Pheo Esrd and Neonate
Transcript of 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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