Test 3 Reproductive, Pulmonary, Endocrine Flashcards by Carley Hernandez

Who’s at risk for pneumonia

young and old COPD Emphysema Asthma Immunocompromised

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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

Pathogenesis of type 2 diabetes

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Hormone Permissiveness

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

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Normal V/Q ratio:

4-5L = 0.8

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Diabetes Insipidus

Clinical Manifestations

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

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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Pneumonia etiology

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

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A 35 yo presents with no history

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

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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Perfusion

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

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Honeycomb Lung

Restrictive vs Obstructive

Diseases

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Classification of Asthma Severity

Intermittent

Symptoms: <2 days a week
Nighttime awakenings: <2x month
Uses inhaler: <2 days/week
Interference with normal activity: None

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Bronchiolitis Clinical Manifestations

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

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What is untrue about asthma

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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Obstructive Lung Disorders

Manifested by increased resistance to airflow

CAN’T GET AIR OUT

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Primary

Secondary

Hyper/Hypo Thyroidism

Primary - thyroid is the problem

Secondary - pituitary is the problem

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Cystic Fibrosis

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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Emphysema

Pathology

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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Croup Clinical manifestations

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

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What are 3 ways that a

Growth Hormone Deficiency can develop

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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Emphysema

Clinical Manifestations

PINK PUFFER

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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Goiter vs Thyroid Nodules

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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What is the biggest risk factor for DM

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

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Clinical Manifestations

Adrenal Insufficiency

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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Clinical manifestations Hand-Foot-Mouth Disease

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

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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

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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

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Epiglottitis Patho

Lift threatening condition Rapid cellulitis of epiglottis and surrounding soft tissue Air blockage into the trachea Children ages 2-4

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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.

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Infective Mono - Epstein Barr Virus Pathology

Cytomegalovirus (CMV) Trans primarily saliva Viral - no abx Incubation is 4-6 weeks

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Adrenal Gland

Located on top of each kidney

Has inner medulla and outer cortex
Hypothalamus regulates function

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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

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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%)

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Virchow’s Triad

Venous stasis/sluggish blood flow Hypercoagulability Damage to the venous wall

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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

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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

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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

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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

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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.

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What hormones

are released

fro the

Posterior Pituitary

•Posterior

ADH (vasopressin)

Oxytocin

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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

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Glycolysis

Breakdown of glucose for energy

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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

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COPD

Criteria

A - no symptoms or hospitalizations

B - mod symptoms no hospitalizations

C - have been hospitalizations

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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.

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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

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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

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Clinical Manifestations of Pulmonary Malignancies

Persistent cough that changes Dyspnea Hemoptysis Hoarseness Frequent URIs

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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

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Elevated prolactin (from anterior pituitary) level

Galactorrhea

Amenorrhea

Headache

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Hormones secreted by the

ANTERIOR PITUITARY

Somoatotropes secrete GH

Gonadotropes secrete LH/FSH

Thyrotropes secrete ACTH

Lactropes secrete prolactin (PRL)

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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

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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

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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

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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

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Emphysema

Classifications

Centriacinar (centrilobular)
- Associated with smoking and chronic bronchitis
- Destroys respiratory bronchioles
Panacinar (panlobular)
- Destroys the alveoli
Paraseptal
- Affects the peripheral lobules

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Type B Influenza

Generally milder Isloated primarily to humans

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How to diagnose Pulmonary HTN

Measurement of pulmonary artery pressure during exercise Stress testing ECHO Big R wave or Inverted T wave

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FEV1

How much air can be expelled in 1 sec

>80% Normal

<70% is obstructive

>70% is normal or restrictive

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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)

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Explain Somogyi phenomenon

Rise in AM glucose as a rebound effect of hypoglycemia

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Best overall ventilation and perfusion occurs in the

Dependant lung fields

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Laryngitis Clinical Manifestations

Throat is NOT red Hoarseness Weak voice Aphonia

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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

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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

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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.

