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Advanced Pathophysiology > Test 3 Reproductive, Pulmonary, Endocrine > Flashcards

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
Q

J-Receptors

A

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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26
Q

Explain

Thyroid storm

A
  • 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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27
Q

Epiglottitis Patho

A

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

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28
Q

Parathyroid

Gland

Disorders

A
  • 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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29
Q

Infective Mono - Epstein Barr Virus Pathology

A

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

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30
Q

Adrenal Gland

A

Located on top of each kidney

  • Has inner medulla and outer cortex
  • Hypothalamus regulates function
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31
Q

Obstructive Lung Disorders

Classifications

A
  • 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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32
Q

How to diagnosis Diabetes Mellitus

A
  • 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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33
Q

Virchow’s Triad

A

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

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34
Q

Adrenocorticotropic Hormone (ACTH)

A
  • 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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35
Q

Restrictive Lung Disease

Cannot get air in

A
  • 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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36
Q

What does the thyroid gland do

A

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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37
Q

How to diagnosis Sarcoidosis

A

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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38
Q

Mechanisms of Lipid Hormone Action

A

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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39
Q

What hormones

are released

fro the

Posterior Pituitary

A

•Posterior

ADH (vasopressin)

Oxytocin

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40
Q

Diagnostic tests for DM

A
  • 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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41
Q

Glycolysis

A

Breakdown of glucose for energy

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42
Q

Pulmonary circulation

A
  • 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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43
Q

COPD

Criteria

A

A - no symptoms or hospitalizations

B - mod symptoms no hospitalizations

C - have been hospitalizations

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44
Q

Hypoparathyroidism

Clinical Manifestations

A
  • 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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45
Q

Acute Bronchitis Pathogenesis

A

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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46
Q

Common Physical Findings

Emphysema

A

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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47
Q

Clinical Manifestations of Pulmonary Malignancies

A

Persistent cough that changes Dyspnea Hemoptysis Hoarseness Frequent URIs

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48
Q

Hyperthyroidism/Graves Disease

Etiology and Pathogenesis

A
  • 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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49
Q

Elevated prolactin (from anterior pituitary) level

A

Galactorrhea

Amenorrhea

Headache

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50
Q

Hormones secreted by the

ANTERIOR PITUITARY

A

Somoatotropes secrete GH

Gonadotropes secrete LH/FSH

Thyrotropes secrete ACTH

Lactropes secrete prolactin (PRL)

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51
Q

Pituitary gland what does it do and where is it located

A

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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52
Q

What are some Diabetic Goals?

A
  • 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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53
Q

CURB-65

A

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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54
Q

Lung Parenchyma Disorders

A

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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55
Q

Emphysema

Classifications

A

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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56
Q

Type B Influenza

A

Generally milder Isloated primarily to humans

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57
Q

How to diagnose Pulmonary HTN

A

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

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58
Q

FEV1

A

How much air can be expelled in 1 sec

>80% Normal

<70% is obstructive

>70% is normal or restrictive

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59
Q

Etiology and Pathogenesis of

Hyperthyroidism

A

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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60
Q

Explain Somogyi phenomenon

A

Rise in AM glucose as a rebound effect of hypoglycemia

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61
Q

Best overall ventilation and perfusion occurs in the

A

Dependant lung fields

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62
Q

Laryngitis Clinical Manifestations

A

Throat is NOT red Hoarseness Weak voice Aphonia

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63
Q

Growth Hormone Excess

A

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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64
Q

Lipid Soluble Hormones

A

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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65
Q

Exercise Induced Asthma

A

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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66
Q

Clinical manifestations Epiglottis

A

High fever Drooling Stridor

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67
Q

Asthma Pathogenesis

A
  • 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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68
Q

Insulin actions:

A
  • 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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69
Q

