Test 3 Reproductive, Pulmonary, Endocrine Flashcards

1
Q

Who’s at risk for pneumonia

A

young and old COPD Emphysema Asthma Immunocompromised

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2
Q

Pathogenesis of Type 2 Diabetes

Liver: Insulin resistance in the liver results in glucose overproduction despite elevation in fasting insulin

Pancreas alpha cells: Increased glucagon secretion from alpha cells stimulates an increased hepatic glucose production and decreased insulin secretion

Pancreas: decrease in beta cell fx leads to decreased insulin secretion

A

Pathogenesis of type 2 diabetes

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3
Q

Hormone Permissiveness

A

the hormone’s ability to increase the number of receptors for other hormones creates a chain of events

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4
Q

Normal V/Q ratio:

A

4-5L = 0.8

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5
Q

Diabetes Insipidus

Clinical Manifestations

A

Clinical manifestations

  • Polyuria, polydipsia (hallmark)
  • Low urine-specific gravity
  • Nocturia
  • Hypernatremia because of water deficit
  • Normal glucose levels
  • Dry mucous membranes, poor skin turgor, decreased saliva and sweat production
  • Disorientation, lethargy, seizures
  • Manifestations from cell shrinkage
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6
Q

Classification of Pulmonary Malignancies Non-small cell (85%)

A

Adenocarcinoma - most common, in lung periphery (doubles every 6 months) Squamous cell carcinoma - center (hilar) region (doubles every 100 days) Large cell carcinoma - develops in periphery (doubles every 100 days)

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7
Q

Pneumonia etiology

A

inflammatory reaction in the alveoli and interstitium cause by an infectious agent

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8
Q

A 35 yo presents with no history

of smoking, chest X-ray is clear. Lungs are hyperinflated with a severely depressed FEV1 @40%

A

Alpha 1 Anti Trypsin Deficiency

If you have a patient that presents as a severe COPDer who never smoked and is young <35. You have to consider Alpha 1 Anti Trypsin Deficiency which is what keeps surfactant and alveoli going

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9
Q

Perfusion

A

Movement of blood into and out of the capillary beds of the lungs to body organs and tissue

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10
Q

Honeycomb Lung

A

Restrictive vs Obstructive

Diseases

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11
Q

Classification of Asthma Severity

Intermittent

A
  1. Symptoms: <2 days a week
  2. Nighttime awakenings: <2x month
  3. Uses inhaler: <2 days/week
  4. Interference with normal activity: None
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12
Q

Bronchiolitis Clinical Manifestations

A

Can be mild to fatal Wheezing Decreased breath sounds Retractions Increased sputum Dyspnea Tachypnea low grade fever

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13
Q

What is untrue about asthma

A

You have a decreased airway reaction in asthma

In asthma, there is s an increased airway reaction which is why you see the bronchospasms

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14
Q

Obstructive Lung Disorders

A

Manifested by increased resistance to airflow

CAN’T GET AIR OUT

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15
Q

Primary

vs

Secondary

Hyper/Hypo Thyroidism

A

Primary - thyroid is the problem

Secondary - pituitary is the problem

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16
Q

Cystic Fibrosis

Diagnosis

A

Diagnosis

  • ABG
    • Hypoxemia and hypercapnia
  • PFT
    • Decreased VC, airflow, TV
    • Increased airway resistance, functional residual capacity
  • Chest x-ray
    • Patchy atelectasis, bronchiectasis, cystic lung fields
  • 72-hour stool collection
    • Determine fat absorption and fecal fat excretion
  • Sweat test (pilocarpine iontophoresis)
    • Elevated Na, Cl levels
  • Genetic testing
    • Genetic marker AF-508 confirms diagnosis
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17
Q

Emphysema

Pathology

A

Pathogenesis

  • Destruction of alveolar ducts (bronchials) and alveolar walls causing enlargement of distal air sacs due to release of proteolytic enzymes from neutrophils and macrophages
  • Ineffective gas exchange (diffusion)
  • Blebs and bullae form
  • Elastin and surfactant are destroyed reducing lung recoil
  • Small airways collapse restricting airflow and trap gas
  • Smoking causes alveolar damage
  • Inactivates α1-antitrypsin (normally protects lung parenchyma)
  • Develop hypercapnia and hypoxia
  • Damage is irreversible
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18
Q

Croup Clinical manifestations

A

URI sx for 1-2 days then: Hoarseness Seal-like barking cough No drooling Respiratory retractions and stridor NO DROOLING

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19
Q

What are 3 ways that a

Growth Hormone Deficiency can develop

A

Etiology

  • Decreased GH secretion from pituitary or GHRH from hypothalmus
  • Defective GH action (structurally abnormal GH or defective GH receptor)
  • Defective IGF-1 (somatomedin) generation
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20
Q

Emphysema

Clinical Manifestations

PINK PUFFER

A

Clinical manifestations

  • Type A COPD
  • “Pink puffer”
  • Progressive, exertional dyspnea
  • Thin due to increased respiratory effort and decreased ability to consume adequate calories
  • Use of accessory muscles
  • Pursed-lip breathing
  • Cough
  • Inspiratory and expiratory wheezing - lack of crackles, breath sounds, hyper resonance
  • Digital clubbing
  • Fatigued
  • Barrel chest
  • Frequent URIs due to loss of cilia
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21
Q

Goiter vs Thyroid Nodules

A

Goiter

  • Abnormal growth of the thyroid gland
  • May cause hypothyroid, hyperthyroid, or a euthyroid state
  • Usually painless
  • Worldwide cause is Iodine deficiency resulting in decreased T3 and T4 production
  • US cause is nodules or autoimmune response

Thyroid nodules

  • Abnormal growths on the thyroid gland
  • May occur without goiter
  • 15% may be malignant
  • May be present in hypothyroid, hyperthyroid, or a euthyroid state
  • Both may cause obstructive trachea or esophageal symptoms
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22
Q

What is the biggest risk factor for DM

A
  • Obesity strongest risk factor for DM
  • Body mass index (BMI) >30 kg/m2
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23
Q

Clinical Manifestations

of

Adrenal Insufficiency

A

Clinical manifestations

  • Early signs include anorexia, weight loss, salt-wasting, weakness, malaise, apathy, electrolyte disturbances, hyperpigmentation of skin, hypoglycemia, and hyperkalemia.
  • Diminished vascular tone, reduced cardiac output, inadequate circulating blood volume, and low blood pressure can lead to cardiovascular collapse.
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24
Q

Clinical manifestations Hand-Foot-Mouth Disease

A

Pharyngitis - vesicles on buccal mucosa & tongue Odynophagia Vesicles on hand and feet Fever Fatique