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Clinical manifestations Epiglottis

High fever Drooling Stridor

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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

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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)

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Residual Volume

amount of gas left in the lungs after expiration – 1.2 L

can’t breathe everything out

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Peritonsillar Abscess

Emergency Abscess of one tonsil can displace uvula Caused by staph or strep Clinical manifestations: drooling, dysphasia

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Lower Airway Structures

Parasympathetic Stimulation

•Parasympathetic stimulation (mediated by acetylcholine) via the vagus nerve leads to constriction of muscle.

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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.

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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

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Obstructive defect for spirometry alone as rated by FEV%

>70% = Mild

60-69% = Moderate

50-59% = Moderate severe

35-49% = Severe

<35% = Very severe

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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.

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Determining Hypothyroidism

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Anterior pituitary gland hormones are regulated

by the hypothalamus

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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

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Pathogenesis of Growth Hormone Deficiency

Pathogenesis

May be idiopathic or related to tumors, radiation, or trauma
Resection of pituitary tumors or head injuries

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Asthma

Etiology

Airway obstruction that is reversible

Airway inflammation

Leukotriene reaction of bronchoconstriction

Increase in bronchial responsiveness to a variety of stimuli

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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.

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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.

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Hypothyroidism

Hyperthyroidism

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Clinical Manifestations

CHRONIC BRONCHITIS

Type B COPD “blue bloater”

Overweight

Dyspnea on exertion

Excess sputum

Chronic cough - WORSE IN AM

Cyanosis - late sign

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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.

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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

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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

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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

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Ventilation

Movement of air in and out of the lungs

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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)

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Chronic Bronchitis - Blue Bloater

Emphysema - Pink Puffer

Chronic Obstructive Pulmonary Diseases

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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.

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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

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Clinical manifestations Pulmonary Embolus

Restlessness Pain on inspiration Tachycardia Hemoptysis Anxiety

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Grade of COPD Symptoms

COPD Assessment Test (CAT)

Impact Level

CAT score-Impact level

< 10 Low

10 – 20Medium

21 – 30 High

> 30 Very high

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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.

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Central Diabetes Insipidus

Nephrogenic Diabetes Insipidus

Central: involves hypothalamus or pituitary gland

Nephrogenic: involves kidneys

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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

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Diagnosis

CT of chest with contrast to light up vessels Pulse OX

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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.

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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

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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

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Clinical manifestations Influenza

Sudden onset Significant fatigue Significant myalgia (muscle pain) Headache Fever >100 Chest congestion and non-productive cough Clear nasal secretions

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Glycogenesis

Excess circulating glucose is converted into glycogen and stored in the liver and muscle cells

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Hypoxia

Decrease in tissue oxygenation

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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

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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

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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

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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)

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Deep labored respirations that are fruity in odor

Kussmaul respirations and they occur in diabetic ketoacidosis

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Etiology

Chronic Bronchitis

BLUE BLOATERS

Cigarette smoking (90%)

Repeated airway infections

Genetic predisposition

Inhalation of physical or chemical irritants

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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)

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Causes of Croup

Flu

Viruses

RSV

Adenovirus

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Influenza

Viral infection of the upper and lower respiratory tract Common Oct - March

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What 4 things enhance the development of neuropathy?

•Hypertriglyceridemia, obesity, smoking, and hypertension enhance development of neuropathy.

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Clinical Manifestations

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

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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

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CURB 65

1 POINT 68 YO

1 POINT HYPOTENSIVE

1 POINT BUN ELEVATED

CUT OFF FOR RESPIRATORY IS 30 TO GET A POINT

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Classification of Pulmonary Malignancies Small cell carcinoma

Oat cell (Extremely aggressive) Central bronchial region Doubles every 30 days Poor prognosis usually found incidentally

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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

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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

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.

Secondary Pulmonary HTN

Stems from a known disease Mitral stenosis Mitral regurgitation LV heart failure Chronic lung diseases Vasculitis

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.