Residual Volume

A

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

can’t breathe everything out

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70
Q

Peritonsillar Abscess

A

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

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71
Q

Lower Airway Structures

Parasympathetic Stimulation

A

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

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72
Q

Diabetic Ketoacidosis

Etiology and Pathogenesis

A
  • 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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73
Q

Diagnosis of Asthma

A
  • 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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74
Q

Obstructive defect for spirometry alone as rated by FEV%

A

>70% = Mild

60-69% = Moderate

50-59% = Moderate severe

35-49% = Severe

<35% = Very severe

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75
Q

Adrenocorticotropic Hormone (ACTH)

A

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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76
Q

Determining Hypothyroidism

A
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77
Q

Anterior pituitary gland hormones are regulated

A

by the hypothalamus

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78
Q

Explain Glucose Metabolism

A

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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79
Q

Pathogenesis of Growth Hormone Deficiency

A

Pathogenesis

  • May be idiopathic or related to tumors, radiation, or trauma
  • Resection of pituitary tumors or head injuries
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80
Q

Asthma

Etiology

A

Airway obstruction that is reversible

Airway inflammation

Leukotriene reaction of bronchoconstriction

Increase in bronchial responsiveness to a variety of stimuli

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81
Q

Hormone Synthesis - Lipid Soluble

A

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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82
Q

Central Chemoreceptors

A
  • 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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83
Q

Hypothyroidism

vs

Hyperthyroidism

A
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84
Q

Clinical Manifestations

CHRONIC BRONCHITIS

A

Type B COPD “blue bloater”

Overweight

Dyspnea on exertion

Excess sputum

Chronic cough - WORSE IN AM

Cyanosis - late sign

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85
Q

Explain Hyposecretion

A

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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86
Q

Secondary Hypercortisolism

A

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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87
Q

Cause and clinical manifestations of

Hyperpituitarism

A

•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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88
Q

GOLD Criteria

Classification for COPD

A

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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89
Q

Ventilation

A

Movement of air in and out of the lungs

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90
Q

Up regulation

A

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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91
Q

Chronic Bronchitis - Blue Bloater

Emphysema - Pink Puffer

Chronic Obstructive Pulmonary Diseases

A
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92
Q

Antidiuretic Hormone Disorder

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

SIADH

Etiology & Pathogenesis

A

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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93
Q

Antidiuretic Hormone Disorder

DIABETES INSIPIDUS

Etiology and Pathogenesis

A

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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94
Q

Clinical manifestations Pulmonary Embolus

A

Restlessness Pain on inspiration Tachycardia Hemoptysis Anxiety

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95
Q

Grade of COPD Symptoms

COPD Assessment Test (CAT)

Impact Level

A

CAT score-Impact level

< 10 Low

10 – 20Medium

21 – 30 High

> 30 Very high

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96
Q

Hyperparathyroidism

Etiology

and

Pathogenesis

A
  • 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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97
Q

Central Diabetes Insipidus

vs

Nephrogenic Diabetes Insipidus

A

Central: involves hypothalamus or pituitary gland

Nephrogenic: involves kidneys

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98
Q

A patient has secondary adrenal insufficiency (not putting out enough cortisol)

A

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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99
Q

Diagnosis

A

CT of chest with contrast to light up vessels Pulse OX

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100
Q

Type 2 Diabetes Mellitus

Etiology and Pathogenesis

A
  • 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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101
Q

Explain IGF-1

A

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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102
Q

Distribution of pulmonary blood flow

A

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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103
Q

Clinical manifestations Influenza

A

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

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104
Q

Glycogenesis

A

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

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105
Q

Hypoxia

A

Decrease in tissue oxygenation

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106
Q

Clinical Manifestations

Asthma

A
  • •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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107
Q

Primary causes of Pulmonary Malignancies Secondary - metastasize from another source

A

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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108
Q

Chronic Bronchitis

Pathogenesis

A

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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109
Q

The Ominous Octect

What is not true about your bodies response to causing high sugar

A

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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110
Q