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25
J-Receptors
Juxtapulonary Capillary Receptors Located in the alveolar capillaries Sense increased pulmonary capillary pressure due to acidosis Initiates rapid deep breathing to reduce CO2 and cause alkalosis with lowers pulmonary pressure
26
Explain Thyroid storm
* Life-threatening thyrotoxicosis that occurs when excessive amounts of thyroid hormones are acutely released into circulation * Clinical manifestations * Elevated temperatures, tachycardia, arrhythmias, congestive heart failure * Extreme restlessness, agitation, and psychosis * Precipitating event: stress, gland manipulation
27
Epiglottitis Patho
Lift threatening condition Rapid cellulitis of epiglottis and surrounding soft tissue Air blockage into the trachea Children ages 2-4
28
Parathyroid Gland Disorders
* Regulates calcium absorption and resorption from bone * Serum calcium levels provide the feedback to regulate parathyroid hormone (PTH) secretion. * **Decrease in calcium causes PTH release.** * **Elevated calcium levels lead to suppression of PTH secretion.**
29
Infective Mono - Epstein Barr Virus Pathology
Cytomegalovirus (CMV) Trans primarily saliva Viral - no abx Incubation is 4-6 weeks
30
Adrenal Gland
Located on top of each kidney * Has inner medulla and outer cortex * Hypothalamus regulates function
31
Obstructive Lung Disorders Classifications
* Obstruction from conditions in the wall of the lumen (Asthma/Bronchitis) * Obstruction resulting from increasing pressure around the outside of the airway lumen (Emphysema) * Obstruction of the airway lumen
32
How to diagnosis Diabetes Mellitus
* DM: endocrine disorder diagnosed by the presence of chronic hyperglycemia * Diagnosis: if any two of the following conditions occurs * Random sampling of blood glucose above 200 mg/dL with classic signs and symptoms * Fasting blood glucose level of greater than 126 mg/dL * Blood glucose concentration greater than 200 mg/dL 2 hours after a 75-g oral glucose load * **HgbA1c : 6.5% or higher (normal \<5.7%)**
33
Virchow's Triad
Venous stasis/sluggish blood flow Hypercoagulability Damage to the venous wall
34
Adrenocorticotropic Hormone (ACTH)
* Produced by corticotropes in the anterior pituitary in response to hypothalamic corticotropin-releasing hormone (CRH) * Binds to G protein-coupled receptors on cells in the adrenal cortex and stimulates the production of **_cortisol and adrenal androgens_**
35
Restrictive Lung Disease Cannot get air in
* Result from decreased lung expansion * Alterations in lung parenchyma, pleura, chest wall, or neuromuscular function * Represent acute or chronic patterns of lung dysfunctions (not a single disease) * ALS, Guillaine-Barre Syndrome * Fibrotic Interstitial Lung Disease * Pulmonary Fibrosis, Sarcoidosis
36
What does the thyroid gland do
Controls growth and metabolism. Hypothalamus releases thyrotropin-releasing hormone (TRH) which stimulates anterior pituitary to release thyroid-stimulating hormone (TSH) which stimulates the thyroid to release T3 and T4 Only 10% of T3 is produced in the thyroid - T4 converts to T3 in body tissues Iodine needed to synthesize the T3 and T4 Thyroid hormones are bound to thyroglobulin (protein) until they are released
37
How to diagnosis Sarcoidosis
Increased eosinophil count, elevated sedimentation rate (ESR), liver enzymes, angiotensin-converting enzyme in active disease Transbronchial lung biopsy shows Noncaseating granulomas (definitive diagnosis) Stages 0 to 4 Progressing from normal to advanced fibrosis with evidence of honeycombing, hilar retraction, bullae, cysts, and emphysema
38
Mechanisms of Lipid Hormone Action
Steroid (lipid) hormones diffuse easily through the lipid bilayer of the cell membrane; cell membrane carriers transport thyroid hormones Thyroid and steroid receptors located in the cytoplasm or in the nucleus of the target cell Once inside the cell lipid hormones have to go through gene expression to have the effect amplified. Lipid acts slower than water-soluble bc of the multiple steps and gene expression that has to take place before amplification can take place.
39
What hormones are released fro the **Posterior Pituitary**
_•Posterior_ ADH (vasopressin) Oxytocin
40
Diagnostic tests for DM
* Glycosylated hemoglobin (HbgA1c) to determine long-term glycemic control and to evaluate therapeutic goals * Glucose freely attaches to RBCs. * Not useful for day-to-day management, reflects glucose average over the past 100 to 120 days * Values of less than 7% without adverse effect are considered desirable. * Capillary glucose testing (\<120 mg/dL) * For day-to-day management * Testing for ketones through urine testing * If glucose \>300; pregnant; ill; suspect ketoacidosis
41
Glycolysis
Breakdown of glucose for energy
42
Pulmonary circulation
* Blood from right ventricle goes to pulmonary arteries (unoxygenated) and then to pulmonary arterioles to the capillary membrane for gas exchange. * Pulmonary venous blood – oxygenated – flows back into the left atrium
43
COPD Criteria
A - no symptoms or hospitalizations B - mod symptoms no hospitalizations C - have been hospitalizations
44
Hypoparathyroidism Clinical Manifestations
* Paresthesias of the distal extremities, muscle cramps, spasms, fatigue, hyperirritability, anxiety, depression, prolonged Q-T intervals, increases in intracranial pressure * Severe symptoms: carpopedal spasm, laryngospasm, and seizures * **Tetany: Chvostek or Trousseau sign** * Manifestations result from low serum calcium levels; increased neuromuscular excitability.
45
Acute Bronchitis Pathogenesis
Airways become inflamed and narrowed from capillary dilation Swelling from fluid exudation Infiltration with inflammatory cells Increased mucus production Loss of ciliary function
46
Common Physical Findings Emphysema
Common physical findings * Thin, wasted individual hunched forward * Using accessory muscles * Decreased breath sounds, lack of crackles and rhonchi * Prolonged expiration * Decreased heart sounds * Hyperresonance - loud b/c of trapped air * Decreased diaphragmatic excursion * Chronic morning cough
47
Clinical Manifestations of Pulmonary Malignancies
Persistent cough that changes Dyspnea Hemoptysis Hoarseness Frequent URIs
48
Hyperthyroidism/Graves Disease Etiology and Pathogenesis
* Most common: autoantibodies bind and stimulate TSH receptors leading to diffuse toxic goiter (Graves disease) * Thyromegaly * Exophthalmos (immune mediated so may not resolve with treatment) * Widening of the palpebral fissure resulting in exposed sclera * Lid lag, vision changes, photophobia
49
Elevated prolactin (from anterior pituitary) level
Galactorrhea Amenorrhea Headache
50
Hormones secreted by the ANTERIOR PITUITARY
Somoatotropes secrete GH Gonadotropes secrete LH/FSH Thyrotropes secrete ACTH Lactropes secrete prolactin (PRL)
51
Pituitary gland what does it do and where is it located
The pituitary gland is located at the base of the brain and controls hormones. Anterior and Posterior pituitary gland Posterior gland is connected to the hypothalamus by the pituitary stalk When the hypothalamus wants to communicate with the Anterior pituitary it has to put hormones out into the system for pituitary gland to receive b/c there is not a direct connection Functions as a intermediary between the hypothalamus and the target organs
52
What are some Diabetic Goals?
* Goals * Achieving metabolic control of blood glucose levels * Preprandial blood glucose level between 70 and 130 mg/dL * Postprandial blood glucose level less than 180 mg/dL for adults (\<160 2 hrs post prandial) * Preventing acute and chronic complications * Accomplished by diet, exercise, medication, and such hygiene practices as daily foot care and smoking cessation
53
CURB-65
CURB-65 Scores * Confusion * BUN\>20 * Respiratory Rate \>30 * BP:SBP \<90mmHg or DBP \<60mmHg * Age\>65 Total Points 0-2 outpatient (2 may have short-stay inpatient) 3 Inpatient 4 most likely ICU 5 Inpatient ICU
54
Lung Parenchyma Disorders
Fibrotic interstitial lung disease Interstitial lung disease Group of disorders (more than 180 disease entities) Characterized by acute, subacute, or chronic infiltration of alveolar walls by cells, fluid, and connective tissue If left untreated, may progress to irreversible fibrosis Characterized by thickening of alveolar interstitium
55
Emphysema Classifications
Classifications * Centriacinar (centrilobular) * Associated with smoking and chronic bronchitis * Destroys respiratory **bronchioles** * Panacinar (panlobular) * Destroys the **alveoli** * Paraseptal * Affects the peripheral lobules
56
Type B Influenza
Generally milder Isloated primarily to humans
57
How to diagnose Pulmonary HTN
Measurement of pulmonary artery pressure during exercise Stress testing ECHO Big R wave or Inverted T wave
58
FEV1
How much air can be expelled in 1 sec \>80% Normal \<70% is obstructive \>70% is normal or restrictive
59
Etiology and Pathogenesis of Hyperthyroidism
Etiology and pathogenesis •Thyroid hyperfunction with increased secretion of T4 and T3 (Graves disease) Thyroid follicular cell destruction with release of preformed T4 and T3 (Hashimoto thyroiditis)
60
Explain Somogyi phenomenon
Rise in AM glucose as a rebound effect of hypoglycemia
61
Best overall ventilation and perfusion occurs in the
Dependant lung fields
62
Laryngitis Clinical Manifestations
Throat is NOT red Hoarseness Weak voice Aphonia
63
Growth Hormone Excess
Etiology and pathogenesis * Uncontrolled GH production by a benign tumor of the pituitary (adenoma) * Stimulates liver to produce IGF-1 * Cause up-regulated growth of soft and bony tissues
64
Lipid Soluble Hormones
Carried in circulation by transport proteins (globulin) poorly soluble Activate intracellular receptors Thyroid hormones (T3, T4) with iodine attached Steroids - derived from cholesterol Hormone detaches at the site of the target cell
65
Exercise Induced Asthma
Intrinsic - Nonatopic Common in children and adolescents * Bronchospasm often occurs within 10-15 minutes after the end of exercise; usually resolves in 60 minutes. * Heat loss, water loss, and increased osmolarity of the lower respiratory mucosa stimulate mediator release from basophils and tissue mast cells causing smooth muscle contraction.
66
Clinical manifestations Epiglottis
High fever Drooling Stridor
67
Asthma Pathogenesis
* Immunohistopathologic features * Edema **_•Mast cell activation starting reaction_** * Inflammatory cell infiltration by neutrophils, eosinophils, and lymphocytes * Inflammation of the airway * Acute bronchospasm (bronchoconstriction) * **_Normal respiratory epithelium replaced by goblet cells,_** resulting in mucosal edema, mucus plug formation - like a callus in respiratory system * Airway wall remodeling: thickening of basement membrane
68
Insulin actions:
* Enhance protein synthesis and prevent muscle breakdown * Inhibit gluconeogenesis * Enhance fat deposition by preventing fat breakdown (lipolysis) and inducing lipid formation * Stimulate growth by enhancing secretion of IGF-1 (somatomedin)
69
Residual Volume
amount of gas left in the lungs after expiration – 1.2 L can't breathe everything out
70
Peritonsillar Abscess
Emergency Abscess of one tonsil can displace uvula Caused by staph or strep Clinical manifestations: drooling, dysphasia
71
Lower Airway Structures Parasympathetic Stimulation
•Parasympathetic stimulation (mediated by acetylcholine) via the vagus nerve leads to constriction of muscle.
72
Diabetic Ketoacidosis Etiology and Pathogenesis
* Continued insulin deficiency leads to lipolysis of body tissues—metabolism of fats leads to free fatty acids (FFA). * FFAs are transformed into ketones, leading to ketoacidosis.
73
Diagnosis of Asthma