Restrictive lung disease

Cannot get air in

Cannot perfuse if there is no oxygen to transfer first

Breathing first - alveolar ventilation

Perfusion is the second process of respiration

Diffusion is third

Normal level of TSH

0.5 - 4.5

Hypoituitarism

Causes and General Manifestations

Causes: Primary Pituitary Secondary Hypothalamus

General Manifestations:

GH deficiency
FSH/LH deficiency
TSH deficiency
ACTH deficiency
ADH deficiency

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

Cause of hypertension that is NOT from a cardiac source

Hyperthyroidism

Explain Dawn phenomenon

Rise in glucose in early morning hours from growth hormone, cortisol, glucagon, and epinephrine release

Examples of low alveolar ventilation but normal perfusion = low V/Q ratio (<0.8)

Atelectasis Pneumonia ARDS example: 3L/5L = 0.6VQ

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

Manifestations Pneumonia

Crackles and decreased breath sounds over affected area Dull to percussion over infilitrate Chills and fever Cough, purulent sputum Dyspnea and tachypnea

Secondary Hyperthyroidism

•Secondary—stimulation of TSH receptors by TSH (hypersecretion of TSH)

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.

Cushing’s Syndrome

Hormone Metabolism/Excretion

Water Soluble

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

What does the epiglottis do

Closes the airway to prevent food from going into trachea

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

Addisonian Crisis

Acute Adrenocortical Insufficiency

Acute adrenocortical Insufficiency

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

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.

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

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

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

Factors affecting hormone secretions

Feeding-fasting cycle

Light dark cycle

Sleep-wake cycle

24 hour (circadian cycle)

Longer cycles (28-day menstrual cycle)

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

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

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

Primary Hyperthyroidism

Primary—Graves disease, autoimmune, tumor related, inflammatory; also malignancy
Autoimmune—related to TSH receptor antibodies

Laryngotracheobronchitis - CROUP - Patho

Subglottic (under epiglottis) area edema leading to airway narrowing and obstruction Children 3 month - 3 years Occurs autumn and early winter

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.

Two types of Asthma

Intrinsic: non-allergic, adult-onset

Extrinsic: allergic, pediatric-onset

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

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

Hormonal regulation of insulin

Insulin is synthesized in the pancreas by the β cells of the islets of Langerhans. (beta)

Diffusion (Respiration)

Movement of gas between air spaces in the lungs and bloodstream

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

Diagnosis of Diabetes Type 1

C peptide level is low along with low insulin levels

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

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)

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

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.

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

Tuberculosis

Clinical manifestations

Clinical manifestations – active primary

Gradual onset
Productive cough
Night sweats, fever, chills
Fatigue
Unexplained weight loss, anorexia

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

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

Expiratory Reserve Volume

gas that can be expired with a maximal expiration – 1.2 L

DEEP expiration beyond normal TV

Lower airway structures

Autonomic nervous system

•Autonomic nervous system: control bronchi and bronchiole musculature

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

Acute Bronchitis Causes

Viral - RSV, Adenovirus, Influenza, Rhinovirus Bacterial not common is usually a secondary infection Inhalation of chemical irritants - bleach Allergic reactions

Types of pneumonia

Community acquired (gram positive - strep pneumonia) Hospital acquired Atypical pneumonia (mycoplasma, legionella-breeds in water) Ventilator associated

What can trigger Asthma?

Aspirin

NSAIDS

Beta Blockers

Tartrazine (yellow #5)

MSG

Sodium or K

Hops in beer

Obesity (fat stores of cytokines)

Classification of Asthma Severity

Moderate

Symptoms: Daily

Nighttime awakenings: 1x week but not nightly

Uses inhaler: Daily

Interference with normal activity: Some limitation

Glycogenesis

Excess circulating glucose is converted into glycogen and

stored in the liver and muscle cells

Opposite of Glycogenolysis

Inspiratory Reserve Volume

gas that can be inspired with maximal inspiration - 2.5 - 3 L

Deep inspiration beyond normal TV 2.5 - 3L

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.

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.