Deep labored respirations that are fruity in odor

A

Kussmaul respirations and they occur in diabetic ketoacidosis

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111
Q

Etiology

Chronic Bronchitis

BLUE BLOATERS

A

Cigarette smoking (90%)

Repeated airway infections

Genetic predisposition

Inhalation of physical or chemical irritants

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112
Q

Cystic Fibrosis

Clinical Manifestations

A

•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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113
Q

Causes of Croup

A

Flu

Viruses

RSV

Adenovirus

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114
Q

Influenza

A

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

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115
Q

What 4 things enhance the development of neuropathy?

A

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

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116
Q

Clinical Manifestations

of

Hypothyroidism in

Adults

A

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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117
Q

Microvascular Diabetic Complications

A

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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118
Q

CURB 65

A

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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119
Q

Classification of Pulmonary Malignancies Small cell carcinoma

A

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

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120
Q

Pheochromocytoma

Clinical Manifestations

A
  • 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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121
Q

Glycogenesis

A

Producing and storing glycogen from the breakdown of excess glucose

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122
Q

When do sinuses fully develop

A

7 years old

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123
Q

Restrictive Pulmonary Disorders

Characteristics

A
  • 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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124
Q

Hypothalamic-Pituitary Axis

A

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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125
Q

Chronic Geriatric Complications of DM

A

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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126
Q

Ventilation

A

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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127
Q

Intrinsic (Nonatopic) Asthma

A
  • 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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128
Q

SIADH

vs

DI

A
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129
Q

Growth Hormone Excess

Diagnosis

A

Diagnosis: High IGF-1 and an elevated GH level that is not suppressed by administration of oral glucose

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130
Q

Alpha cells produce…

A

Glucagon

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131
Q

Hyperthyroidism

Diagnosis

A

•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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132
Q

Hering-Breuer Reflex

A

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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133
Q

Primary (idiopathetic) Pulmonary HTN

A

HTN progresses rapidly (women>men) Long term prognosis poor as med trmt is ineffective

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134
Q

Tuberculosis

Diagnosis

A
  • 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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135
Q

Sarcoidosis

Etiology and Pathogenesis

A

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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136
Q

Glycolysis

A

Breakdown of glucose for energy

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137
Q

Clinical Manifestations of Acute Bronchitis

A

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

138
Q

Complications of Gestational Diabetes

A

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.
139
Q

Secondary Pulmonary HTN

A

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

140
Q

Adrenal insufficiency

Congenital adrenal hyperplasia

A

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.

141
Q

Restrictive lung disease

A

Cannot get air in

142
Q

Cannot perfuse if there is no oxygen to transfer first

A

Breathing first - alveolar ventilation

Perfusion is the second process of respiration

Diffusion is third

143
Q

Normal level of TSH

A

0.5 - 4.5

144
Q

Hypoituitarism

Causes and General Manifestations

A

Causes: Primary Pituitary Secondary Hypothalamus

General Manifestations:

  • GH deficiency
  • FSH/LH deficiency
  • TSH deficiency
  • ACTH deficiency
  • ADH deficiency
145
Q

