
-Buffers: low pH=basic portion of buffer accepts H+. high pH=acidic portion of buffer releases H+.
What is the response of the Respiratory System to maintain acid-base balance?
-Respiratory System: low pH= increased RR to remove carbonic acid. high pH=decreased RR to retain carbonic acid
What is the response of the Renal System to maintain acid-base balance?
-Renal System: low pH=increased secretion of H+ from ECF into renal tubular fluid. increased reabsorption of HCO₃ from renal tubular fluid back to ECF. increased production of NH₃. high pH= decreased secretion of H+. decreased reabsorption of HCO₃. decreased production of NH₃.
What is correction in acid-base balance?
correction of the imbalance occurs when the original problem (cause) is fixed within that system.
What is compensation in acid-base balance?
compensation of the imbalance does not fix the problem, but can restore the imbalance to normal
When the acid-base imbalance is within one system, how does compensation occur?
when the imbalance is offset in one system, the other system kicks in to compensate.
What acid-base imbalance is associated with diarrhea?
probably acidosis bc intestinal fluids are rich in bicarbonate. loss of bicarbonate leads to diarrhea.
What acid-base imbalance is associated with vomiting?
probably alkalosis bc stomach acids are acidic. loss of that would create alkalosis.
What is it when too much carbonic acid accumulates in the blood (increase PaCO₂)?
respiratory acidosis
What might cause respiratory acidosis?
anything that decreases ventilation or respiration (ex.Rt HF)
Why is respiratory acidosis dangerous for the brain?
-excess CO₂ enters the brain cells, leading to intracellular acidosis
-drops the pH of the CSF
-cerebral vasoconstriction (decreases blood flow)
-CNS depression (lethargy/disoriented)
-HA/blurred vision
What do the kidneys do to help compensate for respiratory acidosis?
-excreting more metabolic acid
-causes increased HCO₃ in serum
-takes 3-5 days (slow process)
How can respiratory acidosis be corrected?
therapy required to restore metabolic balance. lactate solution used in therapy is converted to bicarbonate ions in the liver.
What is respiratory alkalosis?
not enough carbonic acid in blood (decreased PaCO₂)
What causes respiratory alkalosis?
anything that causes hyperventilation can lead to decreased carbonic acid.
Why do patients exhibit lightheadedness & mm cramps in respiratory alkalosis?
because the CSF becomes alkaline
What do the kidneys do to compensate with respiratory alkalosis?
kidneys conserve H+ & eliminate the HCO₃ in the urine.
How can respiratory alkalosis be corrected?
HCO₃ are replaced by Cl- (restore lung function)
What is metabolic acidosis?
too much metabolic acid, due to gain of acid or loss of base
What might cause metabolic acidosis?
-intake of acids or substances converted to acids
-increased rate of metabolism
-production of unusual acids secondary to altered normal processes
-decreased renal excretion of acid
-HCO₃ can be lost in urine or through GI tract (vomit/diarrhea)
Why is metabolic acidosis dangerous to the brain?
decreased pH of CSF can lead to
-abdominal pain
-lead to coma
What do the lungs do to compensate with metabolic acidosis?
hyperventilate to excrete carbonic acid
How can metabolic acidosis be corrected?
lactate solution used in therapy is converted to bicarbonate ions in the liver
What is metabolic alkalosis?
too little metabolic acid, from loss of acid or gain of base
What might cause metabolic alkalosis?
-acid can be lost to urine & GI tract
-acid can be moved into cells to decrease levels in blood
Why is the onset of metabolic alkalosis symptoms slower?
bicarbonate ion cross membranes slower than CO₂
What do the lungs do to compensate with metabolic alkalosis?
decrease RR to retain carbonic acid
How can metabolic alkalosis be corrected?
restoring renal function
What are pressure ulcers?
localized injury to the skin and/or underlying tissues usually over a bony prominence. caused by unrelieved pressure that occludes blood flow to the tissues.
What is the Braden Scale and how is it used?
it is a scale used to determine how at risk a pt is to receive a pressure ulcer. it is used by using the 6 categories:
-sensory perception
What Braden scale score corresponds to "at risk", "moderate risk", "high risk" or "very high risk".
at risk: 15-18
moderate risk: 13-14
high risk: 10-12
very high risk: 9 or below
What are the risk factors for pressure ulcers?
-advancing age
-elevated body temp
-impaired circulation
-prolonged surgery
-low diastolic bp
What intervention may be used if a patient is at very high risk for developing a pressure ulcer?
