EXAM 3 Flashcards
Diabetes type 1
- autoimmune dysfunction
- an inadequate production of insulin
- early-onset (age < 30 years), genetic predisposition, race/ethnicity
Diabetes type 2
- body cell’s cannot respond to the production of insulin regardless of making it.
- more common
-obesity, age>30 years, hypertension, smoking alcohol, HDL<35 mg/Dl or triglycerides> 250 mg/dl, or history of gestational diabetes or babies over 9 pounds
Functions of insulin
❖ Transports and metabolizes glucose for
energy
❖ Stimulates storage of glucose in the liver
and muscle as glycogen
❖ Signals the liver to stop the release of
glucose
❖ Enhances storage of dietary fat in adipose
tissue
❖ Accelerates transport of amino acids into
cells
❖ Inhibits the breakdown of stored glucose,
protein, and fat
LADA
-Subtype of diabetes in which progression of autoimmune beta cell destruction in the pancreas is slower than in types 1 and 2 diabetes
-clinical manifestation of LADA shares the features of types 1 and 2 diabetes.
Metabolic syndrome
-Elevated waist circumference (greater or equal to 88 cm for women, greater or equal to 102 cm for men)
-Elevated triglycerides (greater or equal to 150 mg/dl) or drug treatment for elevated triglycerides
-low HDL cholesterol (< 40 mg/dl for men, <50 mg/dl for women) or drug treatment for low HDL
-elevated blood pressure (systolic greater or equal to 130 mm Hg or diastolic greater or equal to 85 mm Hg) or hypertensive drug treatment
-elevated fasting glucose (greater or equal to 100 mg/dl) or drug treatment for elevated glucose
Diabetes mellitus type 1 S/S
- Polyuria, polydipsia, polyphagia
-fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections, fruity breath
-kussmaul respiration
-type 1 may have sudden weight loss, headache, nausea, vomiting or abdominal pain
Type 1 diabetes features
Onset: sudden
Age at onset: mostly in children
Body habits: Thin or normal
Ketoacidosis: common
Auto antibodies: usually present
Endogenous insulin: low or absent
Type 2 diabetes
Onset: gradual
Age at onset: Mostly in adults
Body habits: Often obese
Ketoacidosis: Rare
Auto antibodies: absent
Endogenous insulin: Normal, decreased or increased
Optimal HgbA1c levels for management of diabetes
less than 6.5%-8% would be optimal
Target goal: 7%
Insulin Therapy
Rapid acting- lispro
short acting - regular insulin
Intermediate acting - NPH insulin
Long acting: Glargine insulin
Nursing actions for diabetes
-observe client perform administration
-monitor for hypoglycemia
-Dosages can be adjusted for exercise, fasting procedures, diet
-Rotate the injection site to prevent lip hypertrophy
- inject at 90 angle (45 if thin)
-no need to aspirate for blood
-rapid or short acting (clear) drawn up first, then long acting (cloudy)
-wear medi alert
Methods of insulin delivery
-Traditional subq injections
-Insulin pens
-jet injectors
-Insulin pumps
-Future: implantable insulin pumps, artificial pancreas systems
Complications of insulin therapy
-local allergic reactions
-systemic allergic reactions
-insulin lipodystrophy
-resistance to injected insulin
-hypoglycemia
-Morning hyperglycemia
hypoglycemia s/s
-shaky
-fast heartbeat
-sweaty
-dizzy
-anxious
-hungry
-blurry vision
-weak or tired
-headache
-nervous or upset
hyperglycemia s/s
-extreme thirst
-frequent urination
-dry skin
-hunger
-blurred vision
-drowsiness
-nausea
management of hypoglycemia
-give 15 to 20 g of fast-acting, concentrated carbohydrate
-three or four glucose tablets
-glucose gel, 6-10 hard candies
-4 to 6 ounces of juice or regular soda (not diet soda)
-Emergency measures; if the patient cannot swallow or is unconscious
-subq or im glucacon (1 mg)
-25 to 50 ml of 50% dextrose solution IV
Oral antidiabetic agents focuses
-used for patients with type 2 diabetes who require more than diet and exercise alone
-combinations of oral drugs may be used
-major side effect: hypoglycemia
-Nursing interventions: monitor blood glucose for hypoglycemia and other potential side effects
-patient education
Biguanide (metformin)
counter insulin resistance (especially decrease hepatic glucose output)