Pathogenesis

Cystic Fibrosis

A

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
146
Q

Cause of hypertension that is NOT from a cardiac source

A

Hyperthyroidism

147
Q

Explain Dawn phenomenon

A

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

148
Q

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

A

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

149
Q

How to diagnosis

Adrenal Insufficiency

A

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
150
Q

Manifestations Pneumonia

A

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

151
Q

Secondary Hyperthyroidism

A

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

152
Q

Explain the properties of T3 and T4

A
  • 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.
153
Q

Cushing’s Syndrome

A
154
Q

Hormone Metabolism/Excretion

Water Soluble

vs

Lipid Soluble

A

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

155
Q

What does the epiglottis do

A

Closes the airway to prevent food from going into trachea

156
Q

Hypoglycemia Complications

Causes

&

Clinical Manifestations

A
  • 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
157
Q

Addisonian Crisis

Acute Adrenocortical Insufficiency

A

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
158
Q

Chronic Hyperglycemia can lead to…

A

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.
159
Q

How to diagnosis

Hypercortisolism

A

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
160
Q

Half life of a hormone

A

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

161
Q

Explain Myxedema and when you would see it in Hypothyroidism

A
  • 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
162
Q

Factors affecting hormone secretions

A

Feeding-fasting cycle

Light dark cycle

Sleep-wake cycle

24 hour (circadian cycle)

Longer cycles (28-day menstrual cycle)

163
Q

Pathology of Pulmonary HTN

A

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

164
Q

Chronic Obstructive Pulmonary Disease

COPD

IRREVERSIBLE

A

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
165
Q

What are Incretins and what is their function?

A

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

166
Q

Primary Hyperthyroidism

A
  • Primary—Graves disease, autoimmune, tumor related, inflammatory; also malignancy
  • Autoimmune—related to TSH receptor antibodies
167
Q

Laryngotracheobronchitis - CROUP - Patho

A

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

168
Q

Hypoparathyroidism

Etiology and Pathogenesis

A
  • 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.
169
Q

Two types of Asthma

A

Intrinsic: non-allergic, adult-onset

Extrinsic: allergic, pediatric-onset

170
Q

Down regulation

A

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

171
Q

Explain

INCRETIN EFFECT

A
  • 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
172
Q

Hormonal regulation of insulin

A

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

173
Q

Diffusion (Respiration)

A

Movement of gas between air spaces in the lungs and bloodstream

174
Q

Secondary Pulmonary HTN causes

A

Has to come from something after the lungs so it would be the left side of the heart that would cause secondary pulmonary HTN

175
Q

Diagnosis of Diabetes Type 1

A

C peptide level is low along with low insulin levels

176
Q

What happens with insulin in the fasting state?

A

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

177
Q

Peripheral chemoreceptors

A
  • 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)
178
Q

Hormones

A

Blood-borne chemical messengers that affect target cells anatomically distant from the secreting cell

  • Regulates: Growth and development
  • Metabolism
  • Sexual function
  • Reproduction
  • Mood stability
179
Q

Explain GIP and GLP-1

A

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.

180
Q

Type A Influenza

A

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

181
Q

Tuberculosis

Clinical manifestations

A

Clinical manifestations – active primary

  • Gradual onset
  • Productive cough
  • Night sweats, fever, chills
  • Fatigue
  • Unexplained weight loss, anorexia
182
Q

Pheochromocytoma

(Adrenal Gland Disorder)

Etiology and Pathogenesis

A

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
183
Q

What causes Hypercortisolism

A
  • 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
184
Q

Expiratory Reserve Volume

A

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

DEEP expiration beyond normal TV

185
Q

Lower airway structures

Autonomic nervous system

A

•Autonomic nervous system: control bronchi and bronchiole musculature

186
Q

Acute Bronchitis Etiology

A

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

187
Q

Acute Bronchitis Causes

A

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

188
Q

Types of pneumonia

A

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

189
Q

What can trigger Asthma?

A

Aspirin

NSAIDS

Beta Blockers

Tartrazine (yellow #5)

MSG

Sodium or K

Hops in beer

Obesity (fat stores of cytokines)

190
Q

Classification of Asthma Severity

Moderate

A

Symptoms: Daily

Nighttime awakenings: 1x week but not nightly

Uses inhaler: Daily

Interference with normal activity: Some limitation

191
Q

Glycogenesis

A

Excess circulating glucose is converted into glycogen and

stored in the liver and muscle cells

Opposite of Glycogenolysis

192
Q

Inspiratory Reserve Volume

A

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

Deep inspiration beyond normal TV 2.5 - 3L

193
Q

Fluid balance in the lungs

  • Hydrostatic pressure
  • Colloid osmotic pressure
  • Capillary permeability
A
  • 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.
194
Q

What effect does excessive glucose have on myoinositol in neurons?

