Exam 1 Flashcards

(40 cards)

1
Q

What are nursing implications for the administration of all blood components, including donation, processing, and administration, and complications?

A

DONATION
American Red Cross donation requirements
Type and Cross
A, B, O, AB
Rh+ & Rh –
FFP requires ABO but not Rh compatibility
Platelets are not typically cross-matched for ABO compatibility
Testing
Autologous donation
Intraoperative blood salvage- cannot be stored

TRANSFUSION
Blood Administration
Only with NS, Never medications or other fluids through blood tubing
Never medications or other fluids through blood tubing
Only through appropriate filter tubing, change tubing after 2 units (check hospital policy)
Administration time per unit should not exceed 3 ½ hours
Platelets or FFP:
Infuse each unit over 30-60 minutes
FFP requires ABO but not Rh compatibility testing
Platelets typically not cross-matched
steps:
verify Dr order- hgb of 10- anemic, below 8- needs blood transfusion
Obtain consent
Assess IV site & patency
Obtain blood from blood bank
Check accuracy of blood label and pts ID
Baseline VS & assessment
Start the infusion
VS & assessment recheck
Monitor transfusion reactions

complications: occurs in the first 10-15 minutes or first 50cc of blood
Febrile nonhemolytic reaction- chills, fever, HA, flushing tachycardia, anxiety
Acute hemolytic reaction- low back pain, hypotension, tachycardia, fever & chills, chest pain, tachypnea, hemoglobinuria, can be immediate
Allergic reaction- hives, pruritus, facial flushing, SOA, brochospasm, anxiety
Circulation overload-
Bacterial contamination-
Disease acquisition- Hepatitis, AIDS

implications
stop transfusion (maintain line with normal NS) & notify DR
change IV tubing
treat symptoms
recheck crossmatch record with unit
hemolytic reactions-
obtain 2 blood samples distal to infusion site
obtain first UA- test for hemoglobinuria
monitor F & E
serum calcium levels

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2
Q

bleeding disorders

A

Thrombocythemia- high platelet count resulting from stem cell disorder within BM
Thrombocytopenia- low platelet due to decreased production in BM, increased destruction and increased consumption
Immune Thrombocytopenic Purpura (ITP)- a decreased number of circulating platelets manifests as a bleeding tendency, easy bruising (purpura), or extravasation of blood from capillaries into skin and mucous membranes (petechiae).
Acquired Coagulation Disorders- including vitamin K deficiency and warfarin therapy, liver disease, Disseminated Intravascular Coagulation, platelet disorders and vascular disorders

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3
Q

Most important Labs-rhythm disturbances

A

Potassium: Normal: 3.5-5. mEq/L

Hypokalemia: irregular rate/rhythm, increased ectopy, PVC’s/V. Tach/ V Fib
<2.5

Hyperkalemia: peaked T wave/wide QRS, irregular rate/rhythm, increased ectopy, PVC’s/ V. Tach/heart block, asystole, v tach
>6

Magnesium: Normal: 1.8-3 mg/dL
Hypomagnesemia: tachycardia, atrial or ventricular
<1.2

Hypermagnesemia: bradycardia, decreases contractility, heart blck, asystole
>6.1

Calcium: Normal: 8.5-10.5 mg/dL
Hypocalcemia: dysrhythmias
<7

Hypercalcemia: dysrhythmias
>12

Atrial fibrillation/Atrial flutter
Thyroid, hepatic, and renal function
hyper

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4
Q

Clinical Manifestations-Rhythm Disturbances

A
Atrial fibrillation
May be asymptomatic
Palpitations, SOA, hypotension, dyspnea with exertion, fatigue
Pulse deficit 
Angina

Atrial flutter
Chest pain, SOA, hypotension

Ventricular tachycardia (V. tach)
Nearly always unresponsive/pulseless

Ventricular fibrillation (V. fib)
Absence of audible heartbeat
No palpable pulse
No respirations

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5
Q

Medical management/Medications- rhythm disturbances

A

Atrial fibrillation
Anticoagulants/antiplatelets, Class II and IV antiarrhythmics; Pharmacologic cardioversion
Electrical cardioversion, catheter ablation therapy, Maze/Mini-Maze Procedures
blood pools in atrial, beta blockers & calcium channel blockers (rate control),
Inititate anticoagulants prior to restoring sinus rhythm

Atrial flutter
Adenosine
Antithrombotic drugs, rate and rhythm control similar to atrial fibrillation
Electrical cardioversion

