Exam 3 (detailed) Flashcards
1
Q
What are arrhythmias?
A
Abnormal cardiac rhythms due to:
* Abnormal automaticity
* Triggered activity
* Re-entry (circus pathways)
Arrhythmias can lead to various clinical manifestations and may require intervention.
2
Q
What is abnormal automaticity?
A
Spontaneous depolarization when not supposed to occur
This can lead to premature heartbeats or arrhythmias.
3
Q
What is triggered activity in cardiac rhythms?
A
Occurs during the refractory phase of the cardiac action potential
This can result in additional depolarizations and arrhythmias.
4
Q
What is re-entry in the context of arrhythmias?
A
Electrical impulse circulates through damaged or delayed tissue and reactivates previously excited regions
This mechanism is often involved in tachycardias.
5
Q
What are the pathologic causes of sinus tachycardia?
A
Pathologic causes include:
* Increased body temperature (e.g., fever)
* Cardiac toxicity
* Increased sympathetic discharge
Sinus tachycardia can also be a response to physiological stress.
6
Q
What are the non-pathologic causes of sinus tachycardia?
A
Non-pathologic causes include:
* Medications (e.g., stimulants)
* Caffeine
* Exercise (transient, usually benign)
These factors can increase heart rate without underlying disease.
7
Q
What can cause sinus bradycardia?
A
Causes include:
* Excessive vagal stimulation (e.g., vasovagal syncope)
* Medications (e.g., beta blockers, calcium channel blockers)
* Neurological effects (e.g., elevated intracranial pressure)
Sinus bradycardia may also occur in athletes as a normal variant.
8
Q
What is SA node block?
A
SA node may fire normally, but impulse is blocked from reaching atria (internodal block)
This can lead to a slower ventricular rate as other pacemakers take over.
9
Q
Describe first-degree AV block.
A
Transmission is delayed with a prolonged PR interval (>200 ms) on EKG
This is often asymptomatic but can indicate underlying heart disease.
10
Q
What characterizes second-degree AV block?
A
Intermittent failure of conduction through AV node; some P waves not followed by QRS complexes (‘dropped beats’)
This can occur in Mobitz type I or type II forms.
11
Q
What is third-degree AV block?
A
Atria and ventricles beat independently (AV dissociation); ventricular rhythm maintained by Purkinje fibers or Bundle of His
This is a critical condition requiring immediate intervention, often with a pacemaker.
12
Q
What are premature contractions?
A
Originate from ectopic pacemaker sites (not SA node) and can occur in:
* Atria – premature atrial contractions (PACs)
* AV node – junctional premature beats
* Ventricles – premature ventricular contractions (PVCs)
Frequent PVCs can lead to more severe arrhythmias like ventricular fibrillation.
13
Q
What are paroxysmal tachycardias?
A
Rapid, sudden-onset arrhythmias due to ectopic pacemaker; can be supraventricular or ventricular
Some supraventricular types can be terminated by vagal stimulation.
14
Q
What is ventricular fibrillation (VF)?
A
Most life-threatening arrhythmia; causes include ischemic heart disease and electric shock
VF requires immediate defibrillation to restore normal rhythm.
15
Q
What leads to re-entry circuits in arrhythmias?
A
Healthy tissue becomes refractory and cannot conduct again immediately; diseased/delayed tissue may conduct slower and remain excitable
This can lead to continuous depolarization cycles, contributing to arrhythmias like atrial fibrillation.
16
Q
What are the goals in pharmacologic correction of dysrhythmias?
A
Goals include:
* Suppress ectopic foci or abnormal automaticity
* Slow conduction to promote extinction of abnormal pathways
* Allow normal SA node rhythm to re-establish dominance
This can involve various antiarrhythmic medications.
17
Q
What is the mechanism of action for sodium channel blockers?
A
Decrease the Phase 4 slope of the cardiac action potential
These drugs are often classified as Class I antiarrhythmics.
18
Q
What is decremental conduction in the AV node?
A
The more frequently the AV node is stimulated, the slower it conducts
This property helps protect the ventricles during rapid atrial rhythms.
19
Q
True or False: Many antiarrhythmics are state-dependent.
A
True
They preferentially bind to active or inactivated channels, making them more selective for diseased tissue.