A

Excessive glucose is thought to interfere with myoinositol in neurons and reduced myoinositol in peripheral nerves.

195
Q

Hand-Foot-Mouth Disease

A

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

196
Q

Chronic complications of DM

A

Chronic complications

  • Rarely manifested before adolescence
  • Screening for neuropathy/nephropathy ongoing
  • Counseling on metabolic control before initiation of pregnancy
197
Q

COPD Categories

Group A-D

A

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).
198
Q

How does the hypothalamus function in relation to the thyroid

A
  • 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
199
Q

Growth Hormone Excess

Pituitary gigantism vs acromegaly

A

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

200
Q

Adrenal Gland

Cortex Produces

Salt sugar and sex tells you what comes out of the

Adrenal Cortex

A
  • Mineralocorticoids - Aldosterone (salt and water)
  • Glucocorticoids – Cortisol (sugar)
  • Gnadocorticoids - Androgens and Estrogens (sex)
201
Q

Classification of Asthma

Severe

A

Symptoms: Throughout the day

Nighttime awakenings: Often 7x week

Uses inhaler: Several times a day

Interference with normal activity: Extremely limited

202
Q

Islet of Langerhans

Types of cells

A
  • 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
203
Q

You can have hypoxemia at tissue level but not hypoxemia

A

Yes example is a crushing injury

204
Q

Hyperparathyroidism

Diagnosis

A
  • 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
205
Q

Clinical Manifestations Mono

A

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

206
Q

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

A
207
Q

Hormones secreted by the

POSTERIOR PITUITARY

A

ADH (vasopressin)

Oxytocin

208
Q

Urine Specific Gravity

low number means diluted urine

high number means concentrated urine

A
209
Q

Specificity

A

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

210
Q

Functions of the Pancreas

A
  • Exocrine secretions for digestion
  • Endocrine functions
211
Q

Explain Pulmonary Circulation

A

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

212
Q

Glycogenolysis

A

Breakdown of glycogen into glucose for energy

213
Q

Pharyngitis (Tonsillitis)

A

Fever >100.4 Bacterial - Strep A Viral - RSV

214
Q

Peritonsillar Abscess

A

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

215
Q

Pulmonary HTN Clinical Manifestations

A

Activity intolerance Fatigue Hemoptysis (excess pressure leaks back into alveoli) Syncope Chest pain on exertion When sx appear cannot be reversed focus on prevention

216
Q

Hormone Synthesis - Thyroid Hormone

A

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

217
Q

Diagnosis of Hypoparathyroidism

A
  • Serum calcium (low); phosphorus (high)
  • Antibodies to parathyroid gland present if autoimmune mechanism involved
218
Q

Hypercortisolism

Etiology and Pathogenesis

A
  • 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
219
Q

Screening for Diabetes

A

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

220
Q

What would you see in relation to insulin in

a person with Growth Hormone Excess

A

May cause persistent hyperglycemia and increased insulin production (GH called a diabetogenic hormone)

221
Q

Explain the

Primary Classification of

Endocrine Disorders

A

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.

222
Q

When do you measure cortisol for testing

A

First thing in the morning when its at the highest

223
Q

Risk factors for Diabetes Mellitus

A

Type 2 Diabetes Mellitus

  • Risk factors: female sex, obesity, aging, and sedentary lifestyle
  • Polyuria, polydipsia, and polyphagia may be more subtle
224
Q

Clinical Manifestations of Hypothyroidism in Infants

A

•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
225
Q

Geriatric Complications

A

Increased prevalence of type 2 DM

Increased adiposity, decreased lean body mass, decreased activity levels, decreased insulin secretion, hyperglycemic effect of certain medications

226
Q

How does exercise affect insuln levels

A

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.