Ventricular Tachycardia
Immediate defibrillation for pulseless VT!
CPR
Cardioversion, antiarrhythmic medications, antitachycardia pacing
ICD
Catheter ablation
Torsades de pointes: polymorphic, prolonged QT interval
Correct magnesium imbalance

Ventricular fibrillation
CPR
Defibrillation
Amiodarone, epinephrine

Defibrillate v fib and v flutter
Assess pt
Call code
Initiate cpr

Sinus brady- not a big deal unless they have symtoms

A fib- blood pools- anticoagulants first

A flutter- rare, same as a fib

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6
Q

Most Important lab values for CAD

A

Total Cholesterol <200 mg/dL
LDL (bad) Cholesterol <100 mg/dL
HDL (good) Cholesterol > 40 mg/dL (males) >50 mg/dL (females)
Triglycerides <150 mg/dL

increased = increased risk for coronary artery disease

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7
Q

most important labs for Acute Coronary Syndrome (ACS)/MI

A

Cardiac enzymes/biomarkers
Troponin <0.05 ng/mL- q6h x3
Creatine Kinase (total) Males 50-204 units/L;
Females 36-160 units/L
Creatine Kinase CK-MB 0-5 ng/mL
Myogobin Males 28-72 ng/mL Females 25-58 ng/mL

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8
Q

CORONARY VASCULAR DISORDERS CM, PRIORITY ASSESSMENTS, DIAGNOSTIC TESTS

A

CLINICAL MANIFESTATIONS
Angina
Chest pain, indigestion, choking or heavy sensation
Feeling of impending death/apprehension
MI
Often cannot be distinguished from unstable angina

PRIORITY ASSESSMENTS
Pain
Difficulty breathing
Palpitations
Unusual fatigue
Syncope

DIAGNOSTIC TEST
12-lead ECG
Echocardiogram
Lab Tests (see previous slide)

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9
Q

medical management/medications for coronary vascular diseases

A
CAD
Diet
Physical activity
Medications
Tobacco cessation
HTN management
Diabetes control

Angina
Medications
Oxygen therapy
PCIs/CABG

Medications: Dual antiplatelet therapy: aspirin, clopidogrel (Plavix) or other antiplatelets
STEMI-Emergent PCI
Thrombolytics
Inpatient management
CICU with invasive monitoring
Continuous cardiac monitoring
ASA, beta-blocker, ACE Inhibitor 
BP, Urine output, Na, K, Creatinine
Cardiac Rehab
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10
Q

percutaneous coronary interventions/complications

A

Percutaneous transluminal coronary angioplasty (PCTA)

Coronary artery stent

Coronary artery bypass graft (CABG)
Blood vessel is grafted to an occluded coronary artery so blood can flow beyond the occlusion
Indications
Traditional CABG
Alternative Techniques
priorities
Pain management-Oxygen, morphine
Bed rest with elevated HOB
Fluid volume status
Adequate tissue perfusion
Anxiety
Monitor for complications
complications
hypovolemia
bleeding
cardiac tamponade
fluid overload 
hypothermia
hypertension
tachydysrhythmias 
bradycardia
cardiac failure
MI
PCI
Coronary artery dissection, perforation, abrupt closure, vasospasm
Acute MI
Dysrhythmias
Cardiac arrest
education
Prevention
Non-modifiable/Modifiable risk factors
Medication education
Post-procedure education
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11
Q

structural, infectious, and inflammatory cardiac disorders

A
medications
Antidysrhythmics
CCB, Beta-blockers
ACE Inhibitors, ARBs
Anticoagulation
Valvuloplasty
Valve Replacement
priorities
Assess for s/s heart failure and emboli
Heart sounds
Hemodynamic stability post valve replacement
Neuro, resp, CV are priority assessments
Wound care

complications
Heart failure
Infective endocarditis with mechanical valve prosthesis

education
Prevention
Medication education
Infection prophylaxis
Diet, activity, self-care
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12
Q