sulfonylureas (glimepiride, glidazide, glyburide/gilbenadmine, glipizide)
Stimulate insulin secretion
Meglitinides (repaglinide, nateglinide)
Simulate insulin secretion (faster onset and shorter duration of action than sulfonylureas)
Gliptins (sitagliptin, vildagliptin, saxagliptin)
Increase prandial insulin secretion
thiazolidinediones (pioglitazone, rosiglitazone)
increase insulin sensitivity (especially increase peripheral glucose utilization)
a-Glucosidase inhibitors (acarbose, miglitol, voglibose)
Slow rate of carb digestion
Exercise
-Lower blood glucose-exercise only when levels are between 80-250
-If more than 1 hour passed since eating and planning high intensity work out, consume a carbohydrate snack first
-Ketones in urine- don’t
-Check BS more often
-Benefits: Aids in weight loss, easing stress, and maintaining a feeling of well-being. It also lowers cardiovascular risk
Exercise precautions
-insulin normally decreases with exercise; patients on exogenous insulin should eat a 15 g carbohydrate snack before moderate exercise to prevent hypoglycemia
-patients with type 2 diabetes not taking insulin or an oral agent may not need extra food before exercise
-potential post-exercise hypoglycemia
-need to monitor bg levels more often
gerontologic considerations
Foot care
-Wash daily
-Dry well especially between toes
-feel for bumps or temperature changes
-look between toes; check each toenail
-file toenails straight across
-check for dry cracked skin
-examine bottom of the feet
-track what you find
SICK days
(SUGAR): check your bg level ever 2 to 3 hrs necessary
(INSULIN): always continue to take ur insulin even when you are sick to avoid DKA
(CARBS): Make sure you take in enough carbs and drink enough fluids. If your glucose level is high, stick with sugar-free drinks. If ur glucose level is low, drink carb-containing drinks.
-(KETONES): Check ur blood or urine ketone levels every 4 hrs. Take rapid-acting insulin if ketones are present. Remember to drink plenty of water to flush out ketones out of ur system.
Acute complications of Diabetes
-hypoglycemia
-DKA
-Hyperglycemic hyperosmolar syndrome (HHS)
-Comparison of DKA and HHS
DKA (Type 1) s/s
-Dry and high sugar 250-500 +
-Keytones and Kussmaul resp.
-Abominal pain
-Acidosis Metabolic ph 7.35 or less
HHNS (type 2) s/s
-highest sugar OVER 600+
-Higher fluid loss (extreme dehydration)
- Head Change-Neurological Manifestations “Confusion”
- NO abdominal Pain, NO ketones (NO ACID, NO KUSSMAUL)
-Slower onset and stable potassium
DKA
-Absence or inadequate amount of insulin resulting in abnormal metabolism of carb, protein, and fat
-Clinical features
- hyperglycemia, dehydration, Acidosis, 3 Ps, Abdominal pain, N/V, profound weakness, blurred vision, headache, orthostatic hypotension, fruity breath, mental status changes
Common causes of DKA
-infection (pneumonia, UTI, skin, abdominal)
-Infraction (MI, stroke, bowel infarction)
-infant on board (pregnancy)
-indiscretion (dietary nonadherence)
-insulin deficiency (insulin pump failure or nonadherence)
LAB assessment of DKA
-Blood glucose levels between 250-800 mg/dl
-Ketoacidosis low serum bicarbonate, low pH; low PCO2
-electrolytes vary due to degree of dehydration
-BUN: greater than 30
-creatinine greater than 1.5
-Hct: Increased
-NA: below, within or above;
K: Within or above
Ketones in blood and urine
hyperglycemic hyperosmolar syndrome
-hyperosmolar hyperglycemia is caused by a lack of sufficient insulin; ketosis is minimal or absent
-hyperglycemia (greater than 600) causes osmotic diuresis, loss of water and electrolytes, hypernatremia, and increased osmolality = profound dehydration
Manifestations: 3 Ps, orthostatic hypotension, Tachycardia, weight loss, neurologic signs caused by cerebral dehydration
Lab assessment of HHS
-Blood glucose levels greater than 600 mg/dL
-ABGs: absence of acidosis; pH greater than 7.4; bicarb greater than 20mEq/L
-Electrolytes vary due to the degree of dehydration
-BUN: greater than 30
-Creatinine greater than 1.5
-HCT: increased
-NA: normal or below
