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LICEO DE CAGAYAN UNIVERSITY

COLLEGE OF NURSING
R.N PELEAZ BLVD., KAUSWAGAN, CAGAYAN
DE ORO CITY

IN PARTIAL FULLFILMENT
OF THE REQUIREMENTS FOR
NCM501204 (MS-2 LECTURE)

SUBMITTED BY:
Eusan John P. Nambatac
NCM 501204

PRESENTED TO:
MR. JOEL DEFENSOR, RN
Clinical instructor/Lecturer
Shock - the cardiovascular system fails to perfuse the tissues adequately, resulting in
widespread impairment of cellular metabolism.

PATHOPHYSIOLOGY

Decreased Blood Pressure

STIMULATE SYMPATHETHIC NERVOUS SYSTEM


 Thirst
 Anxiety, restlessness
 Tachycardia
COMPENSATIONS  Vasoconstriction, pallor
To maintain heart and
brain functions RENIN-ANGIOTENSIN-ALDOSTERONE
 Vasoconstriction
 Retention of Sodium and water, oliguria

INCREASED SECRETION
 Retention of water

DIRECT EFFECTS OF DECREASED BLOOD PRESSURE

 Lethargy, Weakness
 Anaerobic Metabolism Metabolic Acidosis

VASODILATION AND DECREASED CELL FUNCTION

 Slow blood flow in Microcirculation Thrombus Forms

 Ischemia in organs Decreased Function


Necrosis (e.g.
Kidney)

DECREASED VENOUS RETURN

FURTHER DECREASED IN CARDIAC OUTPUT

 Severe Acidosis
 CNS depression
 Organ Damage (e.g. acute
renal failure, lung damage)

DECOMPENSATION
Hypovolemic Shock -is caused by loss of whole blood (hemorrhage), plasma
(burns), or interstitial fluid (diaphoresis, diabetes mellitus, diabetes insipidus, emesis,
diarrhea, or diuresis) in large amount.

PATHOPHYSIOLOGY

Decreased Intravascular
volume

Decreased Cardiac output


S/Sx: Decreased BP

Shift of interstitial
fluid Increased HR, Catecholamine
contractility release
Aldosterone, ADH Increased
Volume
Increased SVR

Spleenic Discharge
Increased Cardiac
Output

More volume
loss

Decreased Decreased Systemic


Cardiac output and pulmonic
pressures
Decreased Tissue
perfusion

Impaired cellular
metabolism
EMERGENCY CARE MAMANGEMENT
 Don’t start an I.V infusion in the legs of shock patient who has suffered
abdominal trauma because infused fluid may escape through the ruptured vessel
into the abdomen.
 Place patient in supine position
 Cover and keep warm
 Call for assistance
 Administer Oxygen if possible
 Determine underlying cause and treat if possible, e.g., EpiPen

MEDICAL MANAGEMENT
Diagnostic Test:
Characteristic laboratory findings include
 Low Hct and Decreased Hgb level and RBC and platelet counts.
 Elevate serum, K, Na, Lactate dehydrogenase, creatinie, and BUN levels.
 Increased urine specific gravity (greater than 1.020) and urine osmolality
 Decreased urine creatinie levels
 Decreased pH and partial pressure of arterial oxygen and increased partial
pressure of carbon dioxide.

In addition:
 X-rays
 Gastroscopy
 Aspiration of gastric content
 CBC
Treatment and drugs:
 Blood and fluid replacement
 For severe cases, an intra-aortic balloon pump, ventricular assist device, or
pneumatic antishock garment may be helpful
 Oxygen administration
 Application of pulse site pressure to avoid bleeding
 Dopamnie or another inotropic agent used for vigorous fluid resuscitation.
 Surgery is performed to correct the underlying proble