-turn every hr
-obtain PT consult, out of bed
-moisturize skil daily and PRN
-control moisture
-nutrition consult
-minimize friction/shear
-order low air loss bed
Deep Tissue injury
purple or maroon localized area of discolored intact skin or blood filled blister
Stage I (Deep Tissue Injury)
intact skin with nonblanchable redness of localized area (over bony area)
Stage II
partial thickness loss of dermis presenting as a shallow open ulcer w/red pick wound bed.
Stage III Pressure Ulcer
full thickness tissue loss
Stage IV Pressure Ulcer
full thickness tissue loss with exposed bone, tendon or mm
What do you assess during wound assessment?
-% viable vs. non-viable
You always clean wounds with what?
normal saline
Describe language in which we describe wounds. (standardized language).
-length (head to toe)
-width (hip to hip)
-depth (deepest point)
-tunneling & undermining (use clock)
-color of ulcer base (red, yellow, black)
-drainage (amount, color, odor)
What type of tissue is red, moist, beefy?
granulation tissue
What type of tissue indicates progression to healing?
granulation tissue (red)
What type of tissue is yellow, stringy substance that is attached to wound bed?
slough tissue
What does black tissue indicate?
necrosis & it must be removed for healing
What does periwound mean?
skin around wound
What are some words to describe the periwound (skin around wound)?
If a pt is complaining of increased pain at the wound site. The wound has increased drainage but it is not foul smelling. The RN may suspect what?
possible wound infection
What do we assess with the drains of wounds?
-amount of drainage
-description of drainage
What are some other things needed to be assessed with wound healing?
-circulation (blood volume, etc)
-nutrition (protein intake)
-medication & disease states
How do you know the wound is healing well?
-wound bed is "beefy red"
-wound heals from edges
-decreasing pain
-free of s/s of infection
What is HAPU?
Hospital Acquired Pressure Ulcers (HAPU)
What is the primary difference between a wound and a pressure ulcer?
What are never events?
events that should never happen
What do we use to assess risk for pressure ulcers?
Braden Scale
What is the first step in the prevention of pressure ulcers?
risk assessment
Which cell line are the anemias linked?
3 causes of anemia
-impaired RBC production
-blood loss
-increased RBC destruction
What is anemia?
reduction in the total number of circulating erythrocytes OR decrease in quantity/quality of the Hgb contained in RBC.
Discuss relative vs. absolute anemia.
-increase in plasma volume (pregnancy)
-increase in red cell mass due to blood loss
-decreased production/elevated RBC destruction
Compensation (and why) in anemia: (slide 14)
1. Fluid shift increase in volume ICF to ECF
2. Cardiac -thinner, less viscous blood moves faster
-increase preload to the heart
-increase HR
3. Pulmonary
-works stronger/faster to meet O2 demands
-clear pulmonary congestion
4. Peripheral vasculature -vasoconstriction to shunt blood to essential organs
5. Kidney -renin-angiotensin-aldosterone (RAA) is secreted to retain sodium and water.
-increases volume
6. Oxyhemoglobin dissociation -shift to right
-increase O2 to tissues
What is Sickle Cell anemia?
hemoglobinopathy; AA variant makes RBC "sticky"
What goes wrong in SSA?
precipitating event causes RBC to become sickled. when stimulus is removed; cells return to normal shape unless chronic
What are some precipitating events to a sickle cell crisis?
- low PaO2
-vascular stasis (inactivity)
-cold environmental temp
-strenuous exercise
Micro infarcts produce what?
Describe the vicious cycle in SSA
-increased capillary obstruction
-increased hypoxia
-increased sickling
*RBC live for 20 days vs. 120 days
*cells attempt to pass the spleen; spleen lyses them
*increase cell lysis; jaundice & anemia
*increased hemolysis =anemia= hypoxia
*sickled cells cause micro infarcts (producing pain)
What are the signs and symptoms of SSA?
-low Hct
-ischemia/tissue hypoxia
-hardened spleen
-pulmonary infarcts
-chest pain
-renal ischemia w/low GFR
If blood transfusion is a treatment, these patients are at risk for which hypersensitivity reaction?
type II hypersensitivity
Iron Deficiency Anemia: definition
caused by iron (Fe)deficiency caused by:
-decreased intake
-decreased absorption
-excessive Fe loss
-increased iron needs
What goes wrong with Iron Deficiency Anemia?
wo adequate Fe, new RBC & Hgb are affected. cells become microcytic & hypochromic (small wo much Hgb)
What do cells look like in Iron Deficiency Anemia?