cardiomyopathy

A
diagnostic testing
12-lead ECG
Echocardiogram
Pulmonary artery systolic pressure, pulmonary artery wedge pressure
Central venous pressure
Cardiovascular MRI
clinical manifestations
May be asymptomatic for years
S/S of heart failure
Cough
Orthopnea
Peripheral edema
Nausea
Chest pain, palpitations, dizziness, syncope
priority assessment
Physical assessment focuses on s/s of heart failure
VS
Pulses
Weight
PMI palpation (shifted to left?)
Murmurs, S3/S4
Crackles
JVD
Edema
medications
Antidysrhythmics
Anticoagulation
Beta-blockers
Pacemaker/ICD
Alcohol septal ablation
Surgical Management
Left ventricular outflow surgery
Heart transplantation
Ventricular Assist Devices (VAD)
Total artificial heart
priorities
Improve CO and Peripheral blood flow
Increase activity tolerance
Improve gas exchange
Reduce anxiety
Decrease sense of powerlessness

complications
Severe heart failure
Lethal dysrhythmias
Death

education

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13
Q

aneurism

A
clinical manifestations
Pain most prominent symptom
Dyspnea
Cough
Hoarseness, stridor
Feel heart beating in abdomen
Low back pain

assessment
Dilated veins of chest, neck, arms
Edematous areas on chest wall and cyanosis
Pulsatile mass in middle and upper abdomen
Systolic bruit

tests
Chest X-ray
CTA
MRA
TEE
Duplex ultrasonography

medications
Blood pressure control
Beta-blockers, ACEs, ARBs, diuretics, CCBs
Endovascular repair with graft

priorities
Assessments of baseline prior to surgical repair
Functional capacity of all organ systems
Post operative considerations

complications
Hemorrhage
Shock
Arterial occlusion
Infection
Ischemic bowel
Kidney injury
Impotence

education
Medications
Diet/activity
Fluid intake

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14
Q

dissecting aorta

A

Poorly controlled HTN
Blunt chest trauma
Cocaine use

Sudden and severe
Persistent pain-tearing or ripping
Pale
Sweating
Tachycardia
Elevated BP/may vary greatly from one arm to the other

diagnostics/management

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15
Q

Pericardial Effusion & Tamponade

A
Accumulation of fluid in the pericardial sac
Heart failure, pericarditis, metastatic carcinoma, surgery/trauma
Acute (cardiac tamponade) vs chronic
S/S:  Tamponade
Chest pain
Tachypnea
SOA
JVD
Low CO/hypotension
Tachycardia
Pulsus Paradoxus
management 
Pericardiocentesis
Peri and post procedure monitoring
Possible complications
Puncture, dysrhythmias, plural laceration, gastric puncture
Reaccumulating
Pericardial window
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16
Q

steps in blood transfusion

A
verify Dr order-  hgb of 10- anemic, below 8- needs blood transfusion
Obtain consent 
Assess IV site & patency 
Obtain blood from blood bank
Check accuracy of blood label and pts ID
Baseline VS & assessment 
Start the infusion 
VS & assessment recheck
Monitor transfusion reactions

Get a new set of tubing and start NS after a reaction – document & notify Dr.

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17
Q

Disseminated Intravascular Coagulation

A

A sign of an underlying condition
Initiated by: an infection or a malignancy
May be triggered by: sepsis, trauma, cancer, shock, abruption placentae, toxins, allergic reactions
Clinical Manifestations: bleeding from mucous membranes, venipuncture sites, GI and urinary tracts; multiple organ dysfunction syndrome (MODS) (Chart 33-10, pg. 957).
Diagnostic test: platelet, D-dimer, PT, aPTT, fibrinogen level
STOP THE BLOOD

management
Assess for risks (“triggers”)
Monitor signs and symptoms of thrombi and bleeding
Monitor lab value
Prepare to administer plasma and Platelets

18
Q

common symptoms of leukemia

A

A- anemia
N- neutropenia
T- thrombocytopenia

Weight loss, fever, infection 
Shortness of breath
Weakness
Pain and tenderness in bones or joint
Fatigue
Loss of appetite
Swollen lymph nodes
Liver, spleen enlargement 
Bleeding and bruising, petechiai
19
Q

acute myeloid leukemia

A

over 50 years
Pathophysiology- start in immature forms of myeloid cells – white blood cells (other than lymphocytes), red blood cells, or platelet-making cells (megakaryocytes).