Hand-Foot-Mouth Disease

Enteroviruses, particularly Coxsackievirus Incubation 4-6 weeks (respiratory, contaminated hands, fecal matter)

Chronic complications of DM

Chronic complications

Rarely manifested before adolescence
Screening for neuropathy/nephropathy ongoing
Counseling on metabolic control before initiation of pregnancy

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).

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

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

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)

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

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

You can have hypoxemia at tissue level but not hypoxemia

Yes example is a crushing injury

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

Clinical Manifestations Mono

Sever pharyngitis; exudate (mimics strep) Fever - high Tonsillar and cervical lymphadenopathy Hepatosplenomegaly and elevated LFTs Thrombocytopenia (spleen), elevated WBCs

GOLD Criteria - 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

Hormones secreted by the

POSTERIOR PITUITARY

ADH (vasopressin)

Oxytocin

Urine Specific Gravity

low number means diluted urine

high number means concentrated urine

Specificity

The “fit” of a hormone into a receptor binding pocket

Functions of the Pancreas

Exocrine secretions for digestion
Endocrine functions

Explain Pulmonary Circulation

High flow LOW pressure Coming from the Right Ventricle should be low pressure <25mm/Hg

Glycogenolysis

Breakdown of glycogen into glucose for energy

Pharyngitis (Tonsillitis)

Fever >100.4 Bacterial - Strep A Viral - RSV

Peritonsillar Abscess

Emergency Absess of one tonsil, can displace uvula Caused by staph or strep Clinical manifestations: drooling, dysphasia

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

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

Diagnosis of Hypoparathyroidism

Serum calcium (low); phosphorus (high)
Antibodies to parathyroid gland present if autoimmune mechanism involved

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

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

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)

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.

When do you measure cortisol for testing

First thing in the morning when its at the highest

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

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

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

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.

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

Hypercortisolism

Cushings Syndrome

•Cushing syndrome—term used to describe any other reason for hypercortisolism

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)

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

Diffuse Interstitial Lung Disease

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

Secondary Pulmonary HTN

Stems from a known disease Mitral stenosis Mitral regurgitation LV heart failure Chronic lung diseases Vasculitis

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

FEV 1

amount of forced air exhaled over 1 second

Normal – generally 80% of Forced Vital Capacity

Normal range for Hemaglobin A1c - HgbA1

Normal range 4 - 5.7%

1% reduction decreases microvascular risks by 10%

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

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

Pharmacologic Hormone Concentrations

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

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

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)

Bronchiolitis eitilogoy

Widespread inflammation of the bronchioles (smaller bronchioles) RSV most common cause Winter to spring Common in children Adults for smoking, toxic fumes

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

Etiologies

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

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

Clinical Manifestations of

Prolactinemia

Clinical manifestations

Hypogonadism
Premenopausal female infertility, oligomenorrhea, and galactorrhea
Male decreased libido, impotence, infertility, gynecomastia, and galactorrhea

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

Three mechanisms involved in Secondary HTN

Increased pulmonary blood flow Increased resistance to blood flow Increased left atrial pressures

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

Lower airway structures

Sympathetic stimulation

•Sympathetic stimulation (mediated by β2-adrenergic receptors); leads to relaxation of the smooth muscle

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

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

What may prevent or improve symptoms of diabetic neuropathy?

Glycemic control may prevent or improve symptoms of diabetic neuropathy.

Spermatocele

Lump on testicle that is painless and moveable

What influences resistance in the airway

Resistance influenced by airway radius and the pattern of gas flow

Ventilation

Movement of air in and out of the lungs

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%)

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.

Hypoxemia

Low oxygen in bloodstream

Parathyroid Gland

4 glands
Located behind the thyroid glands
Secrete parathyroid hormone (PTH)

_{<strong>•PTH – regulates calcium</strong>}

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

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

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.