20
Q
Fill in the blank: Frequent PVCs can lead to ______.
A
ventricular fibrillation
This is especially concerning in patients with existing myocardial damage.
21
Q
What is the Gas Exchange Zone?
A
Occurs only in respiratory bronchioles and alveoli
Termed the respiratory zone
22
Q
What is the function of the Conducting Zone?
A
Includes all other airways (trachea, bronchi, terminal bronchioles)
* Serves to warm, humidify, and transport air
* No gas exchange occurs here
23
Q
What role does bronchiolar muscle play?
A
Contains smooth muscle in walls allowing to:
* Regulate airflow resistance
* Respond dynamically to autonomic input
24
Q
What is the intrapulmonary pressure during inspiration?
A
About -3 mmHg
25
What is the intrapleural pressure required to initiate a breath?
Must reach ~ -5 mmHg
26
What is Surface Tension in the context of the lungs?
Created by hydrogen bonding in the thin film of water lining alveoli
* Promotes alveolar collapse, especially during exhalation
27
What is the function of surfactant?
A soapy, phospholipid secretion produced by Type II pneumocytes
* Reduces surface tension
* Increases lung compliance
* Helps prevent alveolar collapse at low lung volumes
28
What condition in premature infants is related to insufficient surfactant?
Infant Respiratory Distress Syndrome (IRDS)
29
What can reduce surfactant production in adults?
Septic shock and inflammatory conditions can reduce surfactant
## Footnote
Results in Acute Respiratory Distress Syndrome (ARDS)
30
What effect does ischemia have on the lungs?
Can damage alveolar cells and surfactant production
31
What is the typical pressure in pulmonary circulation?
Operates at ~15 mmHg
32
What happens in Pulmonary Hypertension?
Occurs when pulmonary pressure increases significantly (e.g., >26 mmHg)
* Can lead to pulmonary edema and right heart strain
33
What causes pulmonary edema?
Results from imbalance between:
* Hydrostatic pressure (↑ in pulmonary HTN)
* Oncotic pressure (albumin concentration)
34
What does sympathetic stimulation do to airways?
Causes bronchodilation via β2 receptors
## Footnote
Crucial in asthma treatment (e.g., β2 agonists like albuterol)
35
What enhances gas exchange efficiency?
Several anatomic and physiologic features:
* Extensive alveolar surface area (~70 m²)
* Short diffusion distance between alveolar air and capillaries
* High capillary density surrounding alveoli
36
What are the two mechanisms that increase available capillary surface area during increased demand?
Recruitment and Distention
* Recruitment – previously unused capillaries open
* Distention – dilation of already-perfused capillaries
37
True or False: Pulmonary capillaries can expand 2–3× their normal volume before pressure rises significantly.
True
38
What is the relationship between airway resistance and radius according to Poiseuille's Law?
Airway resistance is inversely proportional to the fourth power of the radius (Airway resistance ∝ 1 / radius⁴).
39
Where does laminar flow occur and what is its effect on resistance?
Laminar flow occurs in small bronchioles and produces minimal resistance.
40
Where does turbulent flow occur and what is its significance?
Turbulent flow occurs in the nose, mouth, and larger airways, and is the main contributor to airway resistance during inspiration.
41
What happens to alveolar walls in emphysema?
In emphysema, alveolar walls are destroyed, leading to loss of radial traction.
42
What are the consequences of airway collapse during exhalation in emphysema?
Airway collapse during exhalation leads to air trapping.
43
What is pursed-lip breathing and its benefits in emphysema?
Pursed-lip breathing increases positive airway pressure during exhalation, keeps airways open longer, reduces air trapping, and improves gas exchange.
44
What are the general mechanisms of obstruction in obstructive pulmonary disorders?
Obstruction can arise from changes in the vessel wall, external compression, or intraluminal obstruction.
45
What type of lung disease is asthma classified as?
Asthma is classified as a reversible obstructive lung disease.
46
What are the pathophysiological features of asthma?
Asthma features chronic airway inflammation, hyperresponsiveness of airways, and bronchoconstriction leading to airflow limitation.
47
What are common triggers for asthma?
Common triggers include allergens, pollutants, cold air, infections, and exercise.
48
What are the symptoms of asthma?
Symptoms include paroxysmal coughing, wheezing, and dyspnea (shortness of breath).
