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Diabetes Insipidus: A Comprehensive Guide for Nursing Students, Exams of Nursing

Widener University - DelawareNursing

A detailed overview of diabetes insipidus (di), a condition characterized by excessive urination and thirst. It covers the pathophysiology, causes, symptoms, diagnosis, treatment, and nursing care for di. Key features of di, diagnostic tests, medications, and nursing interventions. It also highlights the importance of monitoring i&o, electrolyte levels, and vital signs. Particularly useful for nursing students as it provides a comprehensive understanding of di and its management.

Typology: Exams

2024/2025

Available from 01/18/2025

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NURS 241 Exam 2 Exam Solved 100%
Correct!!
Negative Feedback Loop - ✔️✔️-Helps turn things on as well as turn them off.
Example: Traffic jam. You respond to a message that is already happened and may
start or stop things
-a mechanism by which a system regulates itself. ie. thermostat furnace example. Also
increased glucose and pancreas release of insulin example. Extra glucose is stored in
the liver and saved for future use.
Major Glands - ✔️✔️hypothalamus
pituitary gland
thyroid
parathyroids
adrenal glands
pineal body
reproductive glands (which include the ovaries and testes)
-All glands act in a similar manner. They sense a change in the body, a deviation from
homeostasis, and they release hormone, which then travels through the blood and bind
to their specific receptor and amplifies the signal in the target cell. Then the target cell
releases what the body needs. Then it is started and stopped by negative feedback.
Major Hormones Secreted by Glands - ✔️✔️-estradiol
-testosterone
-insulin
-growth hormone
-epinephrine
Primary vs Secondary Disease - ✔️✔️-Primary directly affects the gland
-Secondary a gland may be affected r/t another gland being affected
Diabetes Insipidus (DI) - ✔️✔️-Decreased response to or decreased release of ADH
(Vasopressin/AVP)
-Can be r/t the body not producing vasopressin = Central diabetes insipidus
-Kidneys not utilizing vasopressin = nephrogenic DI
-This is an uncommon disease
Central DI - ✔️✔️-damage to the pituitary gland or hypothalamus (anything in this area
can affect ADH control i.e. brain surgery, sarcoidosis, tumor, meningitis, head injury, or
inflammation) = damage to the 'central' site of ADH regulation
-body itself is not producing the vasopressin (pituitary)
-the production, storage, and release of ADH is altered
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Download Diabetes Insipidus: A Comprehensive Guide for Nursing Students and more Exams Nursing in PDF only on Docsity!

NURS 241 Exam 2 Exam Solved 100%

Correct!!

Negative Feedback Loop - ✔️ ✔️ -Helps turn things on as well as turn them off. Example: Traffic jam. You respond to a message that is already happened and may start or stop things

  • a mechanism by which a system regulates itself. ie. thermostat furnace example. Also increased glucose and pancreas release of insulin example. Extra glucose is stored in the liver and saved for future use. Major Glands - ✔️ ✔️ hypothalamus pituitary gland thyroid parathyroids adrenal glands pineal body reproductive glands (which include the ovaries and testes)
  • All glands act in a similar manner. They sense a change in the body, a deviation from homeostasis, and they release hormone, which then travels through the blood and bind to their specific receptor and amplifies the signal in the target cell. Then the target cell releases what the body needs. Then it is started and stopped by negative feedback. Major Hormones Secreted by Glands - ✔️ ✔️ -estradiol
  • testosterone
  • insulin
  • growth hormone
  • epinephrine Primary vs Secondary Disease - ✔️ ✔️ -Primary directly affects the gland
  • Secondary a gland may be affected r/t another gland being affected Diabetes Insipidus (DI) - ✔️ ✔️ -Decreased response to or decreased release of ADH (Vasopressin/AVP)
  • Can be r/t the body not producing vasopressin = Central diabetes insipidus
  • Kidneys not utilizing vasopressin = nephrogenic DI
  • This is an uncommon disease Central DI - ✔️ ✔️ -damage to the pituitary gland or hypothalamus (anything in this area can affect ADH control i.e. brain surgery, sarcoidosis, tumor, meningitis, head injury, or inflammation) = damage to the 'central' site of ADH regulation
  • body itself is not producing the vasopressin (pituitary)
  • the production, storage, and release of ADH is altered