227
Q

Emphysema

Etiology

A
  • Smoking >70 packs/year (2pk/dayX30years)
  • Air pollution
  • Certain occupations (mining, welding, working with or near asbestos)
  • α1-Antitrypsin deficiency
  • Expanded “floppy” lungs
228
Q

Hypercortisolism

Cushings Syndrome

A

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

229
Q

STEROID HORMONES

GLUCOCORTICOIDS

A

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)

230
Q

Clinical Manifestations of

Growth Hormone Deficiency

A

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

231
Q

Diffuse Interstitial Lung Disease

Clinical manifestations

A

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
232
Q

Secondary Pulmonary HTN

A

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

233
Q

Growth Hormone Disorders

A
  • 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
234
Q

FEV 1

A

amount of forced air exhaled over 1 second

Normal – generally 80% of Forced Vital Capacity

235
Q

Normal range for Hemaglobin A1c - HgbA1

A

Normal range 4 - 5.7%

1% reduction decreases microvascular risks by 10%

236
Q

What happens after you eat in relation to glucose metabolism

A
  • 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
237
Q

Antidiuretic Hormone Disorders

Syndrome of Inappropriate Antidiuretic Hormone

SIADH

Clinical Manifestations

A

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
238
Q

Pharmacologic Hormone Concentrations

vs

Physiologic hormone concentrations

A

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

239
Q

Describe Type 1 Diabetes Mellitus

A
  • 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
240
Q

Hypothyroidism

Etiology

and

Pathologenesis

A
  • 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)

241
Q

Bronchiolitis eitilogoy

A

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

242
Q

Pre-diabetes classes:

A
  • 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
243
Q

Etiologies

of

Endorine Disorders

A

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

244
Q

Mechanism of Water Hormones with Cell Membrane Receptors

A

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

245
Q

Clinical Manifestations of

Prolactinemia

A

Clinical manifestations

  • Hypogonadism
  • Premenopausal female infertility, oligomenorrhea, and galactorrhea
  • Male decreased libido, impotence, infertility, gynecomastia, and galactorrhea
246
Q

Hormones are categorized by chemical composition

A

Steroids - androgens glucocorticoids, thyroid (lipids)

Proteins/polypeptides - Insulin, growth hormone (water)

Amines/amino acids - epinephrine (water)

Fatty acid derivatives - prostaglandins

247
Q

Three mechanisms involved in Secondary HTN

A

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

248
Q

Acute Geriatric Complications

A
  • 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
249
Q

Lower airway structures

Sympathetic stimulation

A

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

250
Q

Amplification of Hormone Activity

A

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

251
Q

Cross specificity

A

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

252
Q

What may prevent or improve symptoms of diabetic neuropathy?

A

Glycemic control may prevent or improve symptoms of diabetic neuropathy.

253
Q

Spermatocele

A

Lump on testicle that is painless and moveable

254
Q

What influences resistance in the airway

A

Resistance influenced by airway radius and the pattern of gas flow

255
Q

Ventilation

A

Movement of air in and out of the lungs

256
Q

FEV1/FVC RATIO

A

> 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%)

257
Q

What does Calcitonin do?

A
  • 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.
258
Q

Hypoxemia

A

Low oxygen in bloodstream

259
Q

Parathyroid Gland

A
  • 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
260
Q

Gestational Diabetes Mellitus

Risk Factors

A

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

261
Q

Hyperparathyroidism

Clinical Manifestations

A

•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.
262
Q

Pneumonia causes

A

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

263
Q

Water soluble hormones

A

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
Q

FVC

A

Total expiration of air

265
Q

Epiglottis Causes

A

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

266
Q

Adrenal Insufficiency

Etiology & Pathogenesis

A

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
Q

Flu Vaccine information

A

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

268
Q

Negative Feedback for Thyroid System

A
269
Q

Clinical Manifestations

Graves Disease

A
  • 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
270
Q

Pathogenesis

Cystic Fibrosis

CTFR Gene

A

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
271
Q

Comparison of Type 1 and Type 2 Diabetes

A
272
Q

Normal level of

T3 & T4

A

T3 (75 - 195 ng/ml)