What happens to hgb in Iron Deficiency Anemia?
decreases; Fe is necessary for formation of Hgb/hypochromic
What would the CBC show for Iron Deficiency Anemia?
smear will detect hypchromic/microcytic cells
What would the retic count show for Iron Deficiency Anemia?
decreased reticulocytes are immature RBC
Late vs. early signs and symptoms for Iron Deficiency Anemia.
-Hct >30
-poor concentration
-Hct low
-atrophic glossitis (red, swollen, glossy)
-chelitis (inflammed lips)
-pica (eating non-nutritional substances)
Fe is important to help hepatic metabolism of drugs in the P450 system.
no answer, the answer is on the card! :)
Know foods that are enriched in Fe+3 for patient counseling
-lean red meat
-leafy green vegetables
Pernicious anemia: definition
macrocytic anemia due to vitamin B12 deficiency
What goes wrong in Pernicious Anemia?
-vit. B12 & folate are important for DNA development. wo adequate intake; DNA synthesis is impaired & mitosis is dysregulated. result is immature cells only grow in size are released (abnormal) large bone marrow cell.
-deficiency could result from lack of instrinsic factor secreted by stomach for absorption of B12
What do cells look like in Pernicious Anemia?
What are the causes of Pernicious Anemia? (2)
-decreased intake of B12
-decreased absorption of B12
What would the CBC show for Pernicious Anemia?
smear will show macrocytosis, hypersegmented granulocytes
What would the serum B12 level show for Pernicious Anemia?
decreased B12
Vitamin B21 __________be manufactured by the body, it must be obtained from ________ sources.
1. cannot
2. dietary
What is megaloblastic madness?
deficiency of B12 causing neurologic changes.
-altered personality
-spastic weakness
Compare Folate Deficiency to Pernicious Anemia
-Pernicious Anemia
decreased B12 due to decreased intake or decreased absorption.
-Folate Deficiency
malabsorption of dietary folic acid due to lack of intake or absorption
What symptom will pernicious anemia have that FD does not?
neurological impairments
Anemia of chronic disease: definition
chronic inflammatory and infectious diseases, malignancy, can cause anemia of chronic disease
What is hepcidin, and how might it be a mechanism for Anemia of Chronic Disease?
protein that controls Fe absorption and is increased in hypoxia/inflammation. higher hepcidin levels result in less iron absorbed.
How do the cells look on a smear with Anemia of Chronic Disease?
on the smear they are nuclear formation or stacking of cells.
Coagulopathies: definition
deficiencies in one or more components that regulate hemostasis.
What is ITP vs. TTP?
-Immune Thrombocytopenic Purpura (ITP)
autoimmune destruction of platelets
-Thrombotic Thrombocytopenic Purpura (TTP)
rare disorder where platelets clump together inappropriately
Compare the symptoms (bleeding vs. clumping) with ITP and TTP.
ITP Symptoms
-large bruises
-petichial rashes
-bleeding gums
-intracranial bleed
-splenic sequestration (spleen holds 90% of cells vs. 30%)
TTP Symptoms
-purpura (red/purple patches)
-renal failure
What goes wrong with ITP?
normal # of platelets are made. IgG is made that directs toward platelets. the coating on platelets make them more susceptible. spleen attacks and lyses the platelets.
What goes wrong with TTP?
mechanism unknown. platelets clump together which keeps them out of the normal circulation. platelets are unable to respond to injury.
What goes wrong with TTP?
mechanism unknown. platelets clump together which keeps them out of the normal circulation. platelets are unable to respond to injury.
Lab: Hgb count
-usually ordered w/ CBC
-diagnosis chronic anemias or polycythemia
-measures amount of Hgb in the peripheral blood (reflects RBC count in blood)
Lab: Hematocrit (Hct)
measure the % of total blood volume that is made up of RBC
Lab:RBC count
-usually ordered w/CBC
-count of number of circulating RBC in 1mm to the power of 3 of peripheral venous blood.
Lab:CBC w/differential
-series of tests done on peripheral blood.
-provides tremendous information on hematologic system/organs systems.
Lab: WBC count
-has two components
-count of total number of WBC in 1mm to the third power in the peripheral blood.
-the other is differential count which measures the % of each type of leukocyte present
Lab: Platelet count
count of the number of platelets per cubic milliliter of blood
Lab: Erythrocyte Sedimentation Rate (ESR)
-rate at which RBC settle in saline or plasma over a specific time period.