* Pulmonary function tests * Forced expiratory volumes decrease * Peak expiratory flow rate (PEFR) determines index of airway function ratio of FEV1/FVC before and after administration of short-acting bronchodilator * Skin testing * Young patients with extrinsic asthma * Elevated WBCs and eosinophils
74
Obstructive defect for spirometry alone as rated by FEV%
\>70% = Mild 60-69% = Moderate 50-59% = Moderate severe 35-49% = Severe \<35% = Very severe
75
Adrenocorticotropic Hormone (ACTH)
Produced by corticotropes in the anterior pituitary in response to hypothalamic corticotropin-releasing hormone (CRH) Binds to receptors on cells in the adrenal cortex and stimulates the production of **cortisol and adrenal androgens** CRH and ACTH have a _significant diurnal pattern_, with a peak on wakening in the morning and a valley in the evening.
76
Determining Hypothyroidism
77
Anterior pituitary gland hormones are regulated
by the hypothalamus
78
Explain Glucose Metabolism
Glucose is stimulus for insulin release from vesicles. Insulin then binds to its receptor on insulin-sensitive cells (not all cells do this) and it triggers glucose uptake Insulin needs access to insulin receptor cells to allow it to function
79
Pathogenesis of Growth Hormone Deficiency
Pathogenesis * May be idiopathic or related to tumors, radiation, or trauma * Resection of pituitary tumors or head injuries
80
Asthma Etiology
Airway **_obstruction_** that is reversible Airway inflammation Leukotriene reaction of bronchoconstriction Increase in bronchial responsiveness to a variety of stimuli
81
Hormone Synthesis - Lipid Soluble
Steroid (Lipid) Hormones are formed on-demand from cholesterol that is stored in the cell or retrieved from the circulating lipoproteins.
82
Central Chemoreceptors
* Located in the medullary center * Responds to changes in CO2 and pH * Normal stimulus to breathe is small increase in arterial carbon dioxide tension. * Alveolar ventilation can increase tenfold with acute rise in PaCO2.
83
Hypothyroidism vs Hyperthyroidism
84
Clinical Manifestations CHRONIC BRONCHITIS
Type B COPD "blue bloater" Overweight Dyspnea on exertion Excess sputum Chronic cough - WORSE IN AM Cyanosis - late sign
85
Explain Hyposecretion
HYPOSECRETION * Too little secretion of hormone * Primary hyposecretion occurs when an endocrine gland releases an inadequate amount of hormone to meet physiologic needs. * Secondary hyposecretion occurs when secretion of a tropic hormone is inadequate to cause the target gland to secrete adequate amounts of hormone.
86
Secondary Hypercortisolism
Means the anterior pituitary is telling the adrenals to put out a high level of cortisol level and they do this by stimulating it with a High level of ACTH
87
Cause and clinical manifestations of Hyperpituitarism
•Benign pituitary adenomas as most common cause * Manifestations * usually headache and visual field loss * Hormonal manifestations * Diagnosis * History and physical exam with **_vision testing_** * MRI of the brain , CT of the brain, hormone levels
88
GOLD Criteria Classification for COPD
IN PATIENTS WITH FEV1/FVC RATIO \< 0.70 - This is the guide BASE ON PREDICTED LEVEL GOLD 1 MILD - \>80% GOLD 2 MOD - FEV1 is between 50% and 79% predicted GOLD 3 SEVERE - FEV1 is between 30% and 49% predicted GOLD 4 VERY SEVERE - FEV1 \<30% predicted
89
Ventilation
Movement of air in and out of the lungs
90
Up regulation
low level of hormone then we need more of it so the body increases the # of receptors to it Ex: Oxytocin (labor and delivery)
91
Chronic Bronchitis - Blue Bloater Emphysema - Pink Puffer Chronic Obstructive Pulmonary Diseases
92
Antidiuretic Hormone Disorder SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SIADH Etiology & Pathogenesis
Etiology and pathogenesis * Excessive ADH from ectopic production from tumors, notably primary lung malignancies * Excess ADH stimulates renal tubules to reabsorb water despite decreased blood osmolality. * Adrenal insufficiency and hypothyroidism can cause increased ADH secretion and hyponatremia.
93
Antidiuretic Hormone Disorder DIABETES INSIPIDUS Etiology and Pathogenesis
Etiology and pathogenesis Insufficient ADH activity; excessive loss of water in urine Damage to hypothalamus ADH-producing cells Brain injury, tumors, or procedures Some pharmacologic agents Means large diuresis of inappropriately dilute urine Central: involves hypothalamus or pituitary gland Nephrogenic: involves kidneys
94
Clinical manifestations Pulmonary Embolus
Restlessness Pain on inspiration Tachycardia Hemoptysis Anxiety
95
Grade of COPD Symptoms COPD Assessment Test (CAT) Impact Level
CAT score-Impact level \< 10 Low 10 – 20Medium 21 – 30 High \> 30 Very high
96
Hyperparathyroidism Etiology and Pathogenesis
* Idiopathic, genetic, parathyroid adenoma, hyperplasia of parathyroid glands, chronic renal failure (reduced vitamin D) * Bone resorption and formation rates are increased. * Malignant cells can release PTH-like hormones; are a more frequent cause of hypercalcemic crisis. * Despite an elevated calcium level, PTH continues to be secreted. * During pregnancy it can lead to perinatal and neonatal complications. * **Newborn’s PTH production will be suppressed by maternal hypercalcemia, leading to neonatal hypocalcemia and tetany.** * **Some drugs such as lithium and thiazides can increase calcium levels.**
97
Central Diabetes Insipidus vs Nephrogenic Diabetes Insipidus
Central: involves hypothalamus or pituitary gland Nephrogenic: involves kidneys
98
A patient has secondary adrenal insufficiency (not putting out enough cortisol)
Decreased secretion of ACTH Pituitary is not telling the adrenals what to do and the adrenal does not know what to do Secondary - lose weight anorexic pigmented skin
99
Diagnosis
CT of chest with contrast to light up vessels Pulse OX
100
Type 2 Diabetes Mellitus Etiology and Pathogenesis
* Most common form of DM * Non-Caucasian and elderly disproportionately affected * **Insulin resistance and β cell dysfunction** lead to a relative lack of insulin. * Suspect decreased number of insulin receptors or abnormal translocation of glucose transporters * As disease progresses, insulin production may be impaired.
101
Explain IGF-1
Growth hormone * Insulin-like growth factor-1 (IGF-1) also called Somatomedin is stimulated by hypoglycemia, starvation, and exercise to stimulate GH secretion * Affected by estrogen, testosterone, thyroid hormone
102
Distribution of pulmonary blood flow
Gravity affects lung: * Upright position – blood flow is decreased in the apices and increased in the bases. * Supine position - blood flow is decreased anteriorly and increased posteriorly perfusion
103
Clinical manifestations Influenza
Sudden onset Significant fatigue Significant myalgia (muscle pain) Headache Fever \>100 Chest congestion and non-productive cough Clear nasal secretions
104
Glycogenesis
Excess circulating glucose is converted into glycogen and stored in the liver and muscle cells
105
Hypoxia
Decrease in tissue oxygenation
106
Clinical Manifestations Asthma
* •Wheezing - Dyspnea * •Feeling of tightness of chest * •Cough (dry or productive) * •Increased sputum * •Decreased breath sounds * **_•Prolonged expiration_** * •Use of accessory muscles of respiration * •Intercostal retractions * •Distant breath sounds with inspiratory or expiratory wheezing * •Orthopnea, tachypnea * •Tachycardia
107
Primary causes of Pulmonary Malignancies Secondary - metastasize from another source
Bronchial epithelial cell origin Smoking (85%) Asbestosis Radon gas Pollutant Bronchoalveolar (5%) in peripherals metastasize from lymphatics - no correlation to smoking
108
Chronic Bronchitis Pathogenesis
Chronic inflammation and swelling of the LARGE bronchial airway mucosa causing bronchial wall thickness and scarring Goblet cell hypertrophy of bronchial mucous r/i increased prod of mucus w/formation of mucus plugs Increased bronchial wall thickness - increases work of breathing and O2 demands **Ventilation-perfusion mismatch w/hypoxemia and hypercarbia increases pulmonary artery resistance** **Pulmonary hypertension leads to R sided heart failure**
109
The Ominous Octect What is not true about your bodies response to causing high sugar
You have a decreased glucagon secretion (Glucagon comes from the pancreas to raise our sugar. Insulin comes from the pancreas to lower our sugar. So when our body is having an issue with to high of sugar it is because the pancreas puts out too much glucagon)
110
Deep labored respirations that are fruity in odor
Kussmaul respirations and they occur in diabetic ketoacidosis
111
Etiology Chronic Bronchitis **_BLUE BLOATERS_**
Cigarette smoking (90%) Repeated airway infections Genetic predisposition Inhalation of physical or chemical irritants
112
Cystic Fibrosis Clinical Manifestations
•Clinical manifestations * Pancreatic insufficiency, cirrhosis of the liver, diabetes mellitus, gallstones, nasal polyps, and failure of development of the vas deferens in males * Nutritional assessment * Depleted fat stores * Steatorrhea (fatty stools) * Anorexia * Decreased growth rate in children (wt, ht, head circ)
113
Causes of Croup
Flu Viruses RSV Adenovirus
114
Influenza
Viral infection of the upper and lower respiratory tract Common Oct - March
115
What 4 things enhance the development of neuropathy?
•Hypertriglyceridemia, obesity, smoking, and hypertension enhance development of neuropathy.
116
Clinical Manifestations of Hypothyroidism in Adults
Clinical manifestations in adults * Decreased basal metabolic rate * Weakness, lethargy, cold intolerance, decreased appetite * Bradycardia, narrowed pulse pressure, and mild/moderate weight gain * Elevated serum cholesterol and triglycerides * Enlarged thyroid, dry skin, constipation * Depression, difficulties with concentration/memory * Menstrual irregularity - amenorrhea * **Myxedema - generalized facial puffiness**
117
Microvascular Diabetic Complications
*_Microvascular:_* retinopathy and nephropathy from abnormal thickening of the basement membrane in capillaries; may lead to blindness and renal failure * Hyperglycemia disrupts platelet function and growth of the basement membrane. * Thickening of basement membrane may improve with glycemic control. * Urine protein loss occurs in nephropathy. * Preventive: control blood glucose and hypertension
118
CURB 65
1 POINT 68 YO 1 POINT HYPOTENSIVE 1 POINT BUN ELEVATED CUT OFF FOR RESPIRATORY IS 30 TO GET A POINT
119
Classification of Pulmonary Malignancies Small cell carcinoma
Oat cell (Extremely aggressive) Central bronchial region Doubles every 30 days Poor prognosis usually found incidentally
120
Pheochromocytoma Clinical Manifestations
* Hypertension (persistent or intermittent) * **Headache, tachycardia, diaphoresis (classic triad)** * Tremor, nervousness, emotional lability, pallor, fatigue, orthostatic hypotension * Hypermetabolic state with fever, weight loss **Diagnosis** * Abdominal CT/MRI * 24 hour urine for catecholamines
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Glycogenesis
Producing and storing glycogen from the breakdown of excess glucose
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When do sinuses fully develop
7 years old
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Restrictive Pulmonary Disorders Characteristics
* **_Decrease_** in vital capacity (VC), total lung capacity (TLC), functional residual capacity (FRC), residual volume (RV) * The greater the decrease in lung volume, the greater the severity of disease.
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Hypothalamic-Pituitary Axis
Hypothalamus secretes releasing and inhibiting hormones and it regulates what the pituitary gland does. It connects the nervous and endocrine systems
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Chronic Geriatric Complications of DM
Chronic complications * Heart and blood vessel disease * Foot disease * Avoiding foot problems can be challenging from the frequent presence of orthopedic deformity and other common aging-related changes, as well as the decreased ability to perform appropriate foot care. * Eye disease * Kidney disease