Nephrotic DI - ✔️ ✔️ -damage to the "end" site of ADH, the kidneys

  • A defect in the kidney tubules -- the structures in your kidneys that cause water to be excreted or reabsorbed -- will make the kidneys unable to properly respond to ADH
  • Can be due to a genetic disorder of chronic kidney disorder
  • Certain drugs like lithium and demeclocycline can cause nephrogenic DI
  • kidneys are not utilizing vasopressin, IT IS present though. (there can be all of the vasopressin in the world, but the kidneys won't respond to it) Gestational DI - ✔️ ✔️ -Occurs ONLY during pregnancy and when an enzyme made by the placenta destroys ADH Drug-Related DI - ✔️ ✔️ -caused usually by lithium and demeclocycline
  • these drugs interfere with the response of the kidneys to ADH Antidiuretic Hormone (ADH/AVP/Vasopressin) - ✔️ ✔️ -this is a good thing; it holds onto water when needed
  • it is produced in the hypothalamus, and is a normally occurring hormone
  • it moves from the hypothalamus to pituitary to await being used
  • released when the body is dehydrated to hold on to water
  • concentrates the urine
  • i.e. caveman and runner examples Symptoms of Diabetes Insipidus - ✔️ ✔️ -*Extreme thirst (polydipsia)
  • Excretion of an excessive amount of diluted urine (polyuria)*
  • Nocturia (up at night to urinate)
  • Bed wetting in children
  • Dry Skin
  • Dizziness
  • Nausea
  • Fatigue
  • Weakness and muscle weakness Key Features of DI - ✔️ ✔️ Cardiovascular Symptoms
  • Hypotension
  • Tachycardia
  • Weak peripheral pulses
  • Hemoconcentration Kidney/Urinary Symptoms
  • Increased urine output
  • Dilute, low specific gravity Skin Symptoms
  • Poor turgor
  • Dry mucous membranes
  • Ensure baseline testing of pituitary and kidneys to rule out structural defects, injury, or obvious inflammation causing the change in ADH
  • Assess for nausea, vomiting, weakness, fatigue, and seizures
  • Assess for mental health history and medications such as lithium, and demeclocyline which can cause nephrogenic DI Medications/Tests/Other Interventions for DI - ✔️ ✔️ -If the condition is caused by an abnormality in the pituitary gland/hypothalamus/head (such as a tumor), treatment may be surgery
  • Synthetic ADH hormone called Desmospression for central DI. It can be given by nasal spray, oral tablets, or by injection.
  • DO NOT give desmospression for nephrogenic DI
  • Hydrochlorothiazide may improve symptoms. Although this is a diuretic, it can be used to reduced urine output for people with Nephrogenic diabetes insipidus by stimulating aldosterone to work in the tubules
  • Stopping some prescription medications may help nephrogenic DI
  • Fluid replacement for large fluid losses; MUCH OF DI FLUID LOSS CAN BE REPLACED ORALLY Desmopressin - ✔️ ✔️ -Controls central diabetes insipidus
  • Also used after surgery even if no DI is present (especially surgeries of the brain/head) to prevent large amount of urine excretion/development of central DI. Given prophylactically.
  • Can also be used in children to prevent bed-wetting
  • Works as a synthetic version of vasopressin/ADH/AVP
  • Also called DDAVP: can be oral, IV, sublingual, or intranasal
  • May start on a low dose of desmopressin and titrate/increase the dose DOSES ORAL = 0.1 mg, 0.2 mg DOSES IV= 4 mcg DOSES INTRANASAL = 10 mcg/spray DOSES SUBLINGUAL= 25 mcg
  • Can be on this med for 24-36 months The parenteral form is 10x stronger than the oral form, and the dosage must be reduced
  • Teach all patients taking these drugs to weight themselves daily to identify weight gain EXAMPLE TEST Q ON SODIUM/TREATMENT NUGGET - ✔️ ✔️ -Na 145-149 = no IV treatment / use oral solutions
  • Na 150-169 = IV solution D5W or D50.9% = hypoosmolar/hypotonic solutions
  • Na > 170 = critical emergency / ICU = colloids to manage fluid shifts (Plasmalyte, etc)
  • IV rates NOT TOO FAST! Titrate with frequent rechecks of sodium levels (redraw every 1-2 hours and PRN if acute). Rate depends on the patient weight = overall percent of fluid loss (no one right IV answer).
  • Reduction of sodium should be no more than 0.5 mmol/L (0.5 mEq/L) every hour. SLOWLY

Expected DI Outcomes with Treatment - ✔️ ✔️ -Urine osmolality returns to normal (500-800)