-K: normal to high d/t dehydration
-Ketones absent
Long-term complications of diabetes
-Macrovascular (accelerated atherosclerotic changes)
* coronary artery disease, cerebrovascular disease, stroke, MI, peripheral vascular disease
-Microvascular
*microangiopathy; diabetic retinopathy, nephropathy
-Neuropathic
*peripheral neuropathy, autonomic neuropathies, hypoglycemic unawareness, neuropathy, sexual dysfunction
Pituitary gland
- The master gland
- Regulated by the hypothalamus
- Divided into two lobes
- Posterior pituitary
- Anterior pituitary
Anterior pituitary Disorders
ACTH- Adrenocorticotropic hormone
Too much → Cushing’s disease
Too little → Addison’s disease
GH- Growth hormone
Too much → gigantism and acromegaly
Too little → dwarfism
Posterior pituitary Disorders
ADH- Antidiuretic hormone
Too much → SIADH
Too little → DI
Adrenal Gland
Adrenal medulla
- Functions as part of the autonomic nervous system
Catecholamines: epinephrine and norepinephrine
Adrenal cortex
- Glucocorticoids
- Cortisol affects glucose, protein and fat metabolism; responds to stress; affects the immune system
Mineralocorticoids
- Aldosterone increases sodium absorption and potassium excretion in the kidney
Blood Cortisol levels
Higher levels in the morning
- Peak between 0400 and 0800
Lowest levels around midnight or 3 to 5 hours after
the onset of sleep
The 4 pm lab value should be 1/3 to 2/3 of the 8
am value
8:00 am: 5 to 23 mcg/dL
4:00 pm: 3 to 13 mcg/dL
Addison’s disease (Adrenocortical insufficiency)
Damage or dysfunction of the adrenal cortex → decreased aldosterone
and cortisol
Primary Addison’s disease
Idiopathic autoimmune dysfunction- most common
TB
Histoplasmosis
Adrenalectomy
Cancer metastasis
Radiation
Secondary Addison’s Disease
Not producing enough pituitary hormone: tumors, inflammation, etc.
Pituitary cancer
Radiation to the brain
Steroid withdrawal
Addison’s disease clinical manifestations
Weakness & fatigue (lack of energy, lethargy, tiredness)
Muscle weakness
Loss of body hair
Hyperpigmentation of the skin & mucous membranes
Low mood (mild depression) or irritability.
Loss of appetite & intentional weight loss.
Increased thirst &craving for salty foods
Nausea & vomiting
Constipation or diarrhea
Abdominal pain
Low blood sugar
Reproductive- ED, irregular menstrual cycle
Low BP (acute adrenal insufficiency)
Addison’s LAB TESTS
Increased K
Increased WBC
Decreased Na
Increased Calcium
Increased BUN/creatinine
Blood glucose- normal to decreased
Blood/salivary cortisol
ACTH stimulation test(provocation test)
Adrenal Insufficiency Nursing care
-prevent circulatory shock
-Keep room temperature warm
-observe for dehydration
-monitor for hyperkalemia and hypoglycemia
-Administer hydrocortisone
-Administer fludrocortisone
-AVOID STRESS AND GIVE 15 G CARB SNACK
ACTH SIM TEST
Rapid test
1. Obtain a baseline blood cortisol level then wait 30 minutes
2. After 30 minutes administer ACTH
3. Check blood levels at 30 min and 1 hour
Results
- If cortisol levels do not rise indicates primary adrenal insufficiency
- If cortisol levels increase > 7 mg/dL indicates secondary adrenal insufficiency
- An expected response is an increase cortisol after administration
Addisonian crisis
Life-threatening event
The body’s cortisol need is greater than supply (sudden drop in cortisol)
If left untreated can lead to death
Rapid onset of symptoms consistent with Addison’s disease
Triggering factors
- Sepsis/ infection
- Trauma
- Stress
- MI, surgery, anesthesia, hypothermia, volume loss, hypoglycemia
- Adrenal hemorrhage
- Steroid withdrawal
Cushing’s disease
Caused by overexcretion of
adrenal cortex hormones
- Aldosterone
- Cortisol
- Androgens
Cushing’s disease results
from a tumor in the pituitary
gland
Cushing’s syndrome results
from long
-term use of
glucocorticoids
Cushing’s disease s/s
-Moon face
-Purple striae
-osteoporosis
-hyperglycemia
-thinning bald head
-Males (gynecomastia)
-HTN, tachycardia
-hypokalemia
-hypocalcemia
-hypernatremia
Dexamethasone Suppression test
-Rapid testing- high dose
-Prolong testing- low dose