Clinical Manifestations
insufficient prod of normal BC
Low neutrophil count- fever and infection
Anemia- weakness, fatigue, dyspnea, pale
Thrombocytopenia- petechia, ecchymosis, bleeding tendency

diagnostic
Diagnostic- decrease in erythrocytes or platelets
Bone marrow analysis- shows blast cells

Assessment

Prevention/Risk Factors
Smoking, Chemical/Radiation exposures,
Chemotherapy drugs
Certain blood disorders

Management- Chemotherapy

snapshot
Fatigue, weight loss, pallor, bleeding , infection
Labs: blast cells > 20%, anemia, thrombocytopenic 
Tx: Chemotherapy
Complications: bleeding/infection
Nursing
Infection prevention
Assess for bleeding
Prevent bleeding

snapshot
Chronic phase few s/s
leukocytosis on CBC performed for other reason
Acute phase: hepatomegaly, splenomegaly, weight loss, bleeding, fatigue
Tx:
TKI’s

20
Q

chronic myeloid leukemia

A

Increases with age – 65 average
See it rarely under 20
Men more likely to get it

Pathophysiology- a genetic change takes place in an early (immature) version of myeloid cells - the cells that make red blood cells, platelets, and most types of white blood cells (except lymphocytes). The leukemia cells grow and divide, building up in the bone marrow and spilling over into the blood. In time, the cells can also settle in other part of the body, including the spleen.

Clinical Manifestations
Bone pain!!!!
Pale skin
Anemia
Fever 
Bruising
Lethargic/fatigue
Unusual bleeding from nose/gums 
Get infection easy 
Assessment
Prevention/Risk Factors- 
Radiation exposures, age, gender
Management- Imatinib therapy
		 Tyrosine Kinase Inhibitor (TKI)
		 DO NOT MISS THE DOSE
21
Q

acute lymphoid leukemia

A

children- 4 year old peak
Pathophysiology- start in immature forms of lymphocytes. Lymphoid leukemia develops from cells in the bone marrow, lymphomas develop from cells in lymph nodes or other organs.

Clinical Manifestations
Pain from enlarged liver or spleen or pain at the bone area
CNS symptoms- cranial nerve pulses or HA, V

Assessment
Prevention/Risk Factors
Radiation/chemical exposure
Certain viral infections
Inherited syndromes
Management- Chemotherapy, Stem cell transplant
Corticosteroids and vinca alkaloids
snapshot
Usually dx before 15 yr and incidence rises again > 50 yr
Splenomegaly, splenic pain, bone pain, HA, emesis, elevated blast cells
Tx:
Chemotherapy,
Stem cell transplant,
Targeted therapy

22
Q

chronic lymphoid leukemia

A

Pathophysiology- In chronic leukemia, the cells can mature partly but not completely. They generally do not fight infection as well as normal white blood cells do. The leukemia cells survive longer than normal cells, and build up, crowding out normal cells in the bone marrow.

Clinical Manifestations- Fatigue, Increase sensitivity to insets bites
A lot of time asymptomatic
Swollen lymph nodes
Enlarged spleen 
Dying from infection 
Assessment
Prevention/ Risk Factors
Chemical exposure 
Family history
Race (North America and Europe)
Management- Chemotherapy, Stem cell transplant

Progress very slowly (years)
Hard to treat because it could be too late

snapshot
Asymptomatic and dx on assessment for something else
Lymphadenopathy, splenomegaly, lymphocytosis
Tx:
Chemotherapy,
Stem cell transplant

23
Q

lymphoma

A

Pathophysiology- a cancer starts in cells that are part of the body’s immune system,
Lymphoid tissue in spleen, GI, liver or bone marrow

Clinical Manifestations
swollen lymph nodes
night sweats
fatigue
red spots
fever
vomiting
weight loss
backache
shortness of breath
nausea
radiation therapy 
chemotherapy 

Assessment
sx

Prevention/Risk Factors 
prevent infection
Epstein-Barr virus, 
autoimmune diseases, 
HIV/AIDS, 
smoking

Management
Chemotherapy/ Radiation therapy (skin)
Targeted therapy
Surgery

Nursing Management
Help patient with side effects of treatments
Educate to minimize infection risk
Educate to ID s/s of infection
Educate when to call provider
24
Q

non-hodgkins lymphoma

A
Lymphadenopathy, may be asymptomatic
Lymphoid tissue becomes infiltrated with malignant cells (B cells)- unpredictable 
multiple lymph nodes involved
Increases with age, 65
Common in US
Incidence rate has doubled
5 year survival rate -70%
Increased autoimmune problems- organ transplant, viral infection or prior treatment for cancers 