NURSING MANAGEMENT:
 Check for airway and adequate circulation. If blood pressure and HR are absent,
start CPR.
 Record patient’s blood pressure, PR and RR, and peripheral pulses every 15
minutes until the patient’s condition is stabilized. Monitor cardiac rhythm
continuously.
 Increased Oxygen when systole is below 80 mmHg and notify physician
immediately
 Start I.V infusion with NSS or LRS using large-bore (14G to 18G) catheter
 Insert an indwelling urinary catheter to measure urine output.
Cardiogenic shock - is defined as “decreased cardiac output and evidenced of
tissue hypoxia in the presence of adequate intravascular volume

PATHOPHYSIOLOGY

Decreased Cardiac Output

Compensatory
rennin-aldosterone, Adequate or Catecholamine
ADH increased Increased SVR compensatory
blood volume release

Systemic and
pulmonary edema Increased Preload, stroke
volume, and Heart rate

Dyspnea Increased
Myocardial oxygen
requirements

Decreased Cardiac
Increased Blood
output, Decreased
pressure
ejection fraction

Decreased tissue
perfusion

Impaired cellular
metabolism
EMERGENCY CARE MANAGEMENT:

 Don’t start an I.V infusion in the legs of shock patient who has suffered
abdominal trauma because infused fluid may escape through the ruptured vessel
into the abdomen.

MEDICAL MANAGEMENT:

Diagnostic Test:

 Pulmonary artery pressure monitoring reveals Increased PAP and pulmonary


artery wedge pressure.
 Increased in left ventricular end-diastolic pressure and heightened resistance to
left ventricular emptying caused by ineffective pumping and increased peripheral
vascular resistance.
 Thermodilution catheterization reveals a reduced cardiac index (less than 1.8
L/min/mL).
 Invasive arterial pressure monitoring shows hypotension
 ABG analysis shows metabolic and respiratory acidosis and hypoxia
 ECG
 Serum enzymes measurement
 Cardiac catheterization
 Echocardiography

Treatment and drugs:

 I.V drug therapy may include dopamine, a vassopresor to increase cardiac


output, BP, and renal blood flow
 Amrinone or dobutamine, an inotropic agent to increased myocardial contractility
 Norepinephrine
 Intra-aortic ballon pump

NURSING MANAGEMENT

 In ICU, insert I.V infusions with NSS or LRS


 Monitor BP, PR, and RR.
 Insert indwelling urinary catheter to monitor urinary output
 Administer Osmotic diuresis, such as manitol, if ordered
 Check for any signs and symptoms and refer it to the physician.
Septic shock - Septic shock is a serious condition that occurs when an
overwhelming infection leads to low blood pressure and low blood flow. The brain,
heart, kidneys, and liver may not work properly or may fail.

PATHOPHYSIOLOGY

Predisposing Factor: Precipitating Factor:


-Age (1-65 years old) - malnourishment
-Chronic illness - invasive procedure
-Immunosupression -infection

Bacteremia

Gram-negative organism Gram-positive organism

Release of endotoxins, Realse of exotoxins and


protaenases, and other enzymes
products
Act as triggering
molecules and result in
activation of

Complement Coagulation Kinin system Neutrophils,


system cascade endothelial, and
monocytes-
macrophage
cell activity

Release of central endogenous mediators


(Tumor necrosis factor
{TNF}; interleukins-1
[IL-1])

Release of pro- inflammatory cytokines

Endothelial cell damage

Hypotension Decreased Depressed Lactic Leukopenia Thrombo- Vascular Pulmonary


systemic Myocardial acidosis cytopenia leakage congestion
vascular function
resistance Tissue
necrosis

Organ dysfunction
MEDICAL MANAGEMENT:
Diagnostic Test:
 Blood culture
 CBC
 BUN and Creatinine
 PT and PTT
 ECG
 Serum lactate dehydrogenase level
 Urinalysis
 ABG

Treatment and drugs:


 I.V, Intra-arterial, or urinary drainage catheter are in place
 Aggressive antimicrobial therapy
 Granulocytes transfusion may be used to in patients with severe neutropenia
 Oxygen therapy
 Colloid and crystalloid transfusion
 Diuretic (Furosemide) is given to maintain urine output
 Vassopresor (Dopamine)