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Ventilation
Movement of air into the lungs and distributing air to the alveoli for maintenance of oxygenation and removal of carbon dioxide
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Intrinsic (Nonatopic) Asthma
* Develops in middle age with less favorable prognosis * No history of allergies **_•High eosinophil reaction –not allergic_** * Repeated respiratory infections * Aspirin exacerbated asthma reaction * Occupational exposure * Exercise induced
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SIADH vs DI
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Growth Hormone Excess Diagnosis
Diagnosis: High IGF-1 and an elevated GH level that is not suppressed by administration of oral glucose
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Alpha cells produce...
Glucagon
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Hyperthyroidism Diagnosis
•Diagnosis * TSH levels are low * Elevated serum T4 and T3 (confirm) * 24-hour radioactive iodine uptake study can confirm diagnosis of Graves disease and exclude presence of thyroid neoplasms.
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Hering-Breuer Reflex
Stretch receptors in the alveolar septa, bronchi, and bronchioles keep you from taking too deep of a breath that cold rupture your lung
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Primary (idiopathetic) Pulmonary HTN
HTN progresses rapidly (women\>men) Long term prognosis poor as med trmt is ineffective
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Tuberculosis Diagnosis
* Tuberculin skin test – Mantoux test (PPD) * Local reaction typical to a small amount of bacilli 5mm _compromised immunity_ 10mm _at risk_ 15mm _no risk factors_ based on risk * Not used in prior BCG immunization or prior + test * Interferon gamma release assays (Interferon Gold)
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Sarcoidosis Etiology and Pathogenesis
Acute or chronic systemic disease of unknown cause Immunologic basis First degree relative increases risk 5 fold Development of multiple noncaseating epithelioid granulomas Abnormal T-cell fx
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Glycolysis
Breakdown of glucose for energy
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Clinical Manifestations of Acute Bronchitis
Distinct hallmark is recent onset of acute cough Usually mild and self limiting (7-10 days) Cough (productive or nonproductive) Wheezing Low-grade fever Sore throat Postnasal drip Fatigue
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Complications of Gestational Diabetes
Complications * Infant: metabolic abnormalities, stillbirth, macrosomia, and neonatal hypoglycemia * Mother: development of type 2 diabetes mellitus or impairment in glucose tolerance later in life * All pregnant women older than 25 years should be screened during the 24th to 28th weeks.
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Secondary Pulmonary HTN
Stems from a known disease Mitral stenosis Mitral regurgitation LV heart failure Chronic lung diseases Vasculitis
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Adrenal insufficiency Congenital adrenal hyperplasia
Congenital adrenal hyperplasia: rare cause in pediatric populations, because of specific enzymatic defects in the biosynthesis of cortisol by the adrenals Causes severe and life-threatening symptoms Overproduction of ACTH leads to hyperplasia of the adrenal glands and excessive androgen secretion.
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Restrictive lung disease
Cannot get air in
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Cannot perfuse if there is no oxygen to transfer first
Breathing first - alveolar ventilation Perfusion is the second process of respiration Diffusion is third
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Normal level of TSH
0.5 - 4.5
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Hypoituitarism Causes and General Manifestations
Causes: Primary Pituitary Secondary Hypothalamus General Manifestations: * GH deficiency * FSH/LH deficiency * TSH deficiency * ACTH deficiency * ADH deficiency
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Pathogenesis Cystic Fibrosis
Pathogenesis * Recurrent infection of bronchial walls leads to persistent dilation. * Bronchial wall thickening * Inflammation results in the destruction of walls. * Destructive process leads to loss of ciliated epithelium. * Transforms to squamous cell and pus formation * Leads to bronchial obstruction
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Cause of hypertension that is NOT from a cardiac source
Hyperthyroidism
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Explain Dawn phenomenon
Rise in glucose in early morning hours from growth hormone, cortisol, glucagon, and epinephrine release
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Examples of low alveolar ventilation but normal perfusion = low V/Q ratio (\<0.8)
Atelectasis Pneumonia ARDS example: 3L/5L = 0.6VQ
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How to diagnosis Adrenal Insufficiency
Diagnosis * Decreased plasma cortisol levels * ACTH provocation test (chronic AI) * Serum cortisol levels increase following this stimulus if adrenal cortex is normal; failure to produce cortisol indicates primary adrenal insufficiency. * Abdominal CT/MRI to evaluate adrenal gland size
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Manifestations Pneumonia
Crackles and decreased breath sounds over affected area Dull to percussion over infilitrate Chills and fever Cough, purulent sputum Dyspnea and tachypnea
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Secondary Hyperthyroidism
•Secondary—stimulation of TSH receptors by TSH (hypersecretion of TSH)
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Explain the properties of T3 and T4
* Approximately 90% of the thyroid hormone is in the form of T4, whereas 10% is T3. * Remain attached to thyroglobulin until stimulated by TSH * Released T4 and T3 are lipid soluble and diffuse from the follicle into circulation. * Once in the cell, T3 binds to its receptor and exerts its actions.
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Cushing's Syndrome
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Hormone Metabolism/Excretion Water Soluble vs Lipid Soluble
Water-soluble hormones - Finds their way out in urine Lipid- soluble hormones are bound to plasma proteins and stored in adipose tissue so they remain in circulation for longer periods of time Metabolized by kidney and liver; degraded by target cell after binding to receptors
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What does the epiglottis do
Closes the airway to prevent food from going into trachea
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Hypoglycemia Complications Causes & Clinical Manifestations
* Causes * Insufficient food intake, unplanned activity, or an inappropriate insulin or sulfonylurea dose * Manifestations: * Pallor, tremor, diaphoresis, palpitations, and anxiety * Hunger, visual disturbance, weakness, paresthesias, confusion, agitation, coma, death
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Addisonian Crisis Acute Adrenocortical Insufficiency
Acute adrenocortical Insufficiency ## Footnote * Life-threatening condition caused by inadequate levels of glucocorticoids and mineralocorticoids, leading to circulatory collapse * May occur with acute withdrawal of corticosteroids or may be caused by periods of stress/trauma
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Chronic Hyperglycemia can lead to...
Chronic Hyperglycemia * May lead to systemic changes over time and increase the risk of other diseases, including metabolic syndrome, hypertension, cardiovascular disease, and stroke * Complications are categorized as vascular and neuropathic.
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How to diagnosis Hypercortisolism
Diagnosis * ACTH measurement * Primary = low ACTH * Secondary = high ACTH * Plasma cortisol increased * 24-hour urinary free cortisol levels * Renal US/CT ABD can detect adrenal tumor * Dexamethasone suppression test * Differentiate between pituitary causes and ectopic causes
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Half life of a hormone
Duration of hormone activity in circulation expressed in minutes, hours, or days its the time for a hormone to reach one half of its original concentration in the blood and is influenced by the rate uptake by cells, degradation, and excretion Lipids usually have a longer half life Heavier people with more adipose tissue may hold onto hormones a lot longer than someone with no adipose tissue
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Explain Myxedema and when you would see it in Hypothyroidism
* Myxedema occurs in severe or prolonged hypothyroidism. * Generalized, non-pitting edema * Decreased level of consciousness, hypotension, hypothermia, history of precipitating event (trauma, sepsis, certain drugs) * May progress to myxedema coma, a life-threatening condition if treatment not received
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Factors affecting hormone secretions
Feeding-fasting cycle Light dark cycle Sleep-wake cycle 24 hour (circadian cycle) Longer cycles (28-day menstrual cycle)
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Pathology of Pulmonary HTN
Pulmonary vessels become thickened from an increase in the muscle. Pulmonary artery wall becomes fibrotic. Sustained PHTN results in the formation of a network of blood vessels that impedes blood flow
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Chronic Obstructive Pulmonary Disease COPD **_IRREVERSIBLE_**
Irreversible airway or alveolar abnormalities Chronic Bronchitis Emphysema OBSTRUCTIVE * Damage from prolonged inflammation * Smoking history or secondhand smoke exposure * Pollution and chemical irritants * Symptomatic around 60 years of age * Equal presentation in men and women * **_Alpha 1 Antitrypsin presentation – 30 to 40 years of age_**
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What are Incretins and what is their function?
Incretins are released after a meal to stimulate insulin release and inhibit glucagon release Incretins slow gastric emptying and decrease appetite Dipeptidyl Peptidase 4 (DPP-4) causes breakdown of the Incretins There is a new diabetic med that inhibits the breakdown of DPP-4 allowing the incretins to work and natural glucose metabolism
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Primary Hyperthyroidism
* Primary—Graves disease, autoimmune, tumor related, inflammatory; also malignancy * Autoimmune—related to TSH receptor antibodies
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Laryngotracheobronchitis - CROUP - Patho
Subglottic (under epiglottis) area edema leading to airway narrowing and obstruction Children 3 month - 3 years Occurs autumn and early winter
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Hypoparathyroidism Etiology and Pathogenesis
* Primary: may be idiopathic, autoimmune * Secondary: parathyroid or thyroid surgery; may be temporary or permanent * Can occur with removal of parathyroid gland * Congenital lack of parathyroid tissue and idiopathic hypoparathyroidism are causes of hypoparathyroidism in children and infants.
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Two types of Asthma
Intrinsic: non-allergic, adult-onset Extrinsic: allergic, pediatric-onset
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Down regulation