can occur in children & adults

25
Hodgkins lymphoma
``` painless, firm, enlarged lymph node, Reed-Sternberg cells present Anemia & altered WBC count Pruritus Frequent viral infections Rare High cure rate More common in men Fever Weightless Night sweats Chemo, radiation Stem cell for advanced disease Can start with a single lymph node and then develop other places Cad, dysrhythmia, cardiomyopathy seen in later stages ``` Educate about secondary malignancy- stop smoking, drinking, check breast, yearly skin check young adulthood and >55 most patients have a good prognosis
26
multiple myeloma
A malignant disease of the plasma cells Most common symptom is bone pain Most common areas- Back & ribs Increased with movement and decreased with rest No cure; treatment depends on age and includes: corticosteroids chemotherapy PAIN medication is the most important Plasma & pain Bone damage – pelvic, rib cage (prevent falls) Blood issues – anemia, clotting problem, infection Kidney problems – decreased kidney function, monitor UO, blood workhypercalcemia ``` management Pain Management NSAIDS and possible opioids monitor renal function (NSAIDS) Education of activity restrictions Education of manifestations of hypercalcemia Maintain mobility Hydration- to prevent hypercalcemia Infection prevention- Wear a mask Hand hygiene ```
27
Type I Diabetes
Destruction of pancreatic beta cells Decreased insulin production, Increased glucose production by liver Fasting hyperglycemia Glucose derived from food cannot be stored in liver but instead remains in bloodstream = post-parandial (after meals) hyperglycemia
28
Type II Diabetes
Insulin resistance = decreased tissue sensitivity to insulin Intracellular reactions are diminished – making insulin less effective at stimulating glucose uptake by the tissue Impaired insulin secretion Usually a slow progression and can go undetected for many years
29
Diabetic Ketoacidosis (DKA)
1. Hyperglycemia: There is no insulin, so no glucose entering the cells, All the glucose is in the bloodstream , And production and release of glucose by the liver is increased 2. Dehydration and electrolyte loss: The kidneys attempt to rid the body of the excess glucose , Glucose – along with water and electrolytes – are excreted 3. Metabolic acidosis: Breakdown of fat (lipolysis) to free fatty acids and glycerol occur  The free fatty acids are then converted into ketone bodies by the liver  Ketone bodies accumulate leading to metabolic acidosis occurs with type 1 diabetes ``` clinical manifestations Clinical Manifestations Polyuria Polydipsia Marked fatigue Blurred vision Weakness Headache Orthostatic hypotension GI symptoms (nausea, vomiting, abdominal pain) Acetone breath (fruity odor) Hyperventilation w/ very deep (not labored) respirations - Kussmaul Mental status changes ``` Assessment and Diagnostic Findings High blood glucose (300-800 mg/dL) Low serum bicarbonate (0-15 mEq/L) Low serum pH (6.8-7.3) Presence of ketone bodies in blood and urine Depending on amount of water loss: Sodium and Potassium may be low, normal, or high Creatinine, BUN, and hematocrit may be high Decreased or missed dose of insulin Illness or infection Undiagnosed/untreated diabetes Management Rehydration: (Fluid loss from polyuria, hyperventilation, diarrhea, and vomiting) GIVE IV FLUIDS!!! May need as much as 6-10 L Start with NS at rapid rate – 0.5-1L per hour for 2-3 hours Then ½NS for continued rehydration for several more hours When blood glucose reaches 300 or less – switch to D5W to prevent decline in blood glucose level MONITOR FLUID VOLUME STATUS!!! Frequent vital signs Lung assessments Monitoring intake and output Monitor for signs/symptoms of fluid overload Restoring Electrolytes: IV potassium slowly POTASSIUM REPLACEMENT!!!! As much as 40 mEq/hour may be needed for several hours to avoid dysrhythmias that occur with hypokalemia Frequent ECG and lab monitoring Reversing Acidosis GIVE INSULIN!!!! IV Regular insulin is given at a slow, continuous rate Hourly blood glucose measurements Blood glucose levels are usually corrected before acidosis is corrected  IV insulin may be continued for 12-24 H until serum bicarbonate levels increase to at least 15-18 mEq/L SICK DAY RULES Never eliminate insulin doses when nausea and vomiting Take insulin dose and then attempt to consume frequent small portions of carbs Drink fluids every hour to prevent dehydration Assess blood glucose and urine ketones every 3-4 hours If patient cannot take fluids without vomiting, or if elevated glucose or ketone levels persist – call provider! Monitoring and Managing Potential Complications Fluid Overload Hypokalemia Cerebral Edema