(Non-suppression of cortisol indicates Cushing’s disease)
Cushing’s nursing management
Monitor I&Os, daily weights
Assess for hypervolemia-edema, distended neck veins, SOB, hypertension, tachy
Maintain safe environment to decrease the risk of fractures and skin trauma
Turn and reposition the client every 2 hours
Monitor for and protect against skin breakdown and infection
Monitor WBC daily
Treatment
Ketoconazole
- Adrenal corticosteroid inhibitor in high doses
- Monitor LFTs for toxicity
- Hydrocortisone can be used with it
Mitotane
- Produces selective destruction of adrenocortical
cells
- Used for inoperable adrenal carcinoma (lifetime)
- Monitor LFTs and kidney function tests
Chemotherapy
- Used for Cushing’s caused by a tumor
Cushing Client education
Eat foods high in calcium and vitamin D
Avoid infection
Carry emergency card about steroid use
Report black, tarry stools
Thyroid Gland
T3
and T4
are regulated by the anterior pituitary
gland
T3 and T4 affect all body systems by regulating
overall body metabolism, energy production, and
controlling tissue use of fats, protein, and
carbohydrates
Dietary intake of protein and iodine is necessary
for thyroid hormone production
Hypothyroidism
Inadequate amounts of circulating thyroid hormones T3
and T4
Primary hypothyroidism caused by:
Hashimoto’s thyroiditis
Autoimmune disease
Most common cause in adults
Loss of thyroid gland
Use of certain medications
Lithium, amiodarone
Hypothyroidism s/s
Fatigue, lethargy
Irritability
Hair loss, brittle nails, dry skin
Paresthesia’s of fingers
Husky voice, hoarseness
Intolerance to cold
Low body temperature
Bradycardia, hypotension, dysrhythmias
Weight gain without an increase of caloric intake
Hypothyroid management
Levothyroxine
-Synthetic thyroid hormone replacement
-Use caution with older adults- start dose low and
increase gradually
-Monitor for chest pain, SOB
-Dose can be increased every 2 to 3 seeks
-Take on an empty stomach in the morning
-Monitor for manifestations of hyperthyroidism
-Treatment is lifelong
Myxedema Coma
Extreme symptoms of severe hypothyroidism
Life-threatening condition
Occurs when hypothyroidism is untreated, poorly
managed, or can be caused by stress
Hyperthyroidism
Excessive circulating thyroid hormones
Exaggerates normal body functions and produces a hypermetabolic
state
Graves’ disease
- Autoimmune disorder
- Most common cause of hyperthyroidism
Thyroiditis
Toxic adenoma
Exogenous- excessive dose of thyroid hormones
Affects women 8X more frequently than men
Most common during 20s and 40s
hyperthyroidism s/s
Nervousness, irritability, hyperactivity
Emotional liability
Decreased attention span
Weakness, easily fatigued, exercise intolerance
Heat intolerance
Palpitations and tachycardia
Skin is flushed, salmon color, warm, soft, and
moist
Exophtmalmos
Seen with Graves Disease
Wide open eyes
Patient is at risk for injury to the cornea
Priority is to protect the patient’s eyes/cornea
Hyperthyroidism management
Radioactive iodine therapy
- Thyroid cells exposed to the radioactive iodine are destroyed
- Results in reduction of hyperthyroid state and inevitably hypothyroidism
- The degree of thyroid destruction varies and can require lifelong thyroid replacement
Thionamides (methimazole and propylthiouracil/PTU) inhibit the production of thyroid hormones
- Monitor for symptoms of hypothyroidism
- Monitor CBC, LFTs
- With meals
Thyroid storm
Sudden surge of large amounts of thyroid
hormones into the blood stream
Fatal if untreated
Caused by uncontrolled hyperthyroidism,
infection, trauma, emotional stress, DKA,
digitalis toxicity, and thyroidectomy
S/S
- High fever
- Tachycardia, HTN, chest pain, palpations, dyspnea
- Delirium
- Vomiting, abdominal pain
Diabetes Insipidus
Disorder of the posterior
pituitary gland
Often seen as a complication of
brain surgery, head trauma, brain
tumor
Deficiency of ADH reduces the
ability of the distal renal tubules
in the kidneys to collect and
concentrate urine → very large
dilute urine output, even if the
pt’s fluids are restricted
S/S: polydipsia, hypovolemia