49
What are the two types of asthma?
The two types of asthma are extrinsic (allergic) and intrinsic (non-allergic).
50
What are the structural changes associated with asthma?
Structural changes include smooth muscle hypertrophy, increased mucous glands and goblet cells, and edema with thick mucus in the lumen.
51
How is asthma diagnosed?
Asthma is diagnosed by a decrease in Peak Expiratory Flow Rate (PEFR).
52
What are the treatments for asthma?
Treatments include β2 agonists for bronchodilation, anti-inflammatory medications, and both maintenance and emergency therapy.
53
What is the etiology of acute bronchitis?
Acute bronchitis is mostly viral (RSV, influenza), occasionally bacterial.
54
What is the pathology of acute bronchitis?
Acute bronchitis involves inflammation of bronchi, capillary congestion, and increased mucus production.
55
What is the typical course of acute bronchitis?
Acute bronchitis is often self-limiting, but viral infections may predispose to secondary bacterial infection.
56
What is the treatment for acute bronchitis?
Treatment includes supportive care (fluids, rest) and antibiotics only for confirmed bacterial cases.
57
What defines chronic bronchitis?
Chronic bronchitis is defined as a productive cough lasting ≥3 months/year for 2 consecutive years.
58
What are the main etiologies of chronic bronchitis?
The main etiologies include smoking, air pollutants, and recurrent infections.
59
What are the pathological features of chronic bronchitis?
Pathological features include persistent airway inflammation, goblet cell hyperplasia, thickened bronchial walls, and mucus plugs.
60
What are the symptoms of chronic bronchitis?
Symptoms include a chronic productive cough and features of 'blue bloaters' such as cyanosis and edema.
61
What are the complications of chronic bronchitis?
Complications include pulmonary hypertension, cor pulmonale, and jugular venous distension.
62
What are the treatments for chronic bronchitis?
Treatments include inhaled β-agonists, inhaled anticholinergics, oxygen therapy, and smoking cessation.
63
What is emphysema?
Emphysema is the destruction of alveolar walls without fibrosis, leading to loss of gas exchange surface area.
64
What are the main etiologies of emphysema?
The main etiologies are smoking and α1-antitrypsin deficiency.
65
What are the pathophysiological features of emphysema?
Pathophysiology includes loss of radial traction, air trapping, and loss of pulmonary capillaries.
66
What are the types of emphysema?
The types of emphysema are centrilobular (centriacinar) and panlobular (panacinar).
67
What is the clinical presentation of emphysema?
'Pink puffers' present with minimal cyanosis, pursed-lip breathing, thin appearance, and near-normal oxygenation until late disease.
68
What compensatory techniques are used in emphysema?
Pursed-lip breathing maintains airway patency, reduces air trapping, and decreases work of breathing.
69
What is bronchiectasis?
Permanent dilation and thickening of bronchi.
70
What are the etiologies of bronchiectasis?
Repeated infections, poor mucus clearance, often occurs in children.
71
What are the pathological features of bronchiectasis?
Airway damage and epithelial metaplasia, mucopurulent secretions leading to obstruction, turbulent airflow and increased resistance due to airway deformity.
72
What are the complications of bronchiectasis?
Chronic productive cough, recurrent respiratory infections.
73
What is bronchiolitis?
Inflammation of bronchioles, most common in infants and young children.
74
What is the etiology of bronchiolitis?
Typically viral, especially RSV.
75
What are the pathological features of bronchiolitis?
Epithelium is damaged and lost, inflammatory debris and mucus lead to airway obstruction, leads to atelectasis and hyperinflation.
76
What are the symptoms of bronchiolitis?
Cough, wheeze, difficulty breathing.
77
What is the treatment for bronchiolitis?
Supportive: hydration, oxygen; bronchodilators may help in some cases.
78
What is cystic fibrosis (CF)?
An autosomal recessive disorder caused by a mutation in the CFTR gene (chloride channel).
79
What is the pathophysiology of cystic fibrosis?
Impaired Cl⁻ and water transport results in thick, sticky mucus in lungs and other organs.
80
What systems are affected by cystic fibrosis?
Respiratory tract (airway obstruction, infection), pancreas (blocked ducts leading to malabsorption), GI tract, sweat glands (salty sweat), reproductive system.