Cells have been exposed to a high concentration of a hormone so the body to protect itself decreased the # of receptor sites available, so it doesn't have excessive activity example: insulin receptors Chronic high glucose levels so the body is putting out a lot of insulin trying to fix the level so the body shuts down insulin receptor cells. This is how insulin resistance occurs
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Explain INCRETIN EFFECT
* Glucose ingested food causes a brief rise in insulin release (first phase). * Continued glucose causes the second phase: insulin secretion. * Ingestion of nutrients stimulates release of glucose–dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) from cells in the gut. * Effect on blood glucose known as incretin effect
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Hormonal regulation of insulin
Insulin is synthesized in the pancreas by the β cells of the islets of Langerhans. (beta)
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Diffusion (Respiration)
Movement of gas between air spaces in the lungs and bloodstream
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Secondary Pulmonary HTN causes
Has to come from something after the lungs so it would be the left side of the heart that would cause secondary pulmonary HTN
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Diagnosis of Diabetes Type 1
C peptide level is low along with low insulin levels
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What happens with insulin in the fasting state?
In the fasting state, glucose is produced by glycogenolysis, gluconeogenesis, and insulin falls to basal level. Glucagon is responsible for most glucose production in fasting state
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Peripheral chemoreceptors
* Located in the aortic arch and carotid bodies * Respond to decrease in arterial O2 * Also respond to increases in: * Increased Hydrogen ion concentration (decreased pH) * Arterial carbon dioxide level (PaCO2)
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Hormones
Blood-borne chemical messengers that affect target cells anatomically distant from the secreting cell * Regulates: Growth and development * Metabolism * Sexual function * Reproduction * Mood stability
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Explain GIP and GLP-1
GIP and GLP-1 stimulate the production of insulin and GLP-1 inhibits glucagon Insulin stimulates diffusion of glucose into adipose and muscle tissue; inhibits production of glucose by liver.
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Type A Influenza
Most common type Sicker presentation Responsible for epidemics and pandemics Found in humans and animals Went to bed fine woke up very ill Transmission through airborne droplets Incubation 1-4 days Continual antigen changes with gene mutations dev new strains
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Tuberculosis Clinical manifestations
Clinical manifestations – active primary ## Footnote * Gradual onset * Productive cough * Night sweats, fever, chills * Fatigue * Unexplained weight loss, anorexia
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Pheochromocytoma (Adrenal Gland Disorder) Etiology and Pathogenesis
Etiology and pathogenesis * Adrenal medulla secretes catecholamines, norepinephrine, and epinephrine, in response to SNS stimulation. * Catecholamines increase heart rate, blood pressure, and glucose release from the liver. * Pheochromocytoma: adrenal medulla tumor resulting in excessive production and release of catecholamines
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What causes Hypercortisolism
* Microadenomas or adenomas causing excessive production of pituitary ACTH * Nonpituitary tumors can cause ectopic ACTH production (malignancies) * **Exogenous steroid use is the most common cause of Cushing syndrome in the US related to use with allergic and autoimmune diseases**
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Expiratory Reserve Volume
gas that can be expired with a maximal expiration – 1.2 L DEEP expiration beyond normal TV
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Lower airway structures Autonomic nervous system
•Autonomic nervous system: control bronchi and bronchiole musculature
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Acute Bronchitis Etiology
Acute inflammation of the trachea and bronchi Viral 90% of the time Not infectious Sx will improve 7-10 days Cough will linger 3-4 weeks
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Acute Bronchitis Causes
Viral - RSV, Adenovirus, Influenza, Rhinovirus Bacterial not common is usually a secondary infection Inhalation of chemical irritants - bleach Allergic reactions
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Types of pneumonia
Community acquired (gram positive - strep pneumonia) Hospital acquired Atypical pneumonia (mycoplasma, legionella-breeds in water) Ventilator associated
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What can trigger Asthma?
Aspirin NSAIDS Beta Blockers Tartrazine (yellow #5) MSG Sodium or K Hops in beer Obesity (fat stores of cytokines)
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Classification of Asthma Severity Moderate
Symptoms: Daily Nighttime awakenings: 1x week but not nightly Uses inhaler: Daily Interference with normal activity: Some limitation
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Glycogenesis
Excess circulating glucose is converted into glycogen and stored in the liver and muscle cells Opposite of Glycogenolysis
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Inspiratory Reserve Volume
gas that can be inspired with maximal inspiration - 2.5 - 3 L Deep inspiration beyond normal TV 2.5 - 3L
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Fluid balance in the lungs * Hydrostatic pressure * Colloid osmotic pressure * Capillary permeability
* When capillary hydrostatic pressure exceeds colloid osmotic pressure, fluid moves from capillaries into the interstitial space. * If fluid shift is not controlled, fluid will move into the alveoli causing alveolar edema leading to poor gas exchange.
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What effect does excessive glucose have on myoinositol in neurons?
Excessive glucose is thought to interfere with myoinositol in neurons and reduced myoinositol in peripheral nerves.
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Hand-Foot-Mouth Disease
Enteroviruses, particularly Coxsackievirus Incubation 4-6 weeks (respiratory, contaminated hands, fecal matter)
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Chronic complications of DM
Chronic complications * Rarely manifested before adolescence * Screening for neuropathy/nephropathy ongoing * Counseling on metabolic control before initiation of pregnancy
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COPD Categories Group A-D
Based on symptoms and Risk of exacerbation Whether exacerbation landed them in the hospital or not Exacerbation is acute worsening of resp sx/ URI usually * Group A: low risk (0-1 exacerbation per year, not requiring hospitalization) and fewer symptoms (mMRC 0-1 or CAT \<10) * Group B: low risk (0-1 exacerbation per year, not requiring hospitalization) and more symptoms (mMRC≥ 2 or CAT≥ 10) * Group C: high risk (≥2 exacerbations per year, or one or more requiring hospitalization) and fewer symptoms (mMRC 0-1 or CAT \<10) * Group D: high risk (≥2 exacerbations per year, or one or more requiring hospitalization) and more symptoms (mMRC≥ 2 or CAT≥ 10).
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How does the hypothalamus function in relation to the thyroid
* Hypothalamus releases thyrotropin-releasing hormone (TRH) which stimulates anterior pituitary to release thyroid-stimulating hormone (TSH) which stimulates the thyroid to release T3 and T4 * Only 10% of T3 is produced in thyroid – T4 converts to T3 in body tissues * Iodine needed to synthesize the T3 and T4 * Thyroid hormones are bound to thyroglobulin (protein) until they are released
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Growth Hormone Excess Pituitary gigantism vs acromegaly
Pituitary gigantism: occurs in childhood before the skeletal epiphyses close * Accelerated growth velocity (\>95 percentile on pediatric growth chart) * Left untreated, may grow \>8 feet tall with increased risk of cardiomegaly and heart failure Acromegaly: growth hormone excess in adults; progressive over several years
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Adrenal Gland Cortex Produces Salt sugar and sex tells you what comes out of the Adrenal Cortex
* Mineralocorticoids - Aldosterone (salt and water) * Glucocorticoids – Cortisol (sugar) * Gnadocorticoids - Androgens and Estrogens (sex)
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Classification of Asthma Severe
Symptoms: Throughout the day Nighttime awakenings: Often 7x week Uses inhaler: Several times a day Interference with normal activity: Extremely limited
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Islet of Langerhans Types of cells
* Alpha cells – secrete glucagon * Glucagon (opposite of insulin) tells the liver to break down glycogen stores into glucose - raises sugar * Beta cells – secrete insulin and amylin * Insulin works with amylin to control glucose * Delta cells – secrete somatostatin and gastrin * Somatostatin inhibits growth hormone * Gastrin stimulates the stomach to release gastric acid
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You can have hypoxemia at tissue level but not hypoxemia
Yes example is a crushing injury
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Hyperparathyroidism Diagnosis
* Primary hyperparathyroidism: * Serum calcium levels elevated with low to normal phosphorus * Urinary excretion of calcium and phosphorus are elevated; serum PTH levels are elevated * Intact PTH and Ionized calcium * Thyroid US and parathyroid nuclear scan
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Clinical Manifestations Mono
Sever pharyngitis; exudate (mimics strep) Fever - high Tonsillar and cervical lymphadenopathy Hepatosplenomegaly and elevated LFTs Thrombocytopenia (spleen), elevated WBCs
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GOLD Criteria - COPD ## Footnote IN PATIENTS WITH FEV1/FVC RATIO \< 0.70 - This is the guide BASE ON PREDICTED LEVEL GOLD 1 MILD - \>80% GOLD 2 MOD - FEV1 is between 50% and 79% predicted GOLD 3 SEVERE - FEV1 is between 30% and 49% predicted GOLD 4 VERY SEVERE - FEV1 \<30% predicted
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Hormones secreted by the POSTERIOR PITUITARY
ADH (vasopressin) Oxytocin
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Urine Specific Gravity low number means diluted urine high number means concentrated urine
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Specificity
The "fit" of a hormone into a receptor binding pocket
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Functions of the Pancreas
* Exocrine secretions for digestion * Endocrine functions
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Explain Pulmonary Circulation
High flow LOW pressure Coming from the Right Ventricle should be low pressure \<25mm/Hg
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Glycogenolysis
Breakdown of glycogen into glucose for energy
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Pharyngitis (Tonsillitis)
Fever \>100.4 Bacterial - Strep A Viral - RSV
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Peritonsillar Abscess
Emergency Absess of one tonsil, can displace uvula Caused by staph or strep Clinical manifestations: drooling, dysphasia
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Pulmonary HTN Clinical Manifestations
Activity intolerance Fatigue Hemoptysis (excess pressure leaks back into alveoli) Syncope Chest pain on exertion When sx appear cannot be reversed focus on prevention
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Hormone Synthesis - Thyroid Hormone