RISK FOR HYPOVOLEMIC SHOCK
Types of DI
-Primary neurogenic: lack of ADH production or release caused by defects in the hypothalamus or pituitary gland
-Secondary neurogenic: lack of ADH production or release caused by infection, tumors, trauma, or brain surgery
-Nephrogenic: Renal tubules that do not react to ADH caused by genetics, kidney damage, or medications
DI LAB TESTS
(URINE TESTING)
-DILUTE
-DECREASE IN URINE SPECIFIC GRAV, URINE OSMOLARITY, URINE SODIUM, and URINE POTASSIUM
(BLOOD TESTING)
-CONCENTRATED
-INCREASE IN BLOOD OSMOLARITY, SERUM SODIUM, SERUM POTASSIUM
DI MANAGEMENT
Desmopressin
- Treats neurogenic DI
- Synthetic ADH
- Routes- intranasal, PO, or parenterally
- Increases water absorption from the kidneys and decreases Urine Output
Prostaglandin inhibitors and thiazide diuretics
Treats nephrogenic DI
Life long- vasopressin
Daily weight
SIADH
Excessive release of ADH (vasopressin), secreted by the posterior lobe of the pituitary gland
Excess ADH → renal reabsorption of water and suppression of RAAS → water intoxication, cellular edema,
dilutional hyponatremia → fluid shifts within compartments cause decreased blood osmolarity
-RISK FOR SEIZURES
SIADH RISK FACTORs
Malignant tumors
Increased intrathoracic pressure
Head injury, meningitis, stroke
TB
Medications (chemo, TCAs, SSRIs, opioids, fluoroquinolone antibiotics)
SIADH clinical manifestations
Personality changes
Hostility
Sluggish DTRs
NVD
Oliguria with dark urine
SIADH LAB TESTs
(URINE TESTING)
-concentrated
-Urine sodium and urine osmolarity increased
(BLOOD TESTING)
-Dilute
-Blood sodium and blood osmolarity decreased
MED FOR SIADH
-Tetracycline: stimulates urinary flow
-Tolvaptan, conivaptan: used only in acute settings
-Furosemide: used with caution (Can cause NA excretion) WATCH FOR HYPONATREMIA
-Hypertonic saline: Used in severe cases
Normal ABG levels
PH: 7.35-745
PCO2: 35-45
HCO3: 22-26
Metabolic Acidosis: Clinical Manifestations
DUE TO RENAL FAILURE
Neurologic: Headache, Confusion, Drowsiness
Increased respiratory rate and depth (Kussmaul respirations)
Vital signs: Decreased blood pressure, brady, weak pulses
Decreased cardiac output
Dysrhythmias
Shock
Patient may be asymptomatic until bicarbonate is 15 meq/L or less
Metabolic Alkalosis: Clinical Manifestations
DUE TO VOMITING OR GASTRIC SUCTION
Symptoms related to decreased calcium
Respiratory depression
Tachycardia
BP- hypotensive or normo
Symptoms of hypokalemia- PVCs
Neurologic- numbness, tingling, weakness, hyperreflexia
Respiratory Acidosis: Clinical manifestations
CAUSES: Respiratory depression: opioids, poisons
Increased ICP, Brain tumors, cerebral aneurysm, stroke
Inadequate chest expansion due to muscle weakness, pneumothorax,
Chronic resp acidosis- sleep apnea, obesity
PE, ARDS, trauma
(MANIFESATIONS)
With chronic respiratory acidosis, the body may compensate and may be
asymptomatic
Symptoms may include a suddenly increased pulse, respiratory rate, and BP
Bradycardia and hypotension as acidosis worsens
Dysthymia- Ventricular fib
Respiratory Alkalosis: Clinical manifestations
Always due to hyperventilation
Tachypnea- rapid and deep respirations
Tachycardia dysrhythmias: ventricular/atrial
Neurologic
- Lightheadedness
- Inability to concentrate
- Numbness and tingling
- Tinnitus:
- Sometimes loss of consciousness
Epistaxis
-HEMORRHAGE FROM
THE NOSE
-ANTERIOR SEPTUM,
MOST COMMON SITE
-SERIOUS PROBLEM,
MAY RESULT IN AIRWAY
COMPROMISE OR
SIGNIFICANT BLOOD
LOSS
-RISK FACTORS: FACIAL
INJURY/TRAUMA, PHYSICAL OR
CHEMICAL MUCOSAL IRRITATION, SINUSITIS,
ALLERGIC RHINITIS, INFECTIOUS RHINITIS, NASAL TUMORS,
TEMPERATURE, AND HUMIDITY. BLEEDING DISORDERS, ANTICOAGULANTS
Nursing Management of Epistaxis
Airway, breathing, circulation
Vital signs, possible cardiac monitoring
and pulse oximetry
Reduce anxiety
URIs
An infection of the mucous
membranes of the nose,
sinuses, pharynx, upper
trachea, or larynx
Types: Rhinitis and
rhinosinusitis: acute,
chronic, bacterial, viral
Rhinitis and Rhinosinusitis
Inflammation and irritation of the mucous
membranes of the nose and sinuses.