Lab: Prothrombin time (PT)
-used to evaluate the adequacy of the extrinsic system and common pathway in the clotting mechanism.
Lab: Partial Thromboplastin Time (PTT)
-used to assess the intrinsic system and the common pathway of clot formation.
What is the function of the kidneys?
-maintains fluid & electrolyte balance
-disposal of water-soluble wastes
-EPO production
-vitamin D activation
-20% total glucose production
What are the functions of the nephron?
-filter water soluble substances from blood
-reabsorption of filtered nutrients, water, and electrolytes.
-secretion/excretion of wastes or excess substances into filtrate
What are afferent arterioles?
they transport blood into the glomerulus
What are efferent arterioles?
they transport blood out of the glomerulus
What is normal GFR?
125 ml/min
How much Na+ & H₂O absorption occurs at the proximal convoluted tubule (PCT)?
How much Na+ & H₂O absorption occurs at the Ascending Loop of Henle?
How much Na+ & H₂O absorption occurs at the distal convoluted tubule (DCT)?
How much Na+ & H₂O absorption occurs at the collecting duct?
What is the goal of GFR?
to generate enough pressure for urine formation
How does systemic BP affect GFR?
if there is an increase in BP it will in turn increase GFR
What vasoconstricts to keep GFR constant?
afferent arterioles
The driving force of filtration in the glomerulus is what?
hydrostatic pressure
What gets filtered in the kidneys?
-electrolytes (H+, K+)
-solutes (creatinine, urea, glucose)
-organic acids
What does not get filtered in the kidneys?
negatively charged particles (protein) or particles too large to pass (RBC, WBC, platelets)
How does each individual nephron regulate GFR?
the macula densa in the DCT sense changes in the NaCl delivery and JG cells (baroreceptors) they are detecting low or high volume
What happens if the GFR is too low?
-too much tubular filtrate is reabsorbed
-glucose & waste products would be out of balance
What happens if the GFR is too high?
-all filtrate would be lost to urine (good & bad)
What is the role of the JG cells?
-they are baroreceptors
-they synthesize, store, and secrete renin
-smooth mm cells in walls of afferent arteriole
What is the role of the macula densa?
-sense changes in osmolality (NaCl)
-stimulate renin release from JG cells
Renin causes the conversion of what?
AI to AII which leads to potent vasoconstriction
In arterial blood, what is the best indicator of how well the lungs are excreting metabolic wastes?
PaCO₂ in the blood
In the arterial blood, what is the best indicator of how well the kidneys are excreting metabolic wastes?
HCO₃ in the blood
How does the kidneys excrete metabolic wastes?
it can excrete H+ attached to a NH₃ if the body is to acidic.
What is the significance of NH₄?
excess H+ is attached to NH₃ to make NH₄ and excrete it through the kidneys.
What is the significance of HPO₄?
(handbook pg. 619-620)
this is used for an important buffer system. the excretion of H+ will be bound to a filtered phosphate and excreted in the urine. this excretes acid and gain bicarbonate
What is the RAAS pathway?
1. JG cells sense decreased BP
2. JG cells secrete renin
3. renin causes angiotensinogen to be converted to AI
4. AI circulates the lung and ACE converts it to AII
5. AII circulates to adrenal cortex & stimulates secretion of aldosterone
6. aldosterone increases reabsorption of Na+
7. therefore, water is retained & blood volume increases
What is the role of aldosterone in the RAAS pathway and where is it secreted from?
-aldosterone increases reabsorption of Na+ (DCT)
-secreted from adrenal cortex
On which part of the tubular system does aldosterone act on?
-distal convoluted tubule Na+ is reabsorbed(DCT)
-collecting duct K+ is excreted
What is the role of ADH in blood volume maintenance?
-ADH is a vasopressin
-it is secreted from posterior pituitary in response to increased osmolality by the osmoreceptors in the hypothalamus
On which part of the tubular system does ADH act on?
collecting duct where it stimulates water reabsorption
Discuss the process of voiding (micturition).
Most is under ANS and some is under Somatic
1. bladder fills
2.fullness felt (trigone stretched)
3. afferent signal to the brain
4. contraction of detrusor (muscarinic)
5. relaxation of internal sphincter (muscarinic)
What is the SNS control of the bladder?
"hold it" (NE)
-relaxes detrusor mm (Beta 2)
-contracts external sphincter (Alpha 1)
What is the PSNS control on the bladder?