Thyroid hormones (lipid-soluble) are formed on demand but are trapped attached to thyroglobulin and sit and wait until they are told its time to be released by the hypothalamus or anterior pituitary
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Diagnosis of Hypoparathyroidism
* Serum calcium (low); phosphorus (high) * Antibodies to parathyroid gland present if autoimmune mechanism involved
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Hypercortisolism Etiology and Pathogenesis
* Primary: disease of the adrenal cortex * Secondary: hyperfunction of anterior pituitary ACTH-secreting cells * Tertiary: hypothalamic dysfunction or injury * Iatrogenic - long term steroid use * Ectopic ACTH producing tumor – small cell lung cancer
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Screening for Diabetes
Screening for Diabetes -USPSTF * All adults older than age 40 should be screened at least every 3 years for type 2. * Individuals with risk factors should be screened earlier or more frequently. No screening requirements for type 1
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What would you see in relation to insulin in a person with Growth Hormone Excess
May cause persistent hyperglycemia and increased insulin production (GH called a diabetogenic hormone)
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Explain the Primary Classification of Endocrine Disorders
Primary: intrinsic malfunction of the hormone-producing gland In primary, gland fails; an inadequate hormone produced, low levels of circulating hormone, but blood levels of the corresponding trophic pituitary hormone levels very elevated.
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When do you measure cortisol for testing
First thing in the morning when its at the highest
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Risk factors for Diabetes Mellitus
Type 2 Diabetes Mellitus * Risk factors: female sex, obesity, aging, and sedentary lifestyle * Polyuria, polydipsia, and polyphagia may be more subtle
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Clinical Manifestations of Hypothyroidism in Infants
•Clinical manifestations in infants Routine screening in newborns has resulted in increased treatment for congenital hypothyroidism. * Dull appearance, thick, protuberant tongue, and thick lips * Prolonged neonatal jaundice * Poor muscle tone, umbilical hernia * Bradycardia, mottled extremities * Hoarse cry * Mental retardation unless treated early
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Geriatric Complications
Increased prevalence of type 2 DM Increased adiposity, decreased lean body mass, decreased activity levels, decreased insulin secretion, hyperglycemic effect of certain medications
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How does exercise affect insuln levels
Initially insulin levels drop and glucagon and catecholamine levels rise, increasing production of free fatty acids (FFAs) and stimulating glycogenolysis. Glucose from liver meets energy demands. (Glycogenolysis) Muscle contractions increase insulin sensitivity, maintaining normal blood glucose levels in the presence of lower insulin levels.
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Emphysema Etiology
* **Smoking \>70 packs/year (2pk/dayX30years)** * Air pollution * Certain occupations (mining, welding, working with or near asbestos) * **α1-Antitrypsin deficiency** * Expanded "floppy" lungs
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Hypercortisolism Cushings Syndrome
•Cushing syndrome—term used to describe any other reason for hypercortisolism
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STEROID HORMONES GLUCOCORTICOIDS
Primary effect on **glucose metabolism** **Oppose the effects of insulin** and raise blood glucose levels by decreasing glucose uptake by many body cells (decreased glycogenesis) and increasing glucose synthesis in the liver from glycogen and amino acid and glycerol substrates in fat stores (glycogenolysis, gluconeogenesis)
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Clinical Manifestations of Growth Hormone Deficiency
Most clinically relevant in children **_Associated with:_** Birth history of prolonged labor or breech delivery, congenital chromosomal anomaly; nystagmus, retinal abnormalities, midline or midfacial abnormalities (cleft lip or palate) **_Clinical manifestations in children:_** Hypoglycemia Growth below the third percentile Dental eruption delayed Irregular setting of permanent teeth Thin hair, poor nail growth Greater fat mass, decreased muscle mass and delayed bone formation Delayed puberty **_Clinical manifestations in adults:_** Diminished lean body mass Hypercholesterolemia Decreased bone density **_Diagnosis_** Confirmed by decreased serum GH
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Diffuse Interstitial Lung Disease Clinical manifestations
Clinical manifestations * Progressive dyspnea with irritating, nonproductive cough * Rapid-shallow breathing * Clubbing of nail beds * Bibasilar end-expiratory crackles * Cyanosis (late finding) * Anorexia, weight loss * Inability to increase cardiac output with exercise
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Secondary Pulmonary HTN
Stems from a known disease Mitral stenosis Mitral regurgitation LV heart failure Chronic lung diseases Vasculitis
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Growth Hormone Disorders
* Growth hormone (GH) produced in anterior pituitary gland * Regulated by hypothalamic: * Release of growth hormone-releasing hormone (GHRH) * **_Inhibited by Somatostatin_** * Primary target organ is the liver. * Increases lean body mass, reduces fat mass, and induces liver to release glucose under conditions of hypoglycemia * GH acts opposite of insulin and raises glucose
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FEV 1
amount of forced air exhaled over 1 second Normal – generally 80% of Forced Vital Capacity
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Normal range for Hemaglobin A1c - HgbA1
Normal range 4 - 5.7% ## Footnote 1% reduction decreases microvascular risks by 10%
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What happens after you eat in relation to glucose metabolism
* Glucose ingested food causes a brief rise in insulin release (first phase). * Continued glucose causes increased insulin secretion (second phase) * Ingestion of nutrients stimulates release of **glucose–dependent insulinotropic polypeptide (GIP)** and **glucagon-like peptide 1 (GLP-1) from cells in the gut.**_(Incretins stimulates insulin release and inhibits glucagon to lower sugar)_ * Effect on blood glucose known as **incretin effect**
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Antidiuretic Hormone Disorders Syndrome of Inappropriate Antidiuretic Hormone SIADH Clinical Manifestations
Clinical manifestations * Hyponatremia \< 135 mEq/L (135-145) * High urine osmolality * Low serum osmolality * Weakness, muscle cramps, N/V, postural BP changes, poor skin turgor, fatigue, anorexia, lethargy * Confusion, hemiparesis, seizures, coma
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Pharmacologic Hormone Concentrations vs Physiologic hormone concentrations
Physiologic hormones are extremely low due to amplification Pharmacologic levels are much higher Tissue response to pharmacologic hormone concentrations may be significantly different from physiologic levels
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Describe Type 1 Diabetes Mellitus
* Characterized by destruction of the β cells of the pancreas * Usually diagnosed between 5 and 20 years of age * Etiology may be immune-mediated or idiopathic (without autoimmune markers or HLA association). * Autoimmune markers: chromosome 6 * HLA: MHC genes
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Hypothyroidism Etiology and Pathologenesis
* May be congenital or acquired * **Majority are primary,** because of intrinsic thyroid gland dysfunction * Congenital hypothyroidism (cretinism) typically caused by thyroid dysgenesis (lack of development) **•Secondary, as a result of defects in TSH production (hyposecretion)**
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Bronchiolitis eitilogoy
Widespread inflammation of the bronchioles (smaller bronchioles) RSV most common cause Winter to spring Common in children Adults for smoking, toxic fumes
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Pre-diabetes classes:
* Impaired glucose tolerance * 2-hour post-glucose value of 140 to 200 mg/dL * Impaired fasting glucose tolerance * Fasting plasma glucose value of 100 to 125 mg/dL
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Etiologies of Endorine Disorders
Functional disorders - Caused by nonendocrine disease such as chronic renal failure, liver disease, or heart failure Tissue resistance - Occurs when target tissue fails to respond to a hormone (hormone resistance or target tissue resistance) Iatrongenic - Induced by medical treatments such as chemotherapy, radiation therapy, or surgical removal of glands
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Mechanism of Water Hormones with Cell Membrane Receptors
Hormones exert their action by binding to target cell receptor proteins Water-soluble hormones have a hormone-binding site located on the external portion of a specific cell surface receptor Once binding takes place, receptor protein conveys a signal to the interior of the cell to produce a response
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Clinical Manifestations of Prolactinemia
Clinical manifestations * Hypogonadism * Premenopausal female infertility, oligomenorrhea, and galactorrhea * Male decreased libido, impotence, infertility, gynecomastia, and galactorrhea
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Hormones are categorized by chemical composition
Steroids - androgens glucocorticoids, thyroid (lipids) Proteins/polypeptides - Insulin, growth hormone (water) Amines/amino acids - epinephrine (water) Fatty acid derivatives - prostaglandins
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Three mechanisms involved in Secondary HTN
Increased pulmonary blood flow Increased resistance to blood flow Increased left atrial pressures
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Acute Geriatric Complications
* Acute complications * Hyperglycemia: often asymptomatic; dehydration; increased risk of infection; * Non-ketotic hyperglycemic hyperosmolar coma Glucose \>500-600, dehydrated, electrolyte imbalances; arrhythmias, seizures, coma * Hypoglycemia may be atypical and can lead to injury. * Lethargy or focal neurologic dysfunction * Age-related decreases in counter-regulatory function or an inability to report hypoglycemic symptoms
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Lower airway structures Sympathetic stimulation
•Sympathetic stimulation (mediated by β2-adrenergic receptors); leads to relaxation of the smooth muscle
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Amplification of Hormone Activity
Why you can have a very small amount of circulating protein and it can cause a tremendous effect on the body. Progressively larger numbers of chemical reactions occur at each step, resulting in the activation of numerous G proteins
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Cross specificity
One receptor site will respond to two or more different hormones. May occur between hormones Example is growth hormone and prolactin both can bind to a prolactin receptor so if growth hormone take up all the receptors their won't be any for prolactin
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What may prevent or improve symptoms of diabetic neuropathy?
Glycemic control may prevent or improve symptoms of diabetic neuropathy.