Acute or chronic, and allergic or nonallergic
Causes: viral or bacterial or allergens.
Rhinitis and Rhinosinusitis Clinical manifestations
Rhinorrhea (excessive nasal
drainage, runny nose)
Nasal congestion
Nasal discharge (purulent with
bacterial rhinitis)
Sneezing
Itchy, watery eyes
Medical/Nursing management for Rhinitis and Rhinosinusitis
Antihistamines- most common treatment and are
given for sneezing, pruritus, and rhinorrhea.
Brompheniramine/pseudoephedrine- an example
of combination antihistamine/decongestant
medications.
Oral decongestant agents may be used for nasal obstruction.
Allergic rhinitis- avoid or reduce exposure to
allergens/irritants.
Education in the use of all medications.
Vitamins- echinacea, vitamin c, zinc
Pharyngitis
An inflammation of the pharynx,
resulting in a sore throat.
Uncomplicated viral infections
usually subside promptly, within 3 to 10 days after onset.
If caused by bacteria, is a more
severe illness.
Pharyngitis Clinical manifestations
fiery-red pharyngeal membrane and tonsils
lymphoid follicles that are swollen and flecked with white-purple exudate,
enlarged and tender cervical lymph nodes
Influenza
Severe headache
Chills
Fatigue, weakness
Fever
Hypoxia (avian)
Severe diarrhea (Avian)
MEDS:
Amantadine, Rimantadine, Ribavirin
Pathophysiology of
laryngeal cancer
Malignant cancer cells form in the larynx
Most common: well-differentiated squamous cell carcinoma (95%)
*Supraglottic: above vocal cords
*Glottis: area of vocal cords
Subglottic: below vocal cords
laryngeal cancer clinical manifestations
Early symptoms
Sore throat
Voice changes, hoarseness
Pain with swallowing
Nagging cough that won’t go away
Late symptoms:
Mass in neck
Weight loss
Dysphagia
Airway compromise
Asthma
Chronic disorder of airways that result in intermittent
and reversible airflow obstruction of the bronchioles.
Obstruction occurs either by inflammation or airway
hyperresponsiveness.
Risk factors for Asthma
Genetics-inherited component is complex
- Atopy—genetic predisposition to develop IgE-mediated response to common allergens is a major risk factor
Smoking
- Second-hand smoke Environmental allergies
Asthma clinical manifestations
Wheezing, cough, chest tightness, silent chest
Medical/Nursing managements
Albuterol- watch for tremors & tachy
Ipratropium- observe for dry mouth ,increase fluid intake, report HA, blurred
vision or palpitations* (toxicity)
Theophylline- monitor for toxicity. Tachy, nausea & diarrhea.
High fowlers: 90% to maximize
ventilations
Oxygen with humidification to loosen secretions
Face mask
Status asthmaticus
Extreme acute asthma attack characterized by hypoxia,
hypercapnia, and acute respiratory failure; lifethreatening
Wheezing, labored breathing, chest tightness, increased
shortness of breath, distended neck veins, use of
accessory muscles and sudden inability to speak
Without treatment leads to hypotension, bradycardia,
and respiratory/cardiac arrest
Chronic Bronchitis
-overweight and cyanotic, peripheral edema
❖Inflammation of the bronchi and bronchioles due to chronic exposure to irritants.