"void" (Ach)
-contracts detrusor mm (muscarinic)
-relaxes internal sphincter
What is the only anatomic part of voiding that is under somatic/voluntary control?
external sphincter
What are the characteristics of urine?
-specific gravity 1.010-1.030
What are the protective mechanisms associated with urine?
-voiding flushes out pathogens
-pH (acidic)
-high concentration of UREA
Compare gender anatomical differences for risk of UTI's?
women have a shorter urethra then men therefore women are more at risk than men. Prostate secretions are antibacterial.
What are some risk factors for UTI's?
-women: failure to void after sexual activity
-men: rectal sex (no condom)
-kidney stones
-neurobenic bladder (voiding dysfunction)
What risk factor for UTI's are nurses capable of preventing?
What are the s/s of a UTI?
-cystitis (inflammation of bladder lining)
-low back pain
-cloudy and/or strong odor urine
-pyuria (WBC in urine)
-30% is asymptomatic
What is pyelonephritis?
infection of the renal pelvis, calices, parenchyma
What are the s/s of pyelonephritis?
-pt looks sick
-back pain
What is the HALLMARK symptoms of pyelonephritis?
CVA tenderness (costovertebral angle tenderness)
What is any interference with urine flow at any site along the urinary tract leading to accumulation of urine behind the obstruction?
UT obstruction
What is hydronephrosis?
enlarged, swollen kidney from backed up urine
What is hydroureter?
complete obstruction of ureter; accumulation of urine, ureter distended
What are the consequences of UT obstruction?
there can be back pressure into the kidney, which can decrease GFR, leading to renal failure.
Where do stones form?
they can form anywhere but typically in the ureters
What is the most common type of kidney stone?
calcium oxalate stones
What is hypercalciuria?
calcium oxalate stones
What are the risk factors for hypercalciuria?
-increased GI absorption of Ca++
-increased demineralization of Ca++ from bone
-defect in tubular secretion from kidneys
-high levels of uric acid
What characteristic of urine will favor calcium oxalate stone formation?
alkaline urine
What is hyperuricemia?
uric acid stones
What is the significance of a high purine diet with uric acid stones?
increase purine metabolism from high protein intake produces more uric acid (rich in meats, liver)
What characteristic of urine with favor supersaturation and stone formation in uric acid stone?
acidic urine
What is a staghorn calculus?
-a stone formed in the renal pelvis shaped like a horn
-made from magnesium-ammonium-phosphate mix (struvite stone)
-may be caused from a gram - bacteria
What is glomerulonephritis?
inflammation of the glomerulus
Glomerulonephritis is always accompanied by _________ GFR and ____________ creatinine.
What is the cause of acute glomerulonephritis?
strep infection
What is the mechanism of acute glomerulonephritis?
-type III hypersensitivity
-Ab/Ag complex trapped in glomerulus in basement membrane
-inflammatory response (complement cascade)
-glomerulus is compromised & damaged
-the damage allows RBC, WBC & protein into the urine
The glomerular "leakiness" in glomerulonephritis allows what to happen?
RBC, WBC & protein into the urine
What are the clinical manifestations of glomerulonephritis?
-typically 7-10 days after strep throat
-hematuria & proteinuria
-oliguria from lowered GFR (<400mL/24 hrs)
-RBC casts
-increased lipids
Why does edema happen with glomerulonephritis?
-protein loss
-less colloid osmotic pressure
Why is there increased serum lipids with glomerulonephritis?
-decreased albumin
-liver overproduces to compensate
Why does HTN happen with glomerulonephritis?
-increases protein loss
-RAA kicks in
-Na+ & H₂O are retained
What is chronic glomerulonephritis?
fibrotic tissue development in the glomerulus leading to permanent decrease in GFR
Where do casts form?
only in DCT or collecting ducts
Why do casts form in glomerulonephritis?
leakage of RBC from glomerulus or severe tubular damage
What type of casts form in glomerulonephritis?
RBC cast
Why do casts for in pyelonephritis?
inflammation of the kidney
What type of casts are typical in pyelonephritis?
WBC cast
What is acute renal failure (ARF)?
rapid onset renal failure
What is chronic renal failure (CRF)?
slow onset renal failure
In acute renal failure (ARF) what are 2 major problems that can kill your patient quickly?