81
What are the respiratory complications of cystic fibrosis?
Mucus plugging, atelectasis, recurrent lung infections, hyperinflation, accumulated neutrophils leading to increased mucus viscosity.
82
What is the leading cause of death in cystic fibrosis?
Respiratory failure from infections.
83
How is cystic fibrosis diagnosed?
Sweat chloride test.
84
What is the treatment for cystic fibrosis?
Bronchodilators, inhaled DNase, antibiotics, airway clearance techniques.
85
What is epiglottitis?
Bacterial infection, typically Haemophilus influenzae type B (Hib).
86
What are the pathological features of epiglottitis?
Inflammation and swelling of the epiglottis.
87
What is the clinical concern with epiglottitis?
Can rapidly obstruct airway, life-threatening emergency.
88
What is the treatment for epiglottitis?
Immediate airway protection (intubation or tracheotomy), IV antibiotics.
89
What is pneumoconiosis?
Chronic interstitial fibrosis due to inhalation of inorganic dust.
90
What are examples of pneumoconiosis?
Anthracosis (coal dust), silicosis (silica dust), asbestosis (asbestos exposure).
91
What is the mechanism of pneumoconiosis?
Macrophages engulf particles, release lysozymes, leading to inflammatory damage, scarring, and fibrosis of lung tissue.
92
What are the outcomes of pneumoconiosis?
Progressive dyspnea, restrictive and obstructive features.
93
What are the general features of restrictive pulmonary disorders?
Disorders characterized by decreased lung expansion due to lung parenchyma disease, pleural abnormalities, chest wall deformities, or neuromuscular dysfunction.
94
What are the types of restrictive pulmonary disorders?
Can be acute or chronic.
95
What pulmonary volumes are decreased in restrictive pulmonary disorders?
Total Lung Capacity (TLC), Vital Capacity (VC), Functional Residual Capacity (FRC), Residual Volume (RV).
96
What are the arterial blood gas findings in restrictive pulmonary disorders?
Decreased PaO₂ (hypoxemia), normal or decreased PaCO₂.
97
What is interstitial lung disease (ILD)?
Characterized by infiltration of alveolar walls by inflammatory cells, fluid, and connective tissue.
98
What occurs in the pathophysiology of ILD?
Leads to fibroblast proliferation and collagen deposition; fibrosis is irreversible.
99
What is diffuse interstitial disease?
Thickening of alveolar interstitium, replacement of spongy interstitial tissue with stiff, fibrotic stroma, resulting in destruction of normal alveolar architecture.
100
What are the symptoms of interstitial lung disease?
Progressive dyspnea, dry cough, fatigue.
101
What is the etiology of Sarcoidosis?
Unknown; likely autoimmune or antigenic trigger
102
What commonly affects Sarcoidosis?
Lungs and intrathoracic lymph nodes
103
What is the pathology of Sarcoidosis?
Formation of non-caseating granulomas; can become fibrotic over time
104
What are the symptoms of Sarcoidosis?
May be asymptomatic; cough, dyspnea, chest pain
105
What is the treatment for Sarcoidosis?
Corticosteroids to reduce inflammation; symptom management; better outcomes if caught early
106
What is the etiology of Hypersensitivity Pneumonitis?
Occupational exposure to inhaled organic dusts (e.g., moldy hay, bird droppings, silos)
107
Who is more commonly affected by Hypersensitivity Pneumonitis?
Non-smokers
108
What is the pathology of Hypersensitivity Pneumonitis?
Immune-mediated alveolitis and bronchiolitis; thickening of alveolar walls; exudate formation in bronchioles; infiltration by T-cells and macrophages; repeated exposure → fibrosis
109
What are the symptoms of Hypersensitivity Pneumonitis?
Acute: fever, chills, cough, dyspnea; Chronic: progressive pulmonary fibrosis, clubbing
110
What is the etiology of Other Occupational Lung Diseases?
Inhalation of inorganic dust leading to chronic interstitial fibrosis
111
What are examples of Pneumoconioses?
Anthracosis – coal dust → black lung; Silicosis – silica dust (e.g., sandblasting); Asbestosis – asbestos fibers (e.g., shipbuilding, insulation)
112
What is the mechanism of Other Occupational Lung Diseases?