NURSING MANAGEMENT:
 Remove I.V, Intra-arterial, or urinary drainage catheter and send it to the
laboratory to culture the presence of organism.
 Start I.V infusion with NSS or LRS
 Record patent’s BP, PR, and RR
 When blood pressure drop administer Oxygen
 Watch closely for signs of septic shock and refer it immediately to the physician.
 Use sterile technique.
Anaphylactic shock - Anaphylaxis is an severe, whole-body allergic
reaction. After being exposed to a substance like bee sting venom, the person's immune
system becomes sensitized to that allergen. On a later exposure, an allergic reaction
may occur. This reaction is sudden, severe, and involves the whole body.

PATHOPHYSIOLOGY
Antigen (allergen)

Antibody (IgE)
Complement,
Histamine, kinins,
prostaglandins

Constriction of extra vascular


Peripheral
smooth muscle
vasodilatation
(brochoconstriction, laryngo-
Increased Capillary spasm, gastrointestinal
permeability cramps)
Increased SVR

Extravasation of
intravascular fluids

Edema Relative
hypovolemia

Decreased Cardiac
output

Decreased tissue
perfusion

Impaired cellular
metabolism

MEDICAL MANAGEMENT:

Treatment:
 Removing causative antigen
 Administering medications that resolve and restore vascular tone.
 Epinephrine is given
 Benadryl is given
 Nebulized meds., such as albuterol (proventil)
 CPR is performed if cardiac arrest occur
 I.V lines administer

NURSING MANAGEMENT:
 Assess the patient for any allergic reaction and provide precaution
 Prevent further exposure to antigens
 When new allergy identified, the nurse advices the patient to wear or carry
identification that names the specific allergens or antigens
 Observe for any types of symptoms and refer it accordingly
 Maintain Hypoallergenic diet

Neurogenic shock - Anaphylaxis is an severe, whole-body allergic reaction.


After being exposed to a substance like bee sting venom, the person's immune system
becomes sensitized to that allergen. On a later exposure, an allergic reaction may
occur. This reaction is sudden, severe, and involves the whole body.
PATHOPHYSIOLOGY

Predisposing Factor: Precipitating Factor:


-Age -trauma to the spinal cord resulting in the
-gender sudden loss of autonomic and motor
reflexes below the injury level.

Decreased
Sympathetic and/or
Increased
parasympathetic
stimulation

Decreased Vascular
tone

Massive vasodilatation

Decreased
SVR

Inadequate
cardiac output

Decreased
tissue
perfusion

Impaired
cellular
metabolism
MEDICAL MANAGEMENT:

 Restoring sympathetic tone


 Position patient properly
 If hypoglycemia occur, administer glucose

NURSING MANGEMENT:

 Elevate and maintain the head of the bed at least 30 degrees when patient
receive spinal or epidural anesthesia
 Elevate head prevent spread of anesthetic
 Immobilizing the patient to prevent further damage to the spinal cord
 Check for daily pain, redness, tenderness and warmth of the calves.
 Administer drug of heparin or low-molecular-weight heparin (lovenox) as
prescribed

EMERGENCY CARE MANAGEMENT

 If possible treat patient in Trendelenburg position


 Large volumes of fluid may be needed to restore normal hemodynamics
 Dopamine (Intropin) is often used either alone or in combination with other
inotropic agents.
 Vasopressors (Ephedrine)
 Atropine (speeds up heart rate and Cardiac Output)
Hypertension- is an intermittent or sustained elevation of diastolic or systolic blood
pressure. Serial blood pressure measurement used to classify hypertension;
Pre-hypertension Systolic blood pressure is greater than 120 but less than 140 mmHg
or diastolic pressure greater than 80 but less than 90 mmHg. Stage 1 hypertension
systolic pressure greater than 139 but less than 160 mmHg or diastolic greater than 89
but less than 100 mmHg and Stage 2 hypertension systolic blood pressure greater than
159 mmHg or diastolic blood pressure greater than 99 mmHg.