-hyperkalemia (high K+)
-metabolic acidosis (high H+)
What are the levels of GFR with chronic renal failure (CRF)?
decreased by 75%
What determines end-stage renal disease (ESRD)?
when GFR is decreased by 90% with GFR <10ml/min
What are the 2 major causes of chronic renal failure (CRF)?
What is Benign Prostatic Hyperplasia/Hypertrophy (BPH)?
enlargement of the prostate (result of age, exogenous drugs testosterone) that puts pressure on the urethra
What are the clinical manifestations of Benign Prostatic Hyperplasia/Hypertrophy (BPH)?
-weak urinary stream
-abdominal "pushing" to move urine
-urinary hesitancy
-incomplete bladder emptying
-urgency, frequency
Lab: serum creatinine
-test measures creatinine in the blood
-estimates GFR
-normal adult 6-25
Lab: serum BUN
-test measures amount of urea in blood
-BUN is related to liver and kidney function
-BUN will be increased in renal diseases
-normal adult 10-20mg/dL
Lab: urinalysis
-involves multiple tests on the urine
-clean catch is preferred
-color indicates concentration (straw color or amber color)
-clear is normal. cloudy is abnormal (may indicate pus)
-foul odor is abnormal
-pH is normally 4.6-8.0
Lab: UA for stones: what might be seen?
-pH (maybe alkaline or acidic)
Lab: KUB
-x-ray used to detect obstructions
-kidney ureter and bladder
What is shock wave lithrotripsy?
-shock waves breaks stones into smaller pieces to pass through ureters.
-process is very painful
Lab: PSA
-prostate-specific antigen
-increased levels with prostate cancer
-every male has PSA
What is inflammation of the urothelium (lining of the bladder) resulting from infection, irritation, presence of a foreign body, or trauma?
What is an infection of the kidney medulla or cortex?
What is also known as urination?
What is the ability to retain a bodily discharge voluntarily?
What is bladder dysfunction caused by a lesion at any level in the nervous system?
neurogenic bladder
What is the condition where urinary calculi are formed or located anywhere in the urinary system?
What is also known as painful urination?
What is known as pus in the urine?
What is the term used to describe how often a patient is urinating?
What is a strong and immediate urge to void brought about by involuntary detrusor overactivity?
What is it called when a patient abnormally needs to urinate in the middle of the night?
What is it called when a healthcare provider taps on the area over the kidneys and it produces pain?
CVA tenderness
What is it called when swelling of one kidney due to a backup of urine?
What is distention of a ureter with urine , usually resulting from an obstruction process?
What is concretion of crystals of material (uric acid, calcium phosphate) that initially from in the calices or pelvis of the kidneys?
renal calculi
What is the prescence of a stone or calculus anywhere in the urinary tract?
What is point or place at which something originates, accumulates, or develops, as the center around which calculi form?
What are tiny tube-shaped particles made up of WBC, RBC, or kidney cells? They are held together by a protein released by the kidney.
urine casts
What is urine output less than 500ml/day?
What is severe decrease or lack of urine output of less than 100ml/day?
What is it called when protein is present in the urine?
What is it called when blood is present in the urine?
What are increased levels of nitrogens waste products, especially urea nitrogen, in the blood indicative of impaired renal clearance?
What is the breakdown of mm fibers that leads to the release of mm fiber (myoglobin) into the bloodstream?
What is hyperthyroidism?
excess thyroxine production
What is hyperthyroidism also known as? (primary)
Graves' disease
What is the probable mechanism behind most primary hyperthyroidism?
autoimmune process
-increase levels of IgG, which bind to TSH receptors, mimicking TSH & increasing the production of T4
What is a goiter?
condition when thyroid grows larger than normal
-you will see exophthalmos (protrusion of eye) and associated lid lag
What is the most common cause of goiter worldwide?
lack of iodine in diet
What are the clinical manifestations of hyperthyroidism?
-increased metabolism/metabolic rate
-hand tremor
-hair is fine, thinning
-warm, moist baby-butt skin
What will you see in labs for Primary Disorder of Hyperthyroidism?
-TSH decreased
-Free T4 should be increased
What will you see in labs for Secondary Disorder of Hyperthyroidism?
-increased TSH
-increased T4
Why is more radioactive iodine taken up in pt w/hyperthyroidism?
if the thyroid is hyper secreting TSH, then it is more active to take up more iodine.