  • Serum osmolality returns to normal (275-295)
  • Sodium Returns to Normal
  • Specific Gravity Returns to Normal (1.005-1.030)
  • CT/MRI negative for structural damages
  • Stable post-surgical patient
  • Stabilizing I&O
  • Medications delivered and/or taken as ordered
  • Stable patient weight (daily)
  • Free from s/sx of dehydration Outcome Statements and Prognosis DI Long-Term Planning & Discharge DI - ✔️ ✔️ -The pt and family understand medication dosing: can be on demospression/DDAVP for 24-36 months
  • The patient will be instructed how to monitor daily weight
  • The patient and family will verbalize understanding how to monitor for urine color changing (dilution; use color chart)
  • The patient and family will understand how to monitor for dizziness, fatigue, confusion, and other symptoms
  • The nurse will verbalize understanding of why to monitor especially closely in ongoing injury/trauma/structural defects such as brain tumor, surgery, etc
  • The nurse, patient, and family will ensure that there is follow up for lab redraws whether hospitalized or discharged Syndrome of Inappropriate Antidiuretic Hormone (SIADH) - ✔️ ✔️ -there is an INCREASED production of ADH/vasopression/AVP
  • ADH keeps fluid in your body: it is a natural process to maintain homeostasis
  • Too much ADH means too must anti-diresis or anti-water loss = fluid retention
  • Inappropriate ADH = Increased ADH Pathophysiology of SIADH - ✔️ ✔️ -ADH is made in the hypothalamus and is a normally occurring hormone, and moves to the pituitary gland to await being used
  • This is released when the body is dehydrated to anti-diurese; to hold onto water
  • ADH normally concentrates urine to save water if dehydrated: this is a normal process to maintain homeostasis as long as possible
  • By concentrating water in the body, effects are seen on blood pressure, perfusion, osmolality, blood volume, etc.
  • The body can sense changes in circulating volume and will normally release increased ADH to conserve fluids in these situations
  • This is also a good thing in injury situations Causes of SIADH - ✔️ ✔️ -Medications: MAOIs, NSAIDS, SSRIs, vasopressin
  • Associated with respiratory problems such as emphysema, tuberculosis, pneumonia, asthma (hypoxia and hypercapnia increase ADH)
  • Extreme thirst (thirst starts at 290-295 mOsm/kg/osmolality)
  • Irritability and restlessness related to decreasing sodium
  • Cramps or tremors
  • depressed mood or memory impairment
  • personality changes, such as combativeness, confusion, and hallucinations
  • seizures
  • Shock, stupor, or coma Early Symptoms of SIADH - ✔️ ✔️ -hyponatremia
  • loss of appetite
  • N/V
  • weight gain Diagnosis of SIADH - ✔️ ✔️ -Urine osmolality high >800 (500-800)
  • Plasma/serum osmolality is low, <275 (275-295)
  • Serum sodium <135 hyponatremia (r/t increased fluid)
  • Urinalysis including specific gravity (very concentrated: >1.030)
  • CT/MRI (rule out pituitary trauma, injury, or tumor)
  • Can draw an ADH level: not a usual test performed though Assessment: Noticing SIADH - ✔️ ✔️ -Recent Head Trauma
  • Cerebrovascular Disease
  • Tuberculosis or other pulmonary disease
  • Cancer
  • All past and current drug use What you see as a nurse for SIADH - ✔️ ✔️ -I&O (I>O: pt not voiding due to fluid retention
  • Increased thirst (polydipsia)
  • Color of urine (more concentrated with less excretion)
  • Specific Gravity (more concentrated as pre-renal fluids are retained
  • Serum/Plasma osmolality is low/diluted with more fluids on board
  • heart rate (increased to compensate >100)
  • BP increased r/t more fluid
  • Daily Weight Extreme Version of SIADH - ✔️ ✔️ -Fluid volume overload with resultant hyponatremia
  • Confusion
  • Changes in LOC
  • Changes in heart rhythm (working harder with extra fluid)
  • Seizures
  • Coma Nursing Care focus for SIADH - ✔️ ✔️ -monitor I&O
  • Record daily weights
  • Ensure baseline electrolytes have been drawn (management of care)
  • Monitor perfusion (BP/HR/VS) and cognition (neuro checks, assess for changes)
  • Ensure baseline testing of pituitary and kidneys to rule out structural defects, injury, or obvious inflammation
  • Assess for N/V, weakness, fatigue, and seizures
  • Assess mental health hx and medications as MAOIS and SSRIs can cause SIADH Medications/Tests/Other Interventions SIADH - ✔️ ✔️ -If the condition is caused by an abnormality in the pituitary gland/hypothalamus/head (such as a tumor) treatment may be surgery
  • Fluid conservation and restriction with FVE
  • Hypertonic IV fluids 3% NaCl to correct hyponatremia (GIVE SLOWLY)
  • SIADH accounts for 1/3 of all hyponatremia in hospitalized patients = more common (33%)
  • Medications: Demeclocycline, Vaptans, possibly furosemide/Lasix (monitor electrolytes)
  • Monitor the response to therapy to prevent fluid overload from becoming worse, leading to pulmonary edema (life threatening and can occur very quickly!) and heart failure. Any patient with SIADH, regardless of age is at risk for these complications!
  • Provide a safe environment and watch for muscle twitching, increasing irritability, or restlessness before they progress to seizures or coma.
  • Check orientation to time, place and person frequently. Demeclocycline - ✔️ ✔️ -an antibiotic: a tetracycline derivative which induces drug induced diabetes insipidus by acting on the collecting tubule cell to diminish its responsiveness to ADH (so we can rid of fluid it acts as a diuretic in SIADH)
  • The role is limited in emergency care due to the slow onset of action
  • May start on a low dose of demeclocycline and titrate/increase the dose: 150-300 mg orally TID or QID for 7-14 days
  • Can be on for many months
  • this drug is not approved for this use Vasopressin Receptor Antagonists (Vaptans) - ✔️ ✔️ -work to block ADH (Vasopressin); sometimes used for correction of hypervolemic hyponatremia by increasing urine volume/increasing excretion
  • These drugs promote water excretion without causing sodium loss
  • Only administer these drugs in the hospital setting so sodium serum levels can be monitored closely
  • Tolvaptan (samsca)
  • oral
  • has black box warning that rapid increases in serum sodium levels (>12mEq/L in 24 hours) have been associated with central nervous system demyelination that can lead to serious complications and death
  • When this drug is used at higher dosages or for longer than 30 days, there is a significant risk for liver failure and death