❖Cough and sputum production for at least 3 months in each of 2
consecutive years
❖Ciliary function is reduced, bronchial walls thicken, bronchial airways narrow, and mucous may plug airways
Emphysema
-severe dyspnea, older and thin
Loss of lung elasticity & hyperinflation of lung tissue.
Causes a destruction of the alveoli, increased air spaces leading to decreased surface area for gas exchange, carbon dioxide retention
and respiratory acidosis.
Right sided heart failure
Respiratory Infection
- Result from increased
mucous production &
poor oxygen levels
-cor pulmonale
bronchiectasis
❖ Bronchiectasis is a chronic, irreversible
dilation of the bronchi and bronchioles
❖ Caused by:
▪ Airway obstruction, pulmonary
infections
▪ Diffuse airway injury
▪ Genetic disorders
▪ Abnormal host defenses
▪ Idiopathic causes
Bronchiectasis clinical manifestations/medical management
Chronic cough
Purulent sputum in copious
amounts
Clubbing of the fingers
Postural drainage
Chest physiotherapy
Smoking cessation
Antimicrobial therapy
Bronchodilators and mucolytics
cystic fibrosis
-Cystic fibrosis (CF) is a genetic disorder that causes problems with breathing and digestion
(autosomal recessive)
-Genetic mutation changes chloride
transport which leads to thick,
viscous secretions in the lungs,
pancreas, liver, intestines, and
reproductive tract
Medical management of CF
-Chronic: control of infections; antibiotics
-Acute: aggressive therapy involves airway clearance and antibiotics based on results of sputum cultures
-Anti-inflammatory agents
-Corticosteroids; inhaled, oral, IV during exacerbations
-Inhaled bronchodilators
-Oral pancreatic enzyme supplementation with meals
-Cystic fibrosis transmembrane conductance regulator (CFTR) modulators are a new class of drugs and help to improve function of the defective
CFTR protein
Pneumonia
Inflammation of the lung parenchyma caused by various
microorganisms, including bacteria, mycobacteria, fungi, and viruses
Clinical Manifestations of Pneumonia
Pleuritic chest pain (sharp)when you breathe or
cough
Confusion or changes in mental awareness (in adults
age 65 and older)
Cough, which may produce purulent, blood-tinged
Fatigue
Fever, sweating and shaking chills
-crackles, wheezing
Pulmonary Tuberculosis
Caused by Mycobacterium tuberculosis bacillus (TB)
Spreads by airborne transmission through droplets to primarily lungs then
moves to other parts of the body such as the kidneys, bones, and cerebral cortex via blood.
clinical manifestations of TB
Low‐grade fever
Cough; nonproductive or mucopurulent lasting
longer than 3 weeks
Night sweats, fatigue, weight loss
Cough may be nonproductive, or mucopurulent sputum may be expectorated
Mantoux test
Used to see if one is positive with TB
Medications for TB
Rifampin (RIF) 10 mg/kg (600 mg maximum daily)
SE: Hepatitis, febrile reaction,
purpura (rare), nausea, vomiting
Bactericidal/bacteriostatic antibiotic
Pyrazinamide 15–30 mg/kg (2 g
maximum daily)
SE: Hyperuricemia, hepatotoxicity, skin rash, arthralgias, GI distress
Bactericidal/bacteriostatic antibiotic
military TB
Usually affects the lungs, but almost any organ can be involved.
Symptoms
Headaches, neck stiffness,
drowsiness (life threatening)
Pericarditis: dyspnea, swollen
neck veins, pleuritic pain,
hypotension
Chest tubes
Function
- Inserted into the pleural space todrain fluid, blood or air
- Reestablish a negative pressure
- Facilitate lung expansion
- Restore normal intrapleural
pressure.
Indications
-Pneumothorax
- Hemothorax
- Post op drainage
- Pleural effusion
- Pulmonary empyema
MANIFESTATIONS FOR THOSE NEEDED FOR A CHEST TUBE
Dyspnea
JVD
Hemodynamic instability
Pleuritic chest pain
Cough
Absent or reduced breath sounds on affected side
Dullness on percussion on the affected side
(hemothorax, pleural effusion)
Asymmetrical chest wall motion
