Pheo Esrd and Neonate

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    Diabetic Ketoac

    Ivan T.

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    Diabetic

    an acute complication of DM type 1 character1. Hyperglycemia

    2. Ketonuria

    3. Acidosis4. Dehydration

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    Diabetic Ketoacidosis: Path

    1. Insulin deficiency prevents glucose from beinenergy, forcing the body to metabolize fat for

    2. Free fatty acids, released from the metabolis

    are converted to ketone bodies in the liver

    3. Ketone bodies are organic acids that cause m

    acidosis

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    Diabetic Ketoacidosis:Path

    4. Osmotic diuresis caused by hyperglycemia cre

    shift in electrolytes, with losses in potassium,

    phosphate, and water

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    Diabetic

    Clinical Manifstations:

    Early Stage Late StagPolydipsia, polyuria

    Fatigue, malaise,

    drowsiness

    Anorexia, N/V

    Abdominal pains, muscle

    cramps

    Kussmaul respirat

    Fruity, sweet brea

    Hypotension, wea

    Stupor and coma

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    Diabetic

    DIAGNOSTIC EVALUATION:

    1. Serum glucose elevated over 300 mg/dL up to 1,000 mg/dL

    2. Serum and urine ketone bodies (+)

    3. Serum HCO3 and p

    pCO

    4. Serum Na and K= low, normal or high

    5. BUN, creatinine, hemoglobin, and hematocrit = elevated

    6. Urine glucose (+) in high

    Specific gravi

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    Diabetic

    MANAGEMENT:

    I.V. fluids for fluid replacement

    I.V. insulin drip (regular insulin)

    Electrolyte replacement

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    Diabetic Ketoacidosis: NURSING INT

    Assess for signs of dehydration

    Monitor intake and Output

    Monitor urine specific gravity and blood gluco

    frequently

    Assess for symptoms of hypokalemia.

    Administer replacement electrolytes and insu

    ordered

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    Diabetic Ketoacidosis: NURSING INT

    Monitor serum glucose, bicarbonate, and pH le

    Provide reassurance about improvement of co

    and that correction of fluid imbalance will help

    discomfort

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    Hypergly

    Hyperos

    Nonk

    Synd

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    Hyperosmolar Hyperglycemic Nonketotic Syndrom

    an acute complication of DM type 2characterized by hyperglycemia,

    dehydration, and hyperosmolarity,

    with little or no ketosis

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    Hyperosmolar Hyperglycemic Nonketotic Syndrome: Path

    1. Prolonged hyperglycemia with glucosuria pro

    osmotic diuresis2. Loss of H2O, Na and K results in severe dehyd

    causing hypovolemia and hemoconcentration

    3. Hyperosmolarity d/t increased glucose and so

    4. Insulin continues to be produced at a level th

    prevents ketosis

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    Hyperosmolar Hyperglycemic Nonketotic Syndrome: Path

    Increased blood viscosity causes tissue hypoxia.

    Caused by inadequate amounts of endogenous/exoge

    to control hyperglycemia.

    Use of therapeutic agents that increase blood gluco

    (eg, glucocorticoids, immunosuppressive agents).

    Use of therapeutic procedures that cause stress or

    blood glucose levels (eg, hyperosmolar hyperalime

    peritoneal dialysis).

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    Hyperosmolar Hyperglycemic Nonketotic Syndrome: Ma

    Early Late

    Polyuria, dehydration

    Fatigue, malaiseNausea, vomiting

    Hypothermia

    Seizures, stupoMuscle weakne

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    Hyperosmolar Hyperglycemic Nonketotic Syndrome

    Diagnostics EvaluationSerum glucose and osmolality = elevated

    Serum and urine ketone bodies = minimal to abs

    Serum Na and K levels = may be elevatedBUN and creatinine = may be elevated

    Urine specific gravity = elevated

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    Hyperosmolar Hyperglycemic Nonketotic Syndrome: M

    1. Correct fluid and electrolyte imbalances with I.V. fluid

    2. Provide insulin via I.V. drip to lower plasma glucose

    3. Evaluate complications, such as stupor, seizures, or shtreat appropriately

    4. Identify and treat underlying illnesses or events that

    HHNS

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    Hyperosmolar Hyperglycemic Nonketotic Syndrome: C

    1. Too rapid infusion of I.V. fluids can cause cerebral ede

    death

    2. HHNS is a medical emergency that, if not treated pro

    cause death

    3. Patients who become comatose will need nasogastric

    to prevent aspiration

    Criteria DKA H

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    Criteria DKA H

    Age Any age > 50 yrs old

    S/Sx 3Ps, orthopneic hypotension,

    LOC changes, N/V

    Same as DKA

    slower onse

    PA Dry flushed skin, poor turgor,

    decreased BP, dry mucous

    membranes, Kussmauls

    respiration and acetone breath

    Same with D

    without Kus

    respiration a

    breath

    Dxtics Glucose, Ketones(+), BUN,

    Creatinine, WBC

    Ketones abs

    normal with

    Onset Hours to days Days to wee

    Mortality

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    Pheochromocy

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    pheoch

    A benign tumor

    Originates from the chromaffincells of the adr

    medulla

    80% to 90%, tumor arises in the medulla

    10% occurs in the extra-adrenal chromaffintis

    the aorta, ovaries, spleen, or other organs

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    pheoch

    May occur at any age (peak: 40 and 50 years)