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Spermatocele
Lump on testicle that is painless and moveable
254
What influences resistance in the airway
Resistance influenced by airway radius and the pattern of gas flow
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Ventilation
Movement of air in and out of the lungs
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FEV1/FVC RATIO
\> 70% Normal Ratio of how much you exhaled in the first second divided by how much you exhale Less than 70% is obstructive Greater than 70% is either normal or restrictive (FVC \<80%)
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What does Calcitonin do?
* Calcitonin produced by thyroid parafollicular cells; also influences the processing of calcium by bone cells * Calcitonin increases bone formation by osteoblasts and inhibits bone breakdown by osteoclasts. * Calcitonin decreases blood calcium levels and promotes conservation of hard bone matrix.
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Hypoxemia
Low oxygen in bloodstream
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Parathyroid Gland
* 4 glands * Located behind the thyroid glands * Secrete parathyroid hormone (PTH) •PTH – regulates calcium * Can cause calcium release from bones when serum calcium levels are low (makes bones weak) * Can increase calcium absorption from the GI tract and in the renal system * PTH stimulates Vitamin D which is needed for calcium GI absorption
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Gestational Diabetes Mellitus Risk Factors
Most likely precipitated by placental hormones and weight gain Risk factors Severe obesity, history of gestational diabetes, previous offspring weighing more than 9 lbs at birth, presence of glycosuria, or a strong family history of type 2 diabetes
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Hyperparathyroidism Clinical Manifestations
•Clinical manifestations * Kidney stones * Bone demineralization (osteoporosis) * Polyuria and dehydration * Anorexia, nausea, vomiting, constipation * Bradycardia, heart block, and cardiac arrest * Manifestations result from high serum calcium levels and bone demineralization. * High serum calcium levels decrease neuromuscular excitability.
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Pneumonia causes
Bacterial, viral, fungi Aspiration of secretions or gastric contents Inhalation of smoke or chemicals
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Water soluble hormones
Bind to cell surface receptors Peptides (small proteins) majority of endocrine hormones Easily transported in the bloodstream ACTH FSH LH, Growth Hormone, TSH PTH
264
FVC
Total expiration of air
265
Epiglottis Causes
Haemophilus influenzae type b (HIB) GABHS bacteria Throat trauma Hot liquids Foreign objects
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Adrenal Insufficiency Etiology & Pathogenesis
Etiology and pathogenesis * Primary: hyposecretion caused by disease of adrenal cortex; idiopathic or autoimmune (Addison disease), surgical removal * Secondary: inadequate secretion of ACTH from anterior pituitary; usually iatrogenic, related to corticosteroid therapy (suppresses ACTH) followed by sudden withdrawal of steroids * Tertiary: lack of secretion of CRH from hypothalmus * Cortisol insufficiency is most clinically relevant
267
Flu Vaccine information
Quadrivalent (2 strains both A and B) Intranasal for ages 2-49 its a live vaccine (no for pregnant, immunocompromised or chronic resp prob) If over 65 4 dose series of not live vaccine
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Negative Feedback for Thyroid System
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Clinical Manifestations Graves Disease
* Clinical manifestations * Insomnia, restlessness, tremor, irritability, palpitations, heat intolerance, diaphoresis, diarrhea, inability to concentrate that interferes with work performance; enlarged thyroid gland * Increased basal metabolic rate leads to weight loss, although appetite and dietary intake increase. * Amenorrhea/scant menses
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Pathogenesis Cystic Fibrosis CTFR Gene
Pathogenesis * Dysfunction of CFTR gene * Normally CFTR encodes a membrane chloride channel and is in sweat glands, lungs, and pancreas * CFTR gene mutations result in alteration in chloride and water transport across epithelial cells. * Primarily affects the pancreas, intestinal tract, sweat glands, and lungs, and in males causes infertility * High concentrations of sodium and chloride in sweat, salivary, and lacrimal secretions
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Comparison of Type 1 and Type 2 Diabetes
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Normal level of T3 & T4
T3 (75 - 195 ng/ml) T4 (5-12 mcg/dL)
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Classifications of Rhinosinusitis
Most infections are viral Acute sx \<4 weeks Chronic sx =12 weeks Recurrent \>4 year
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The Adrenal Glands Medulla Produces
Epinephrine Norepinephrine
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Diabetes Mellitus
* Hyperglycemia from insulin production and/or action defects * Type 1 diabetes - autoimmune * Destruction of pancreatic beta cells * Type 2 diabetes - herideratary * Insulin resistance and loss of insulin production * Gestational diabetes * Glucose intolerance during pregnancy * Ineffective pancreatic function to overcome insulin resistant state
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Types of ventilation - perfusion imbalances
High (under perfused) Ventilation \> perfusion - Alveolar unit is ventilated, but not perfused. Happens with PE (lack of blood flow) Low (underventilated) Ventilation
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Grade of COPD Symptoms Modified British Medical Research Council mMRC Questionnaire on breathlessness
0 minimal sx 1-2 slowing down 3 -4 - symptomatic to very symptomatic
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Proprioceptors
* Located in muscles and tendons of movable joints * Respond to body movement (exercise) and increase rate and depth of respiration Muscle movement stimulates you to take a breath HTN slows down respiration Hypotension increases respiration - venous return
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Cystic Fibrosis Pathogenesis
* Mucous-producing glands in the GI tract enlarge * Generates excessive secretions * Thick eosinophilic mucus secretions plud the glands and ducts of the GI tract, causing dilation and fibrosis * Leads to decreased production of pancreatic enzymes, causing increased FAT and PROTEIN IN THE STOOL
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Steroid Hormones MINERALCORTICOIDS ALDOSTERONE
* Maintain normal salt and water balance by promoting sodium retention and potassium excretion at the distal renal tubules * Aldosterone secretion regulated primarily by the renin-angiotensin system associated with the juxtaglomerular cells of the kidney * Released in response to low blood pressure, reduced renal perfusion and a high serum potassium level
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Diagnosis of Chronic Bronchitis
Diagnosis * Chest x-ray * Increased bronchial vascular markings * Congested lung fields * Evidence of previous pulmonary infection * Pulmonary function tests * Normal total lung capacity (TLC) * **Increased residual volume (RV)** * **Decreased FEV1** * ECG - right ventricular hypertrophy * CBC – polycythemia due to hypoxia * Chronic or recurrent productive c**ough \>3 months** \>2+ successive years * Persistent, **irreversible** when paired with emphysema
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Diagnosis for Hypothyroidism
Diagnosis •Primary: elevated TSH (0.5-4.5 normal levels) May have elevated TPO/Thyroglobulin * Secondary: decreased TSH (Pituitary failure) * Low levels of T3 and T4 may not occur until later in the disease course. * T3 (75-195 ng/ml) T4 (5 -12 mcg/dL)
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Sarcoidosis Clinical Manifestations
* Malaise, fatigue * Weight loss * Fever * Dyspnea of insidious onset * Dry, nonproductive cough * Erythema nodosum * Macules, papules, hyperpigmentation, and subcutaneous nodules * Hepatosplenomegaly, lymphadenopathy
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Tuberculosis
Caused by Mycobacterium tuberculosis Transmission via aerosol droplets with active TB patient Can survive weeks in dry sputum Florida 4th state for positive cases
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Diagnosis Pneumonia
CURB - 65 WBC \>15,000 (bacterial) Chest Xray shows white shadows (Parenchymal infiltrates)
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Risk factors for Pulmonary Embolus
Immobility Trauma Pregnancy Cancer Heart Failure Estrogen Use Smoking
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Causes of Restrictive Lung Diseases
1. Stiff lungs (can't inflate) 2. Stiff chest wall (kyphosis, obesity, rigidity) 3. Elasticity of lungs (can't snap back) -Decreased (COPD) Increased - (Pulmonary fibrosis, Sarcoidosis, SLE, Asbestos)
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What hormones are released from the Anterior Pituitary
**_•Anterior_** ## Footnote Somoatotropes secrete GH Gonadotropes secrete LH/FSH Thyrotropes secrete TSH Corticotropes secrete ACTH Lactropes secrete prolactin (PRL)
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Extrinsic (Atopic) Asthma (E)xtrinsic = IgE (A)topic = allergy
1/3 to 1/2 of asthma cases A genetic IgE-mediated exaggerated response in many cases Allergic rhinitis, atopic dermatitis and eczema
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Prolactinemia Cause Primary vs Secondary
Primary is a disorder of the anterior pituitary Secondary is a disorder of the hypothalamus Normal range = Men 10-20 Women 10-25
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Diffusion
Respiration Movement of gas between air spaces in the lungs and the bloodstream
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Hormone Synthesis - Water soluble
Peptide hormones are contained within the bilayer of the vesicles and stored until a trigger results in the exocytosis of the hormone into the extracellular space
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Hormones are classified by
Action - the effect they have (insulin lowers glucose) Source - Anterior or posterior pituitary Chemical structure
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What is the most common cause of acquired hypothyroidism:
Lymphocytic thyroiditis (Hashimoto or autoimmune thyroiditis); may result in a goiter Irradiation of the thyroid gland Surgical removal of thyroid tissue Iodine deficiency
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Where do we get energy how is it metabolized
Energy requirements are met by glucose and fats Glucose is produced from glucose stores or glycogen in liver primarily it is coming from the bloodstream from the GI tract and liver
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Tidal Volume
amount of gas entering or leaving in a normal breath – 500 ml Increases with exercise
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Hypercortisolism Clinical Manifestations
Clinical manifestations * Round face with flushed cheeks, “moon face” * Weight gain with excess total body fat, particularly in the abdomen, thin extremities * Cervical fat pad, capillary friability, thin skin with formation of purple striae and ecchymosis over the abdomen, arms, and thighs * Decreased muscle mass, muscle weakness * Glucose intolerance, hyperglycemia * Hypertension (salt-retaining activity of cortisol) * Demineralization of bone (osteoporosis) * Increased androgen production causing excessive hair production, acne, menstrual irregularities * Emotional lability, anxiety, irritability, depression