Pneumonia causes

Bacterial, viral, fungi Aspiration of secretions or gastric contents Inhalation of smoke or chemicals

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

FVC

Total expiration of air

Epiglottis Causes

Haemophilus influenzae type b (HIB) GABHS bacteria Throat trauma Hot liquids Foreign objects

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

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

Negative Feedback for Thyroid System

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

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

Comparison of Type 1 and Type 2 Diabetes

Normal level of

T3 & T4

T3 (75 - 195 ng/ml)

T4 (5-12 mcg/dL)

Classifications of Rhinosinusitis

Most infections are viral Acute sx <4 weeks Chronic sx =12 weeks Recurrent >4 year

The Adrenal Glands

Medulla Produces

Epinephrine

Norepinephrine

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

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

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

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

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

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

Diagnosis

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 cough >3 months >2+ successive years
Persistent, irreversible when paired with emphysema

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)

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

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

Diagnosis Pneumonia

CURB - 65 WBC >15,000 (bacterial) Chest Xray shows white shadows (Parenchymal infiltrates)

Risk factors for Pulmonary Embolus

Immobility Trauma Pregnancy Cancer Heart Failure Estrogen Use Smoking

Causes of Restrictive Lung Diseases

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)

What hormones are released

from the

Anterior Pituitary

•Anterior

Somoatotropes secrete GH

Gonadotropes secrete LH/FSH

Thyrotropes secrete TSH

Corticotropes secrete ACTH

Lactropes secrete prolactin (PRL)

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

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

Diffusion

Respiration

Movement of gas between air spaces in the lungs and the bloodstream

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

Hormones are classified by

Action - the effect they have (insulin lowers glucose)

Source - Anterior or posterior pituitary

Chemical structure

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

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

Tidal Volume

amount of gas entering or leaving in a normal breath – 500 ml

Increases with exercise

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

What are secondary complications of the flu

Secondary pneumonia Reye Syndrome in children

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

Perfusion

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

Glycolysis

Body is breaking down sugar so the cells can use it

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

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

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.

Gluconeogenesis

No sugar in system and glycogen used up so the body gets sugar from other non sugar substances

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

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

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

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

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

Acidosis can result in

Hyperkalemia

Examples of normal ventilation but low perfusion = high V/Q ratio (>0.8)

Pulmonary emboli SLE Sarcoidosis Alveolar carcinoma example: 4L/3L = 1.3VQ

Normal range for HgbA1c

5.7%

Gluconeogenesis

Generation of glucose from

non-sugars

Sleep Apnea

Etiology

Obstructive (OSA) or Central (CSA)

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

What are etiologies of Endocrine Disorders

Congenital

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.

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

Beta cells produce…

β cells produce proinsulin.

Stored in granules, where it is cleaved into insulin and C-peptide
1:1 RATIO OF INSULIN AND C-PEPTIDE

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)

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

Disorders/Diseases

of the

Thyroid Gland

Hyposecretion

Hypersecretion

Target cell hypo-responsiveness

Delta cells produce…

Somatostatin (counteracts growth hormone)

Hypercortisolism

Cushing’s Disease

•Cushing disease—term only used for pituitary hyperstimulation of adrenal cortex; secretes excess cortisol

Glycogenolysis

Breakdown of glycogen into glucose for energy

Opposite of Glycogenesis

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

What happens when glucose levels rise?

Glucose levels rise, leading to polyuria (increased urination), polydipsia (thirst), and polyphagia (hunger): classic signs.

Laryngitis

Inflammation of the larynx - vocal cord Noninfectious - screaming, singing, vomiting Infectious form - Rhinovirus, Strep

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.

What does an overproduction of glucagon stimulate?

Glycogenolysis

and

Gluconeogenesis

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

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

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.

Hydrocele

Excess fluid

What is the ideal Ventilation to Perfusion ratio

Ventilation 4L/min

Perfusion 5L/min

4/5-0.8

Thyroid Gland follicles

Thyroxine – T4
Triiodothyronine – T3
Thyrocalcitonin – Calcitonin (regulates calcium levels)

Persistent Asthma Classification

Mild X2 week

Moderate X1 day

Severe multiple X a day

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%

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.

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

Diffuse Interstitial Lung Disease

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

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

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