30
Hyperglycemic Hyperosmolar Syndrome (HHS)
1. Hyperglycemia: Lack of effective insulin to prevent hyperglycemia , but enough insulin is present to prevent the breakdown of fat , So no ketosis and acidosis occur 2. Hyperosmolarity: Persistent hyperglycemia causes osmotic diuresis , results in loss of water and electrolytes ``` Clinical Manifestations Hypotension Dehydration Tachycardia Variable neurologic signs ``` Assessment and Diagnostic Findings High blood glucose (600-1200 mg/dL) Osmolality (>320 mOsm/kg) High BUN and Creatinine Causes Infection or acute illness Medications that exacerbate hyperglycemia Treatments such as dialysis Management Rehydration Restoring Electrolytes Insulin Administration Rehydration Very similar to management in DKA Restoring Electrolytes Very similar to management in DKA Insulin Administration Less of important role because not needed for reversal of acidosis Insulin is given at a continuous low rate Monitoring and Managing Potential Complications Fluid Overload Hypokalemia Cerebral Edema
31
DKA VS HHS
DKA More common Type 1 Rapid onset (<24 H) Blood Glucose >250 Arterial pH Level < 7.3 Serum and urine ketones present Serum osmolality 300-350 mOsm/L Plasma bicarbonate level <15 mEq/L BUN and creatinine elevated HHS More common in Type 2 Slower onset (over several days) Blood Glucose > 600 Arterial pH Level is normal Serum and urine ketones absent Serum osmolality >350 mOsm/L Plasma bicarbonate level is normal BUN and creatinine elevated
32
Long Term Complications of DM
``` Macrovascular Complications Results from changes in the medium-large blood vessels Coronary artery disease Myocardial infarction Cerebrovascular disease Transient ischemic attacks Strokes Peripheral vascular disease Occlusive peripheral arterial disease Prevention and treatment of atherosclerosis Nutrition therapy and exercise to manage obesity, HTN, HLD Medications to control HTN and HLD Smoking cessation Control of blood glucose levels MORE COMMON IN TYPE 2 ``` Microvascular Complications Results from changes in the capillary basement membrane (thickening) Diabetic Retinopathy Nephropathy ``` Routine eye exams Annual urine analysis for albumin Annual serum creatinine and BUN Control of HTN Prevention/Treatment of UTIs Avoidance of nephrotoxic Rx and contrast dye Low-sodium and Low-protein diet Smoking cessation Control of blood glucose levels MORE COMMON IN TYPE 1 ``` ``` Diabetic Neuropathies Results from changes in the nerves Peripheral Neuropathy Distal portion of the nerves, especially in lower extremities, affects both sides symmetrically Autonomic Neuropathy Broad range of dysfunction affecting almost every organ system COMMON IN BOTH TYPES parathesia burning decreased sensation of light touch decrease proprioception decrease pain & temperature Intensive insulin therapy FALL PRECAUTIONS! Pharmacologic treatment Foot checks and care ``` AUTONOMIC NEUROPATHY Ranges from tachycardia, orthostatic hypotension, to MI Urinary retention, decreased sensation of bladder fullness, neurogenic bladder Delayed gastric emptying “diabetic gastroparesis”, bloating, N/V, constipation or diarrhea Discontinue meds that interfere with autonomic nervous system responses Use sympathomeimetic meds that stimulate an autonomic response Low-fat diet, frequent small meals Use meds that increase gastric motility Frequent glucose monitoring Meds to help treat constipation/diarrhea Intermittent straight caths Foot and Leg Problems and Infections Results from neuropathy, peripheral vascular disease, and immunocompromised Neuropathy = loss of pain and pressure sensation PVD = poor circulation contributes to poor wound healing Immunocompromise = lowers resistance to infections FOOT CARE!!!! Inspect feet daily Do not allow moisture to accumulate between toes Wear closed-toed shoes that fit well Trim toenails frequently Protect feet from hot/cold Keep blood flowing to feet DO NOT – walk barefoot, use heating pads, wear open-toed shoes, soak the feet, shave calluses
33
diabetes in the hospital