What is thyrotoxicosis?
special case of hyperthyroidism but with the added complications of co-morbidities such as infections, pregnancy, emotional stress, CV
What is hypothyroidism?
decreased thyroxine production
What is hypothyroidism also known as? (primary)
Hashimoto's thyroiditis
What is the probable mechanism behind most primary hypothyroidism?
autoimmune destruction of the thyroid gland by circulating anti-thyroid Ab's.
What are potential causes of primary hypothyroidism?
failure of the gland itself to produce thyroxine
-hasimoto's thyroiditis
-pt treated w/RA12 for Graves disease
-iodine deficiency
-medications: sulfonamides, lithium carbonate
What are potential causes of secondary hypothyroidism?
failure of the HPT axis
-hypothalamic lesion
-pituitary lesion
What will you see in labs for Primary Disorder of Hypothyroidism?
-increased TSH
-decreased T4
What will you see in labs for Secondary Disorder of Hypothyroidism?
-decreased TSH
-decreased T4
What are the clinical manifestations of hypothyroidism?
-slow mental activity
-weight gain
-dry coarse skin
-menorrhagia (heavy periods)
What is myxedema (fat face)?
cutaneous and dermal edema secondary to increased deposition of connective tissue components (hypothyroidism) also note it is non-pitting edema (especially noticed around eyes)
What does the adrenal cortex control? (3)
Hypersecretion of adrenal gland is also known as what?
Cushing's Disease
What is Cushing's Disease?
hypersecretion of the adrenal cortex. excess secretion of cortisol.
What is the mechanism behind hypersecretion of cortisol?
Normally the levels of ACTH are low due to negative feedback regulation. However, when this pathway is compromised, Cushing's syndrome might result because of hypersecretion of ACTH, which leads to higher free cortisol in the body
Why does having high ACTH and cortisol negatively affect the body?
The body becomes desensitized to the increased ACTH/cortisol levels & is unable to respond appropriately to stressors.
What is the role of exogenous glucocorticoid therapy?
it is a synthetic hormone that when used excessively you can develop Cushing's Disease.
What are the clinical manifestations of Cushing's Disease (hypersecretion of adrenal glands)?
-accumulation of adipose tissue
-protein wasting
-MS changes
Why would a pt become HTN with Cushing's Disease (hypersecretion of adrenal glands)?
cortisol increases the effects of catecholamines and aldosterone (retention of salt and water), increasing vasoconstriction and BP.
Hyposecretion of the adrenal cortex also known as what?
Addison's Disease (hypocortisolism)
What is the most concerning manifestation with Addison's Disease (hypocortisolism)?
-decreased cortisol
-decreased aldosterone
What is primary adrenal insufficiency?
-decreased cortisol, aldosterone & androgens
-increased ACTH
What is secondary adrenal insufficiency?
-decreased ACTH
-decreased cortisol
What are the clinical manifestations of Addison's Disease (hypocortisolism)?
-weakness & fatigue
-hypotension & hypovolemia (salt cravings)
Why do we see salt cravings in Addison's Disease (hypocortisolism)?
-decreased aldosterone
-the loss of Na+ and K+ causes excessive thirst
What is addisonian crisis?
severe hypotension leading to hypovolemic shock
What is hyperparathyroid?
excess PTH
What is primary hyperparathyroid?
adenoma/tumor in parathyroid gland
-increased PTH
-increased calcium
What is secondary hyperparathyroid?
r/t overstimulation of parathyroid gland
-chronic decreased calcium
-increased PTH (excess)
-this is often related to renal failure
What are the clinical manifestations of primary hyperparathyroid?
-abdominal groans
-psychic overtones
Describe mechanism of primary and secondary hyperparathyroidism.
Primary: increased PTH with increased serum calcium (the tumor keeps secreting PTH regardless of
serum level)
Secondary: increased PTH with decreased serum calcium. Chronic low serum Ca++ (from less absorption,
renal failure, or external cause) stimulates PTH secretion from parathyroids
What is hypoparathyroidism?
-decreased PTH
-decreased calcium
What are the most common causes of hypoparathyroidism?
-removal of thyroid or parathyroid gland
-ablation of gland
What happens to serum calcium with hypoparathyroidism?
What is the mechanism of primary hypoparathyroidism?
decreased PTH with decreased serum Ca++ (the parathyroid cannot respond to the
low Ca++)
What is the mechanism of secondary hypoparathyroidism?
decreased PTH with increased serum Ca++ (if serum Ca++ is high for some
reason, parathyroid does not respond Would be corrected with correction of serum Ca++)
What are the clinical manifestations of hypoparathyroidism?