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What are secondary complications of the flu
Secondary pneumonia Reye Syndrome in children
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Pleural Effusion Etiology & Pathogenesis
Collection of fluid or pus in pleural cavity as a result of another disease process Changes in pleural capillary hydrostatic pressure, colloid oncotic pressure, or intrapleural pressure Imbalance in pressure associated with fluid formation exceeding fluid removal
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Perfusion
Movement of blood into and out of the capillary beds of the lungs to body organs and tissues
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Glycolysis
Body is breaking down sugar so the cells can use it
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Acute Pediatric Complications of DM
* Dehydration: diabetic ketoacidosis * When blood glucose is \>240 mg/dL or during illness, test for ketones. * Hypoglycemia may be difficult to detect; subtle behavioral changes. * Lethargy, pallor, and sleep disturbances
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Causes of impaired diffusion
Thickening of alveolar cap membrane - pneumonia, pulm edema; also aging Surface – Emphysema – areas destroyed Activity - less blood flow time in the lungs Elderly – decreased lung capacity, blood flow Newborn - thick alveolar membrane
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Explain Hypersecretion of the Thyroid Disease
HYPERSECRETION * Excess secretion of hormone * Primary hypersecretion occurs when there is a dysfunction of the endocrine gland that results in abnormally high secretion of hormone. * Secondary hypersecretion occurs when there is an elevation in the tropic level of one hormone that results in an increased plasma concentration of another hormone.
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Gluconeogenesis
No sugar in system and glycogen used up so the body gets sugar from other non sugar substances
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Cystic Fibrosis Etiology
Autosomal recessive disorder of exocrine glands Most common genetic lung disease in the US Classified as airflow or suppurative (pus-forming) Hypersecretion of abnormal, thick mucus that obstructs exocrine glands and ducts Median survival age: 31 years
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Diabetic Neuropathy Patho and Etiology
Diabetic neuropathy * Autonomic dysfunction: GI disturbances, bladder dysfunction, tachycardia, postural hypotension, and sexual dysfunction * Sensory dysfunction includes carpal tunnel syndrome, paresthesias in extremities, especially feet. * Amputation 15 to 40 times higher than in nondiabetic individuals
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Growth Hormone Excess Clinical Manifestations
Clinical manifestations of acromegaly * Increased ring or shoe size * Enlargement of frontal sinus causes prominent brow. * Growth of mandible leads to progressive underbite (prognathism). * Coarse facial features and skin tags * Increased size of internal organs * Deepening of the voice and enlarged tongue
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How to diagnosis Diabetes Insipidus
Diagnosis * Dilute urine, hypernatremia along with abnormally low serum ADH levels (diagnostic of central DI) * Renal US or MRI Brain
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Affinity
The degree of "tightness" or the hormone receptor bond or the inclination of the hormone to remain bound to the receptor i.e. Old key locks you put key in a jiggle it around present-day locks have a high affinity with tight locks only fitting the intended key When you have a high affinity you don't need as much of the hormone you can use a very small amount
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Acidosis can result in
Hyperkalemia
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Examples of normal ventilation but low perfusion = high V/Q ratio (\>0.8)
Pulmonary emboli SLE Sarcoidosis Alveolar carcinoma example: 4L/3L = 1.3VQ
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Normal range for HgbA1c
5.7%
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Gluconeogenesis
Generation of glucose from non-sugars
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Sleep Apnea Etiology
Obstructive (OSA) or Central (CSA) ## Footnote OSA - associated with obesity oral or pharyngeal obstruction CSA - associated with heart or brain abnormalities (rare) Risk factors - neck circumference 17" in men 16" in women
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What are etiologies of Endocrine Disorders
Congenital ## Footnote Inborn genetic defect that causes excessive production of hormone precursors Autoimmune Involves genetic predisposition and environmental trigger; antibodies made against antigens on self-tissue cells Neoplastic Hormones may be produced by abnormal tissue sites (ectopic) such as malignancies.
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Explain Negative feedback control
The body says it need so much of a hormone the body reacts to it and it sends a signal back to the anterior pituitary and hypothalamus that fx at a good level. If we don't need as much hormones it will send a message back that to the anterior pituitary to slow down production If deficient in hormone sends signal to anterior pituitary and hypothalamus that we need more How we keep hormone level fx and at level we want
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Beta cells produce...
β cells produce proinsulin. ## Footnote * Stored in granules, where it is cleaved into insulin and C-peptide * 1:1 RATIO OF INSULIN AND C-PEPTIDE
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Diffuse Interstitial Lung Disease
Pathogenesis Begins with injury to alveolar epithelial or capillary endothelial cells Persistent alveolitis leads to obliteration of alveolar capillaries, reorganization of lung parenchyma, irreversible fibrosis Leads to large air-filled sacs (cysts) with dilated terminal and respiratory bronchioles (honey-comb lung)
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Diagnosis Emphysema
Diagnosis * Pulmonary function tests (PFTs) -BIG LUNGS- * Increased functional residual capacity * Increased RV, TLC * Decreased FEV1, FVC * Chest x-ray * Hyperventilation * Low, flat diaphragm * Presence of blebs or bullae * Narrow mediastinum * ECG * Normal, show **tall P waves** * Sinus tachycardia: first sign of decreased oxygenation * Supraventricular and ventricular arrhythmias
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Disorders/Diseases of the Thyroid Gland
Hyposecretion Hypersecretion Target cell hypo-responsiveness
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Delta cells produce...
Somatostatin (counteracts growth hormone)
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Hypercortisolism Cushing's Disease
•Cushing disease—term only used for pituitary hyperstimulation of adrenal cortex; secretes excess cortisol
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Glycogenolysis
Breakdown of glycogen into glucose for energy Opposite of Glycogenesis
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Regulation of Receptor Responses What determines the ability of a cell to respond to a particular hormone
Cell response to a hormone depends on the presence of specific receptors on very specific cells for that hormone on the cell called the target cells A cell can change how it wants to respond to a hormone by changing the # of receptors or an affinity for the hormones
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What happens when glucose levels rise?
Glucose levels rise, leading to polyuria (increased urination), polydipsia (thirst), and polyphagia (hunger): classic signs.
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Laryngitis
Inflammation of the larynx - vocal cord Noninfectious - screaming, singing, vomiting Infectious form - Rhinovirus, Strep
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Macrovascular damage r/t Diabetic Vascular Complications with DM
*_Macrovascular:_* damage to large blood vessels; leads to cardiovascular disease, peripheral vascular disease, and stroke * Preventive: caloric restriction, exercise, possibly drugs, control dyslipidemia, and hypertension * DM is an independent risk factor for coronary artery disease (CAD). * Dyslipidemia, hypertension, and impaired fibrinolysis are present in uncontrolled DM; improve with blood glucose control.
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What does an overproduction of glucagon stimulate?
Glycogenolysis and Gluconeogenesis
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Metabolic Syndrome
* Cluster of risk factors * Hyperglycemia, hypertension, hypercholesterolemia, increased waist circumference * Chronic complications * Directly result from long-term excessive glucose levels * Thickening and hardening of vessel walls * Causing diffuse ischemia and necrosis * Macrovascular complications * Microvascular complications * Miscellaneous complications
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Tuberculosis Pathogenesis
* Lymphocytes and macrophages form a granuloma around bacilli to contain it * Caseating granuloma * Intact immune system inhibits granuloma formation and develop Ghon complexes that calcify * Latent TB – infected but asymptomatic and not contagious
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When are CRH and ACTH at their peak and lowest point?
CRH and ACTH have a significant diurnal pattern, with a peak on wakening in the morning and a valley in the evening.
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Hydrocele
Excess fluid
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What is the ideal Ventilation to Perfusion ratio
Ventilation 4L/min Perfusion 5L/min 4/5-0.8
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Thyroid Gland follicles
* Thyroxine – T4 * Triiodothyronine – T3 * Thyrocalcitonin – Calcitonin (regulates calcium levels)
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Persistent Asthma Classification
Mild X2 week Moderate X1 day Severe multiple X a day
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Pre-Diabetes --- Impaired Glucose
Impaired glucose tolerance and impaired fasting glucose tolerance Intermediate stages between normal glucose metabolism and diabetes •HgbA1c : 5.7 – 6.4%
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Explain the Secondary Classification of Endocrine Disorders
* Secondary: malfunction of the hypothalamus/pituitary cells that control the target gland * In secondary, pituitary gland fails to release trophic hormone, secondarily reducing primary gland production, so both levels are abnormally low. * Since clinical manifestations are similar, laboratory results can help distinguish between primary and secondary.
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Classification of Asthma Severity Mild
Symptoms: \>2 days a week, but not daily Nighttime awakenings: 3-4x month Uses inhaler: \>2 days/week but not daily, and not more than 1x day Interference with normal activity: Minor limitation
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Diffuse Interstitial Lung Disease Diagnosis
Diagnosis * Chest x-ray * PFTs (decreased VC, TLC; normal FEV1/FVC ratio * Open lung or transbronchial biopsy * Gallium-67 scan lung scan * High-resolution computed tomography (HRCT) and bronchoalveolar lavage
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Cystic Fibrosis Clinical Manifestations
Clinical manifestations * Persistent, daily, chronic, productive cough * Purulent, foul-smelling, green, or yellow sputum * Hemoptysis * Fever, night sweats * Moist crackles, rhonchi * Halitosis (bad breath) * Skin pallor