Blood glucose levels tend to increase due to stress Management of glucose control very important during perioperative period Frequent blood glucose monitoring May need to use IV insulin Monitor closely post-operative for cardiovascular complications, wound infections, and skin breakdown change in diets NPO Usual dosage of rapid or intermediate acting insulin must be changed Continue to give basal dose insulin Frequent blood glucose monitoring Clear Liquids A lot of clear liquids contain simple carbohydrates – try to use diet types Glucose tests and insulin administration should match mealtimes Enteral Tube Feeding Often results in increased levels of glucose If continuous tube feeding, regularly scheduled intervals of insulin given Must be cautious if tube feeding is temporarily discontinued or paused HYPERGLYCEMIA DURING HOSPITALIZATION Reasons: Changes in usual treatment regimen New medications introduced or routine medications changed Use of IV dextrose in fluids Overly vigorous treatments for hypoglycemia Inappropriate withholding of insulin Inappropriate use of “sliding scales” Mismatched timing of meals and insulin NURSING INTERVENTIONS Nursing Interventions: Assess patient’s usual home routine and try to mimic Monitor blood glucose levels Test blood glucose before a meal served and administer insulin at that time Use NS as much as possible, and not IV fluids with dextrose Avoid overly vigorous treatment of hypoglycemia HYPOGLYCEMIA DURING HOSPITALIZATION Reasons: Overuse of “sliding scale” insulin Not changing insulin dosage when dietary intake is decreased Overly vigorous treatment of hyperglycemia Delayed meal after administration of insulin NURSING INTERVENTIONS Nursing Interventions: Follow hospital protocol Assess patient’s pattern of glucose levels Avoid giving doses of insulin repeatedly Arrange for snacks to be giving if meals are going to be delayed
34
osmolality
high osmolality > High concentration of particles Low concentration of water > high adh > KIDNEYS KEEP WATER URINE MORE CONCENTRATED low osmolality > Low concentration of particles High concentration of water > low adh > KIDNEYS EXCRETE WATER URINE LESS CONCENTRATED 1.005-1.030- normal specific gravity Urine Osmolality 100-900
35
Diabetes Insipidus
DEFICIENCY OF ADH ``` CAUSES Head Trauma Brain Tumor Surgical/Irradiation of pituitary gland Infections of CNS Failure of renal tubules to respond to ADH ``` Diagnosis: Urine specific gravity Urine osmolality Fluid deprivation test Treatment: Replace ADH Desmopressin (DDAVP) – synthetic vasopressin, intranasally once to twice daily Ensure adequate fluid replacement Identify and correct underlying pathology ``` LARGE VOLUMES OF DILUTE URINE: Greater than 250 mL per hour Low urine specific gravity(1.001-1.005) POLYDIPSIA: Intense thirst Drinking 2-20 L daily Craves cold water ``` OSMOLALITY <100 for DI DRY INSIDE
36
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
EXCESS OF ADH ``` Causes: Non-endocrine origin Disorders of the lungs (pneumonia, pneumothorax) Head injury Brain surgery/tumor CNS infection Some medications ``` ``` Treatment: Identify and correct underlying pathology Restrict fluid intake Use of hypertonic IV solution Diuretics may be used ``` CANNOT EXCRETE A DILUTE URINE: Urine is very concentrated Elevated urine specific gravity RETAIN FLUIDS Euvolemic No edema present ``` DILUTIONAL HYPONATREMIA Nausea Vomiting Headache Weakness Fatigue Confusion ``` Sticky and stinky pee Not going to see edema, see body holding water in intravascular space- hypertension Watch for seizures – seizure precautions SIADH- soaked inside 3% NS
37
DI VS SIADH
``` DI low ADH, low water in body High UO, polyuria high sodium high h&h and serum osmolality from dehydration risk: hypovolemic shock tx: DDVAP (ADH) ``` ``` SIADH high ADH, water intoxication low UO, oliguria low sodium (dilution) weight gain risk: seizures tx: hypertonic saline ```
38
hypovolemic shock
drink plenty of fluids when exercising or in hot weather obtain early medical attention with illness or trauma and with any evidence of dehydration or bleeding educate about manifestations of dehydration, including thirst, decreased UO, and dizziness ``` chest pain lethargy somnolence restlessness anxiety dyspnea diaphoresis thirst muscle weakness nausea constipation ```
39
cariogenic shock
educate about ways to reduce the risk of a MI, such as exercise, diet, stress, reduction, and smoking cessation ``` chest pain lethargy somnolence restlessness anxiety dyspnea diaphoresis thirst muscle weakness nausea constipation ```
40
hemoglobin & hematocrit
hgb: men: 13.5 to 17.5 women: 12.0 to 15.5 hct: men: 41% to 50% women: 36% to 48%