-mm cramps
-chvostek's sign (facial twitching)
-trousseau's sign (bp cuff & fingers cramp)
Describe the role of insulin in energy metabolism.
-insulin allows glucose into the cell
-glucose allows for energy metabolism
How does insulin effect lipolysis?
suppresses lipolysis (break down of fat cells)
How does insulin effect glucoregulatory?
-CHO are broken down into glucose
-insulin turns on the glucose receptors
-receptors bring in glucose
Do RBC's and neural tissue need insulin?
no because those cells have GLUT 1 receptors which do not require hormone insulin for activation
Does adipose tissue, skeletal mm need insulin?
yes, to store glucose, lipids, and proteins
What is glucagon?
-secreted by alpha cells in pancreas when detected decrease blood glucose
-they stimulate liver to breakdown glycogen into glucose
Name 3 things that can cause hyperglycemia.
-ingestion of food
-gluconeogensis (production of glucose from fat or protein)
-glycogenolysis (glycogen broken into glucose)
What is the effect of the SNS and cortisol on blood glucose?
-blood sugar increases with increased cortisol levels
-stressful times the body needs more energy to fight or flight
What are ketones? Where and why are they made?
when cells break down fat to get energy because the cells are insulin resistance. the fat is broken down to free fatty acids and then broken down to ketones. ketones are acidic and prolonged release causes body to go into metabolic acidosis. they are made in the liver. they need to be used for energy. ketones then circulate in the blood.
A normal FBG is below__________mg/dL
FBG (fasting blood glucose) 60-100mg/dL
A normal postprandial (after eating) glucose does not rise above_____________mg/dL
What is Type I Diabetes?
hyperglycemia: destruction of beta cells in the pancreas. no insulin.
What are the clinical manifestations of Type I Diabetes?
-polydipsia (thirst)
-polyphagia (hunger)
What is osmotic diuresis?
increased urination caused by the presence of certain substances (glucose) in the small tubules of the kidney. glucose cannot be reabsorbed. osmotic pressure increases in tubule and causes water retention and reduces water reabsorption, increases urine output.
What is DKA (diabetic ketoacidosis)?
-increased ketones
-breath may have alcohol odor (fruity)
What may cause DKA?
-discontinue insulin medication
What is the mechanism of DKA?
when cells break down fat to get energy because the cells are insulin resistance. the fat is broken down to free fatty acids and then broken down to ketones. ketones are acidic and prolonged release causes body to go into metabolic acidosis. they are made in the liver. they need to be used for energy. ketones then circulate in the blood.
What is Type II Diabetes?
hyperglycemia with insulin resistance, lack of insulin
What is insulin resistance?
is increase over long time of insulin that receptors down regulate. the receptors that are available are very sensitive to insulin
Metabolic syndrome is also known as the___________syndrome
insulin resistance
What is the significance of metabolic syndrome?
increased risk of CAD, stroke and Type II Diabetes
Type 2 diabetes is increasing in parallel with_____________
What are the clinical manifestations of T2DM?
-polydipsia (thirst)
-polyphagia (hunger)
-peripheral neuropathy (careful for silent MI)
-blurred vision
-proteinuria, hematuria
What is HHNC?
-hyperosmotic, hyperglycemic, non-ketotic coma
-FBG >800mg/dL
-severe dehydration from osmotic diuresis and electrolyte shifting
-hypotension, hypovolemia
What is the mechanism of blood vessel damage in diabetes?
-chronic increased blood glucose
-glucose combines with RBC (glycosylation)
-increase in glycosylation
-end products of glycosylation is AGE's
-AGE's accumulate and allow for accelerated atherosclerosis
_______________will kill your patient faster than hyperglycemia
What are the clinical manifestations of hypoglycemia?
-MS changes
-poor focus
-sweating, cool
How do we treat it hypoglycemia?
conscious pt: glucose paste, OJ, coke
unconscious pt: IV glucose, IM glucagon
Principle of hemoglobin A1C test: how would you explain it to a patient?
this test will give us the average BS levels over 3 months
What are AGE’s?
advanced glycosylation end products
Macro vs. microvascular complications of diabetes
macro: accelerated atherosclerosis, HTN, CAD (gangrene and loss of digits)
micro: capillary membrane hypertrophy (diabetic nephropathy) AGE caused damage in glomerulus which results in leaky capillaries allowing RBC and protein to get into urine.
then diabetes retinopathy same mechanism as nephropathy. can cause hemorrhage and can lead to blindness.
diabetic neuropathy