MEDICAL MANAGEMENT:

Diagnostic Test:

 Urinalysis
 Excretory Urography
 Serum potassium level
 ECG
 Opthalmoscopy
 Oral captopril to test for renovascular hypertension

Treatment and drugs:

 Beta-adrenergic blocker
 Calcium channel blocker
 ACE inhibitors
 Weight reduction
 Alcohol, smoke and salt restriction
 Promote compliance of medication

NURSING MANAGEMENT:

 Ask patient if he/she is taking prescribed hypertensive drugs


 Monitor Blood pressure
 Monitor Pulse pressure
 Avoid patient that can provoke increased blood pressure like prohibition of
alcohol, smoking, salt-intake, fatty-foods, and high cholesterol foods and also
avoid caffeine-beverages.
 Promote health Teachings on proper compliance of medication and prohibition
PATHOPHYSIOLOGY

RISK FACTORS:
Diabetes Mellitus
Family History
Advance age
Obesity
Sedentary Lifestyle
Stress
Smoking
High intake of Na, saturated fats
and alcohol

Kidney release RENIN into the


bloodstream

RENIN helps convert angiotensin I


in liver

Angiotensin I is converted to
angiotensin II (a potent
vasoconstrictor) in lungs

Angiotensin
II

Aldosterone: Causes Na and water


retension

Retained Na and Water Increased Blood Volume

Arteriolar constriction Increased Peripheral vascular resistance

Increased Blood pressure and vascular resistance to


hypertension
MEDICAL MANAGEMENT:

Diagnostic Test:

 Urinalysis
 Excretory Urography
 Serum potassium level
 ECG
 Opthalmoscopy
 Oral captopril to test for renovascular hypertension

Treatment and drugs:

 Beta-adrenergic blocker
 Calcium channel blocker
 ACE inhibitors
 Weight reduction
 Alcohol, smoke and salt restriction
 Promote compliance of medication

NURSING MANAGEMENT:

 Ask patient if he/she is taking prescribed hypertensive drugs


 Monitor Blood pressure
 Monitor Pulse pressure
 Avoid patient that can provoke increased blood pressure like prohibition of
alcohol, smoking, salt-intake, fatty-foods, and high cholesterol foods and also
avoid caffeine-beverages.
 Promote health Teachings on proper compliance of medication and prohibition
Acute Respiratory Failure – is characterized by acute lung inflammation and
diffuse alveolocapillary injury with non-cardiogenic pulmonary edema.

PATHOPHYSIOLOGY

ALVEOLAR OR PULMONARY CAPILLARY WALL INJURY

Increased capillary Cell Damage


permeability

Fluid protein leaks into


alveoli and interstitial tissue

PULMONARY EDEMA
DECREASED SURFACTANT
PRODUCTION

Decreased compliance, labored RESPIRATORY


inspiration INSUFFIECIENCY

Decreased Oxygen Exchange


Hypoxemia RESPIRATORY
Decreased Lung volume
FAILURE
Atelectasis
MEDICAL MANAGEMENT:

Diagnostic Test
 ABG analysis
 CXR
 ECG
 Pulse oximetry
 CBC
 Serum electrolytes
 Pulmonary artery catheterization

Treatment and drugs:

 Cautious oxygen therapy (nasal prongs or Venturi mask)


 If Respiratory Acidosis persist, Mechanical ventilation with an Edotracheal is
attached or Tracheostomy
 Antibiotics
 Bronchodilators
 Corticosteroids
 If cor pulmonale and cardiac output decreased administer Inotropic agents,
vasopresors, and diuretics may ordered

NURSING MANAGEMENT:

 Orient the patient to the treatment unit to prevent anxiety


 To reverse hypoxemia, administer oxygen as ordered
 Maintain patent airway
 Monitor BP, RR and PR
 Place patient in semi-fowlers position
Diabetic Ketoacidosis – is caused by an absence or markedly inadequate amount
of insulin. This results in orders in the metabolism of carbohydrates, protein and fats.
The three main clinical features of DKA are HYPERGLYCEMIA, DEHYDRATION AND
ELECTROLYTE LOSS AND ACIDOSIS.