    Affects men and women equally

    High incidence in family members 10% are malignant

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    Pheochromocytoma: Signs an

    Typical triad of symptoms: headache, diaphorepalpitations

    HPN and cardiovascular disturbances

    Tremor, headache, flushing, and anxiety

    Hyperglycemia results from glycogenolysis (ma

    insulin to control glucose levels)

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    Pheochromocytoma: Signs an

    acute, unpredictable attacks: seconds to hours

    Manifestations: extremely anxious, weak, hevertigo, blurring of vision, tinnitus, air hunger,

    dyspnea, polyuria, nausea, vomiting, diarrhea,

    abdominal pain, and a feeling of impending do

    Palpitations and tachycardia

    BP exceeds 250/150 mmHg

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    pheoch

    5 Hs of Assessment: Hypertension

    Headache

    Hyperhidrosis (excessive sweating)

    Hypermetabolism

    Hyperglycemia

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    Pheochromocytoma: Laboratory E

    Urinary catecholamine metabolites measurem

    (metanephrines [MN] and vanillylmandelic aci

    or free catecholamines are the standard diagn

    24-hour urine specimen

    Medications and foods (eg, coffee, tea, banana

    chocolate, vanilla, aspirin) may alter the resulttests

    Anti HPN drugs are not given prior to testing o

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    pheoch

    CT scans, MRI, and ultrasound to localize disea

    assess number of tumors

    131I-metaiodobenzylguanidine (MIBG) scintigr

    determines location of tumor and metastasis

    MIBG: a specificisotope for catecholamine-pro

    tissue

    MIBG scintigraphy is: noninvasive, safe has inc

    the accuracy of diagnosing tumors

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    Man

    Patient is placed on bed rest with the he

    the bed elevated to promote an orthosta

    decrease in blood pressure

    ICU for monitoring of ECG

    administration of alpha - adrenergic bloc

    agents or smooth muscle relaxants to lo

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    Man

    Phenoxybenzamine (Dibenzyline), long-a

    alpha-blocker if BP is stable for surgery

    Beta-adrenergic blocking agents used in

    patients with dysrhythmias

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    Man

    Hypotension and hypoglycemia may occ

    OP

    Manipulation of glands during surgery (?

    Corticosteroid therapy (?)

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    Chronic Renal

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    A large proportion of the nep

    damaged due to acute or chrkidney disease

    Nephrons die off, the undam

    increase their work capacity

    Pt may have significantkidnewithout showing symptoms ofailure

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    C

    Hypertension (prolonged & s

    Diabetes mellitus Glomerulopathies (from SLE a

    disorders)

    Nephritis

    Hereditary renal disease

    Obstructive uropathy

    Developmental or congenital

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    CRF: Consequences of Decreasing R

    1. Progression varies on unde

    cause & severity2. Stages: decreased renal re

    renal insufficiency, renal fa

    ESRD3. Retention of Na and H2O

    4. Decreased GFR (RAAM)

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    CRF: Consequences of Decreasing R

    5. Metabolic acidosis

    6. Decreased GFR increasesphosphate, with reciproca

    in serum Ca & bone resorp

    7. Erythropoietin decreases8. Uremia affects CNS

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    CRF: Clinical Ma

    GI: anorexia,N/V, hiccups, ulcers and

    Cardiovascular: hyperkalemia, HPN,

    pericardial effusion and tamponade

    Respiratory: pulmonary edema, pleu

    and rub

    Neuromuscular: fatigue, sleep disord

    headache, lethargy, muscular irritab

    peripheral neuropathy, seizures, com

    Metabolic and endocrine: glucose in

    hyperlipidemia, sex hormone disturb

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    CRF: Clinical Ma

    FE & acid base: salt and water

    acidosis, hyperK, hypocalcemia Hematologic: anemia, defect in

    platelets, increased bleeding te

    Psychosocial: personality and b

    changes, alteration in cognitive

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    CRF: Diagnostic

    Complete blood count : anemia Elevated creatinine, BUN, phos

    Decreased Ca, HCO3 and CHON

    ABG level: low blood pH, low p 24-hour urine for creatinine, pr

    creatinine clearance

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    CRF: Nursing

    Excess Fluid Volume

    Imbalanced Nutrition: Less ThaRequirements

    Impaired Skin Integrity

    Constipation

    Risk for Injury

    Ineffective Therapeutic Regime

    Management

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    CRF: Nursing In

    GOAL: Conservation of renal func

    Maintain F/E and acid base Maintain Nutrition

    Maintain Skin Integrity

    Detection of reversible cause a Treatment of Anemia

    Dialysis

    Renal Transplant

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