T4 (5-12 mcg/dL)

273
Q

Classifications of Rhinosinusitis

A

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

274
Q

The Adrenal Glands

Medulla Produces

A

Epinephrine

Norepinephrine

275
Q

Diabetes

Mellitus

A
  • 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
276
Q

Types of ventilation - perfusion imbalances

A

High (under perfused) Ventilation > perfusion - Alveolar unit is ventilated, but not perfused. Happens with PE (lack of blood flow)

Low (underventilated) Ventilation

277
Q

Grade of COPD Symptoms

Modified British Medical Research Council

mMRC

Questionnaire on breathlessness

A

0 minimal sx

1-2 slowing down

3 -4 - symptomatic to very symptomatic

278
Q

Proprioceptors

A
  • 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

279
Q

Cystic Fibrosis

Pathogenesis

A
  • 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
280
Q

Steroid Hormones

MINERALCORTICOIDS

ALDOSTERONE

A
  • 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
281
Q

Diagnosis

of

Chronic Bronchitis

A

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
282
Q

Diagnosis for Hypothyroidism

A

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)
283
Q

Sarcoidosis

Clinical Manifestations

A
  • Malaise, fatigue
  • Weight loss
  • Fever
  • Dyspnea of insidious onset
  • Dry, nonproductive cough
  • Erythema nodosum
  • Macules, papules, hyperpigmentation, and subcutaneous nodules
  • Hepatosplenomegaly, lymphadenopathy
284
Q

Tuberculosis

A

Caused by Mycobacterium tuberculosis

Transmission via aerosol droplets with active TB patient

Can survive weeks in dry sputum

Florida 4th state for positive cases

285
Q

Diagnosis Pneumonia

A

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

286
Q

Risk factors for Pulmonary Embolus

A

Immobility Trauma Pregnancy Cancer Heart Failure Estrogen Use Smoking

287
Q

Causes of Restrictive Lung Diseases

A
  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)
288
Q

What hormones are released

from the

Anterior Pituitary

A

•Anterior

Somoatotropes secrete GH

Gonadotropes secrete LH/FSH

Thyrotropes secrete TSH

Corticotropes secrete ACTH

Lactropes secrete prolactin (PRL)

289
Q

Extrinsic (Atopic) Asthma

(E)xtrinsic = IgE

(A)topic = allergy

A

1/3 to 1/2 of asthma cases

A genetic IgE-mediated exaggerated response in many cases

Allergic rhinitis, atopic dermatitis and eczema

290
Q

Prolactinemia

Cause Primary vs Secondary

A

Primary is a disorder of the anterior pituitary

Secondary is a disorder of the hypothalamus

Normal range = Men 10-20

Women 10-25

291
Q

Diffusion

A

Respiration

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

292
Q

Hormone Synthesis - Water soluble

A

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

293
Q

Hormones are classified by

A

Action - the effect they have (insulin lowers glucose)

Source - Anterior or posterior pituitary

Chemical structure

294
Q

What is the most common cause of acquired hypothyroidism:

A

Lymphocytic thyroiditis (Hashimoto or autoimmune thyroiditis); may result in a goiter