Predisposing Factor: Precipitating Factor:


-Hereditary -surgery
-Age (19 below) -diabetes 1 and 2
-Type A personality -stress
-Obesity -alcohol/drug abuse
-Genetics -infection

PATHOPHYSIOLOGY

Decreased Insulin Increased levels of hormone associated with


stress

Increased Decreased
Release of fatty insulin use Increased cathecholamines,
acids cortisol, and growth hormone

Increased glucose
Increased ketone production
formation Increased glucagon

Accumulation of
β-hydroxybutyrate
and acetoacetic
acids in the blood
Increased blood glucose level

Metabolic Acidosis Ketones


Sugar in Solute diuresis
in urine
urine
Kussmaul Polyuria Hyperosmolality
respirations CNS
depression
Dehydration
hypovolemia
Increased thirst

Shock
Polydepsia
MEDICAL MANAGEMENT:

Diagnostic Test:

 Blood glucose level


 Na and K serum level
 Creatinie
 BUN
 CBC
 ECG
 Urinalysis
 FBS

Treatment and drugs:

 Rehydration (fluid replacement NSS)


 When glucose level reaches to 300 mg/dL Iv solution may change to Dextrose of
5% in water (D5W) to prevent precipitous decline in blood glucose level.
 Regular insulin
 Human insulin

NURSING MANAGEMENT:

 Monitor Intake and Output


 Monitor vital signs
 Monitor diabetic effects on cardiovascular system
 Provide meticulous skin care
 Provide Health Teaching
Hepatic Encephalopathy-a life-threatening complication of the liver disease,
occurs with profound liver failure and may result from the accumulation of ammonia and
other toxic metabolites in the blood.

PATHOPHYSIOLOGY
Ammonia

Entering the blood stream

Converting ammonia
to urea

Absorption GI tract Liberation from


Muscle cells
kidney
S/Sx:
Edema, bleeding

Increased ammonia
concentration in the blood

Brain dysfunction
S/Sx:
Motor disturbances, minor mental
changes

Damage

HEPATIC ENCEPHALOPATHY

EMERGENCY CARE MANAGEMENT:


 Don’t give a semi-comatose or comatose patent sedative because these depend
the coma. Protect the comatose patient’s eyes from corneal injury by using
artificial tears or eye patches.

MEDICAL MANAGEMENT:

Diagnostic Test:

 Serum ammonia level


 ECG
 CT Scan
 MRI

Treatment:

 Elimination of ammonia from the GI tract include SORBITOL-INDUCED


CATHARSIS
 Reduction of dietary protein
 Continuous aspiration of blood in the stomach
 Administration of lactulose to reduce serum ammonia level.
 Administer Neomycin through retention enema
 Potassium supplements
 Diuretics
 Salt-poor album to maintain fluid and electrolyte balance.
 Hemodialysis
 Exchange Transfusion

NURSING MANAGEMENT:

 Frequently assess the patient’s level of consciousness


 Promote rest, comfort and quiet atmosphere
 Administer medication as ordered
 Use appropriate safety measures.
 Provide Health Teaching

Chronic Renal Failure (End-stage Renal Failure)-is the progressive loss of renal
function over a period of months or years in which there is less than 10% of remaining
renal function and dialysis or kidney transplant is required to sustained life.

PATHOPHYSIOLOGY

Predisposing Factors: Precipitating Factors:


-Genetics -diabetic nephropathy
-Age -hypertensive nephrosclerosis
-Gender

Renal Injury

Loss of nephrons Increased angiotensin II.