Urine Output: < 200 mL/2 hours: >250mL/2 hours Serum Na: <135:> Urine Na: <25-30: Decreased Urine Osmolality: >800: <200- 300 Plasma Osmolality: <275: > Blood Pressure: Normotension : Hypotension Fluid Status: No dehydration: Dehydration Neuro Symptoms: confusion, delirium, coma : Seizures coma Warfarin Sodium/Coumadin Antidote - ✔️ ✔️ Vitamin K Heparin Antidote Dalteprin/Fragmin Antidote - ✔️ ✔️ Protamine sulfate Rivaroxaban/Xarelto Antidote - ✔️ ✔️ Andexxa Dabigatran/Pradaxa Antidote - ✔️ ✔️ Idarucizumab (Praxbind) Angiomax Antidote - ✔️ ✔️ NONE Streptokinase Antidote tPA Agents Antidote - ✔️ ✔️ Aminocaproic Acid (in emergency only) Thrombolytic Events - ✔️ ✔️ -create a possibility for DIC to occur

  • Examples include: Stroke, MI Disseminated Intravascular Coagulation (DIC) - ✔️ ✔️ -widespread clotting across many vessels
  • the body clots abnormally and form in small vessels of the body (pretty much anywhere)
  • Once clots forms, they can stop blood flow and cause problems like tissue necrosis, etc.
  • Once clots form, they use up clotting factors in the body
  • If clotting factors are used up, it increases the risk for internal bleeding!
  • Therefore, the patient with DIC is at risk for BOTH clotting and bleeding problems DIC is not really it's own disease, but a complication of other processes gone wrong DIC Pathophysiology - ✔️ ✔️ -The balance between clotting and bleeding is altered, resulting in irregular activation of the clotting cascade
  • Activated clotting factors are circulating (normal)
  • Clotting factors get used up (consumption)
  • Fibrin continues its process unregulated and causes fibrin degration products, which interfere with platelets
  • As platelets are used up in clots, this starts a thrombocytopenia (low platelets)
  • As clotting factors are used up in clots, feedback mechanism to body DOES NOT WORK to make more clotting factors
  • Lack of clotting factor replacement causes bleeding Etiology/Causes of DIC - ✔️ ✔️ -Cancer, sepsis, surgery, trauma, turns, motor vehicle accidents
  • Less frequently caused by frostbite, poisonous snake bites, and child birth
  • Can also be caused by a blood transfusion reaction
  • Can be caused by pancreatitis or liver disease
  • Can be caused by artificial devices such as artificial heart valves
  • *Sepsis caused DIC can be from bacterial, fungal, or protozoal sources (especially gram positive and gram negative; BE SURE TO PULL THESE CULTURES TO FIGURE OUT WHICH)
  • SIRS patients (Systemic inflammatory response syndrome) have a higher rate of DIC*
  • Can be caused by obstetrical emergencies such as pre-eclampsia or placental abruption
  • Most common cause is sepsis and cancer
  • DIC is found in 30-50% of sepsis patients Etiology/Causes of Chronic DIC - ✔️ ✔️ -chronic DIC is most often seen with cancer/tumors as body adjust more slowly over time
  • Can be caused by myocardial infarction
  • Can also be caused by inflammatory/autoimmune processes:

Rheumatoid arthritis Ulcerative colitis/Chron's disease Sarcoidosis Symptoms/Presentation of DIC - ✔️ ✔️ Clotting

  • Clots can form in vessels: peripheral in organs, in heart, lung, brain, kidneys or the vessels that supply any organ (basically anywhere)
  • Peripheral blocked blood flow can look like petechiae/purpura
  • Blocked blood flow can cause MI, PE, stroke, kidney infarction, liver infarction or other organ complications (impaired blood flow to these organs) Bleeding
  • Common bleeding sites are in urine, stool, and at IV sites
  • Can have bleeding from nose, gums, and other mucosa
  • Can have internal/unseen bleeding
  • Internal bleeding and resultant hypovolemia can cause hypovolemic/hemorrhagic shock Nursing Assessment of DIC - ✔️ ✔️ -Assess for hypotension, tachycardia
  • Respiratory signs to assess for: pleural friction rub, signs of acute respiratory distress (ARDs)
  • GI signs include abdominal bruising, bloody emesis, and bloody stools
  • Give anti-bleeding treatments (IV blood products, clotting factors)
  • Trend lab draws for improvement or decline Medications/Tests/Other Interventions DIC - ✔️ ✔️ Clotting:
  • give heparin: may be LMWH (Dalteparen/Fragmin) SQ, or IV
  • Heparin helps prevent the conversion of fibrinogen to fibrin
  • AntiThrombin: given with heparin (IV) to work better
  • Anticoagulants/antifibrinolytics: aminocaproic acid Amicar Bleeding:
  • Give platelets
  • Give other blood products such as packed red blood cells, FFP
  • FFP contains coagulation factors
  • Give specific clotting factors Other medications in DIC - ✔️ ✔️ -Coumadin/warfarin sodium - contraindicated with DIC: blood thinner and may make bleeding worse: inhibits activated clotting factors (nonspecific)
  • Xarelto/rivaroxaban-more specific in regards to clotting factors thrombin and factor 10/X
  • Pradaxa/dabigatran - thrombin inhibitor; good clot preventer. Not a first line treatment
  • Angiomax/bivalrudin- thrombin inhibitor - used with cardiac procedures to prevent heparin induced thrombocytopenia, used with aspirin, used after MI to prevent clots, may be used with DIC when device is in place such as an aortic balloon pump or ventricular assist device (something artificially inserted)
  • Streptokinase/tPA - tPA already naturally occurring in DIC process; extra tPA as medication can be given to prevent clots. SUPER CLOT BUSTER. Side effects: bleeding
  • Recombinant Human Soluble Thrombomodulin (RHSTs): new class of anticoagulants for DIC DIC Expected Outcomes - ✔️ ✔️ -Stable VS
  • Continued central and tissue perfusion (circulation intact)
  • Stable urinary function and excretion
  • Stable I&O
  • Blood products will be given accurately as ordered
  • Labs will be trended and followed
  • Anticoagulation therapy as ordered
  • Free from S/Sx of bleeding
  • Stable tissue integrity
  • Free from injury
  • Discharged on anticoagulation regimen while being monitored closely for bleeding
  • Pt can verbalize s/sx of both bleeding and clotting Fibrinogen - ✔️ ✔️ -a protein and a coagulation factor
  • normal range 60-100 (If this is increased, so is the risk for a clot. If this is decreased, so is the risk for a clot.)
  • Lower fibrinogen levels correlate with DIC
  • High fibrinogen shows less activation of secondary fibrinolysis which can explain organ failure
  • Fibrinogen activity level = how well does blood clot, how well is fibrinogen working. Normal Range 150-400
  • Fibrinogen Antigen level = amount of fibrinogen in blood. Normal range: 149-353 Thrombin - ✔️ ✔️ -a clotting enzyme
  • normal range is 12-14 seconds
  • Time increases/gets prolonged with heparin
  • Time increases/gets prolonged with fibrindegrationproducts and/or deficiency of fibrinogen Fibrinolysis - ✔️ ✔️ breakdown of fibrin by enzymes in blood clots Fibrin Degradation Products (FDPs) - ✔️ ✔️ stuff left after a clot dissolves. Normal process for a clot to dissolve
  • Low FDPs=body not dissolving clots normally
  • Normal FDPs = <10 mcg/mL
  • High FDPs = (subtype is D-Dimer) = rises after thrombotic event = too many clots Reticulocyte Count - ✔️ ✔️ how hard your body works to replace immature RBCs