Irradiation of the thyroid gland

Surgical removal of thyroid tissue

Iodine deficiency

295
Q

Where do we get energy how is it metabolized

A

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

296
Q

Tidal Volume

A

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

Increases with exercise

297
Q

Hypercortisolism

Clinical Manifestations

A

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
298
Q

What are secondary complications of the flu

A

Secondary pneumonia Reye Syndrome in children

299
Q

Pleural Effusion

Etiology & Pathogenesis

A

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

300
Q

Perfusion

A

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

301
Q

Glycolysis

A

Body is breaking down sugar so the cells can use it

302
Q

Acute Pediatric Complications of DM

A
  • 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
303
Q
A
304
Q

Causes of impaired diffusion

A

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

305
Q

Explain Hypersecretion of the Thyroid Disease

A

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.
306
Q

Gluconeogenesis

A

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

307
Q

Cystic Fibrosis

Etiology

A

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

308
Q

Diabetic Neuropathy

Patho and Etiology

A

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
309
Q

Growth Hormone Excess

Clinical Manifestations

A

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
310
Q

How to diagnosis

Diabetes Insipidus

A

Diagnosis

  • Dilute urine, hypernatremia along with abnormally low serum ADH levels (diagnostic of central DI)
  • Renal US or MRI Brain
311
Q

Affinity

A

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

312
Q

Acidosis can result in

A

Hyperkalemia

313
Q

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

A

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

314
Q

Normal range for HgbA1c

A

5.7%

315
Q

Gluconeogenesis

A

Generation of glucose from

non-sugars

316
Q

Sleep Apnea

Etiology

A

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

317
Q

What are etiologies of Endocrine Disorders

A

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.

318
Q

Explain Negative feedback control

A

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

319
Q

Beta cells produce…

A

β cells produce proinsulin.

  • Stored in granules, where it is cleaved into insulin and C-peptide
  • 1:1 RATIO OF INSULIN AND C-PEPTIDE
320
Q

Diffuse Interstitial

Lung Disease

A

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)

321
Q

Diagnosis

Emphysema

A

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
322
Q

Disorders/Diseases

of the

Thyroid Gland

A

Hyposecretion

Hypersecretion

Target cell hypo-responsiveness

323
Q

Delta cells produce…

A

Somatostatin (counteracts growth hormone)

324
Q

Hypercortisolism

Cushing’s Disease

A

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

325
Q

Glycogenolysis

A

Breakdown of glycogen into glucose for energy

Opposite of Glycogenesis

326
Q

Regulation of Receptor Responses

What determines the ability of a cell to respond to a particular hormone

A

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

327
Q

What happens when glucose levels rise?

A

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

328
Q

Laryngitis

A

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

329
Q

Macrovascular damage r/t Diabetic Vascular Complications with DM

A

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.
330
Q

What does an overproduction of glucagon stimulate?

A

Glycogenolysis

and

Gluconeogenesis

331
Q

Metabolic

Syndrome

A
  • 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
332
Q

Tuberculosis

Pathogenesis

A
  • 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
333
Q

When are CRH and ACTH at their peak and lowest point?

A

CRH and ACTH have a significant diurnal pattern, with a peak on wakening in the morning and a valley in the evening.

334
Q

Hydrocele

A

Excess fluid

335
Q

What is the ideal Ventilation to Perfusion ratio

A

Ventilation 4L/min

Perfusion 5L/min

4/5-0.8

336
Q

Thyroid Gland follicles

A
  • Thyroxine – T4
  • Triiodothyronine – T3
  • Thyrocalcitonin – Calcitonin (regulates calcium levels)
337
Q

Persistent Asthma Classification

A

Mild X2 week

Moderate X1 day

Severe multiple X a day

338
Q

Pre-Diabetes — Impaired Glucose

A

Impaired glucose tolerance and impaired fasting glucose tolerance

Intermediate stages between normal glucose metabolism and diabetes

•HgbA1c : 5.7 – 6.4%

339
Q

Explain the

Secondary Classification of

Endocrine Disorders

A
  • 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.
340
Q

Classification of Asthma Severity

Mild

A

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

341
Q

Diffuse Interstitial Lung Disease

Diagnosis

A

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
342
Q

Cystic Fibrosis

Clinical Manifestations

A

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

Advanced Pathophysiology (8 decks)

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