Glomerular capillary hypertension

Increased Glomerular permeability


and filtration

Proteinuria Systemic
hypertension

Increased Tubular protein


reabsorption

Tubulointerstitial
inflammation and
fibrosis

Renal scaring

EMERGENCY CARE MANAGEMENT:

 Careful monitor of serum level to detect hyperkalemia


 Emergency treatment is Dialysis Therapy
 Administration of 50% hypertonic glucose I.V, regular insulin, calcium glocunate
I.V, sodium bicarbonate I.V and cation exchange resins such as sodium
polystyrene sulfate.
 Cardiac tamponade resulting from pericardial effusion may result require
emergency pericardial tap or surgery.

Diagnostic Test:

 Elevated BUN, serum Creatinine, sodium and potassium level


 Decreased arterial pH and bicarbonate levels
 Low Hct and Hgb
 Increased blood glucose level
 ABG analysis
 X-RAY
 Kidney-ureter-bladder radiography
 Excretory urography
 Nephrotomography
 Renal scan
 Renal arteriography show reduced kidney size
 Abdominal X-RAY
 Abdominal CT Scan
 MRI
 Ultrasonography
 Renal biopsy
 EEG

Treatment and drugs:

 Low-protein diet
 High-calorie diet prevents Ketoacidosis
 Restrict sodium, phosphorus and potassium
 Maintaining fluid balance
 Monitoring vital signs, weight changes and urine volume
 Loop diuretic (furosemide)
 Cardiac glycosides in small amount does used to mobilize the fluids causing the
edema
 Antihypertensive
 Antiemetics given before meals
 Cimitidine, omreprazole or ranitidine may decrease gastric irritation
 Methylcellulose or docusate can help prevent constipation
 Folate supplements
 Severe anemia requires infusion of fresh frozen packed cells or washed packed
cells
 Synthethic erythropoietin (epoietin alfa)
 Antipruritic, such as trimeprazine or diphenydramine, can relieve itching,
 Aluminum hydroxide gel can lower serum phosphate levels
 Supplementary vitamins and essential amino acids
 Calcium and phosphorus imbalance may be treated with phosphate binding
agents, calcium supplements and reduction of phosphorus in the diet
 Hemodialysis or peritoneal dialysis
 Kidney transplantation best choice of treatment

NURSING MAMNGEMENT:

 Provide good skin care, bath patient daily


 Provide good oral hygiene
 Offer small, palatable, nutritious meal
 Monitor patients hyperkalemia, watch for cramping of the legs and abdomen and
for diarrhea
 Carefully assess the patient’s hydration status
 Monitor for bone or joint complications
 Encourage the patient to perform deep-breathing and coughing exercise to
prevent pulmonary congestion
 Maintain aseptic technique
 Carefully observe and document seizure activity
 Observe for sings of bleeding
 Schedule medication administration carefully
 If patient requires dialysis, check the vascular access every 2 hours for patency
and the arm used for adequate blood supply and intact nerve function
 Withhold the morning dose of antihypertensive on the day of dialysis, check for
disequilibrium syndrome.
Hypothyroidism – results from suboptimal levels of thyroid hormone. Thyroid
deficiency can affect all body functions and can range from mild , subclinical
forms to myxedema, an advanced form.

PATHOPHYSIOLOGY

Hypothyroidism

Primary Hypothyroidism Secondary hypothyroidism

Caused by the pituitary’s


Loss of thyroid tissue failure to synthesize
adequate amounts of TSH

Decreased TH,
Increased secretion of Pituitary Tumors
TSH, and goiter

MEDICAL MANAGEMENT
Diagnostic Test:
 Serum TSH levels
 Serum cholesterol
 Serum sodium level
 Radioisotope scanning
 Skull X-RAY

Treatment and drugs:


 Thyroid hormone replacement
 I.V administration
 Hydrocortisone therapy
 Iodine supplements
NURSING MANGEMENT:
 Keep accurate vital signs
 Monitor cardiovascular status
 Encourage patient to cough and breath
Hypoglycemia - (abnormally low blood glucose level) occurs when the blood
glucose falls to less than 50- 60 mg/dL. It can be caused by too much insulin or oral
hypoglycemic agents, too little food, or excessive physical activity. Hypoglycemia
may occur at any time of the day or night. It often occurs before meals especially if
meals are delayed or snacks are omitted.

EMERGENCY CARE MANAGEMENT:

 For patient with severe hypoglycemia (producing confusion or coma), initial


treatment is usually I.V administration of a bolus of dextrose 50% solution.
 This is followed by continuous infusion of glucose until the patient can eat a
meal.
 A patient who experience adrenergic reactions without CNS symptoms may
receive oral carbohydrates (parenteral therapy isn’t required)

Diagnostic Test:

 Glucometer readings
 5-hour glucose tolerant test
 C-peptide assay

Treatment:

 Dietary modification
 Frequent meals
 Avoid simple carbohydrates
 Anticholinergic to slow gastric emptying
 For fasting hypoglycemia, surgery and drug therapy may be required
 Nondiuretic thiazide (diazoxide)
 Administer I.V

NURSING MANAGEMENT:

 Watch for and report any signs and symptoms of hypoglycemia


 Implement measure to patient who is unconscious
 Monitor infusion of hypertonic glucose
 Measure patient blood glucose with the use of HGT
 Monitor effect of drug therapy, and watch for development of any adverse
reactions
 Provide family health teaching
PATHOPHYSIOLOGY
RISK FACTORS:
Too much insulin or oral hypoglycemic
agents
Too little food
Excessive exercise

hypoglycemia Blood glucose level drops


rapidly

Cells break down fatty and amino Brain cells can’t use ATP for
acids into adenosine triphosphate energy
(ATP) for energy

Neuroglycopenia Early CNS symptoms These include


glucose deprivation in brain headache, dizziness, restlessness,
tissue causes mild cerebral and decreased mental capacity.
dysfunction

AUTONOMIC NERVOUS SYSTEM STIMULATION

Pancreas Sympathetic Adrenal glands Sympathetic nerves stimulate Stomach


nerves and epinephrine epinephrine secretions (rapid response). Hypothalamus
rapid stimulate Hypothalamus stimulates pituitary gland to stimulates hunger;
glucagons secretions; secrete corticotrophin, which acts on the adrenal parasympathetic
epinephrine inhibits cortex to cause cortisol secretions (delayed nerves increase
insulin secretions response). gastric juices
contractions.

Liver Sympathetic nerves directly Muscle Hypothalamus stimulates pituitary


stimulate glycogenolysis; epinephrine, to secrete growth hormone (delayed
glucagons, cortisol, and growth response), which –along with epinephrine
hormone increase gluconeogenesis; and cotisol-inhibits glucagons use
glucagons also stimulates
glycogenolysis

Adrenergic changes these include hunger,


weakness, diaphoresis, tachycardia, pallor,
anxiety, and rebound hyperglycemia.

EMERGENCY CARE MANAGEMENT:


 For patient with severe hypoglycemia (producing confusion or coma), initial
treatment is usually I.V administration of a bolus of dextrose 50% solution.
 This is followed by continuous infusion of glucose until the patient can eat a
meal.
 A patient who experience adrenergic reactions without CNS symptoms may
receive oral carbohydrates (parenteral therapy isn’t required)

Diagnostic Test:

 Glucometer readings
 5-hour glucose tolerant test
 C-peptide assay

Treatment:

 Dietary modification
 Frequent meals
 Avoid simple carbohydrates
 Anticholinergic to slow gastric emptying
 For fasting hypoglycemia, surgery and drug therapy may be required
 Nondiuretic thiazide (diazoxide)
 Administer I.V

NURSING MANAGEMENT:

 Watch for and report any signs and symptoms of hypoglycemia


 Implement measure to patient who is unconscious
 Monitor infusion of hypertonic glucose
 Measure patient blood glucose with the use of HGT
 Monitor effect of drug therapy, and watch for development of any adverse
reactions
 Provide family health teaching

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