Alveolar macrophages engulf particles; inflammatory response → lysozyme release → tissue injury; cannot degrade particles → granuloma and fibrosis
113
What are the outcomes of Other Occupational Lung Diseases?
Progressive fibrosis; can present with restrictive and/or obstructive features; increased risk of lung cancer (especially with asbestosis)
114
What is the etiology of Acute Respiratory Distress Syndrome (ARDS)?
Direct or indirect injury to alveolar-capillary membrane (e.g., sepsis, trauma, pneumonia, aspiration, pancreatitis)
115
What is the pathophysiology of ARDS?
↑ Capillary permeability → protein-rich edema; hyaline membrane formation within alveoli; alveolar collapse, pulmonary vascular damage
116
What is the gas exchange issue in ARDS?
↓ PaO₂; refractory to oxygen therapy
117
What are the lung mechanics in ARDS?
↓ lung compliance; ↑ work of breathing
118
What is the treatment for ARDS?
Oxygen therapy with PEEP; mechanical ventilation
119
What is the etiology of Infant Respiratory Distress Syndrome (IRDS)?
Prematurity → immature lungs with insufficient surfactant
120
What is the pathophysiology of IRDS?
Pulmonary edema and alveolar collapse (atelectasis); decreased lung compliance; hypoxemia that does not improve with supplemental oxygen; surfactant deficiency → fluid imbalance and protein-rich leakage into alveoli
121
What are the clinical signs of IRDS?
Grunting, nasal flaring, retractions, cyanosis
122
What is the treatment for IRDS?
Prenatal corticosteroids; mechanical ventilation with PEEP; exogenous surfactant administration
123
What are the two main body fluid compartments?
Intracellular fluid (ICF) – ~2/3 of total body water; Extracellular fluid (ECF) – includes plasma, interstitial fluid, and other transcellular fluids
124
What is the composition of Intracellular fluid (ICF)?
High in: K⁺, Mg²⁺, phosphates, and proteins
125
What is the composition of Extracellular fluid (ECF)?
High in: Na⁺, Cl⁻, HCO₃⁻; plasma is protein-rich, interstitial fluid contains few proteins
126
What are the sources of water intake?
Ingested via food and fluids; metabolic water produced during cellular respiration
127
What drives capillary to interstitial fluid exchange?
Capillary hydrostatic pressure; interstitial hydrostatic pressure; capillary oncotic pressure; interstitial oncotic pressure
128
What drives intracellular to interstitial fluid exchange?
Osmotic gradients; plasma membranes are freely permeable to water, but not solutes
129
What are the excretion routes for fluid output?
Skin (sweat), Lungs (water vapor), GI tract (feces), Kidneys (urine – major route of fluid regulation)
130
What is the role of Antidiuretic Hormone (ADH)?
Produced in hypothalamus, stored and released by posterior pituitary. Stimulated by ↑ Plasma osmolality and ↓ Blood volume/pressure.
131
How does ADH function?
Increases water reabsorption in distal tubules & collecting ducts, inserts aquaporin-2 channels into nephron cell membranes, resulting in concentrated urine and water retention.
132
What stimulates Aldosterone secretion?
↑ K⁺ levels and ↑ Angiotensin II (RAAS system).
133
What is the mechanism of Aldosterone?
Promotes Na⁺ reabsorption in distal tubules and collecting ducts; water follows Na⁺ → volume expansion.
134
What are Natriuretic Peptides (ANP, BNP)?
Released by atria (ANP) and ventricles/brain (BNP) in response to stretch, promoting Na⁺ and water excretion.
135
What causes ECF Volume Deficit (Hypovolemia)?
Hemorrhage, vomiting, diarrhea, diuretics, 3rd spacing.
136
What is ECF Volume Excess (Hypervolemia)?
Caused by saline retention, heart failure, renal disease, aldosterone excess; isotonic expansion of ECF volume.
137
What is Hyponatremia?
↓ Na⁺ concentration in plasma caused by excess water retention or loss of Na⁺.
138
What is Hypernatremia?
↑ Na⁺ concentration in plasma caused by excess sodium intake or water loss.
139
What is edema?
Accumulation of fluid in interstitial space.
140
What are the mechanisms of edema?
↑ Capillary hydrostatic pressure, ↓ Capillary oncotic pressure, ↑ Interstitial oncotic pressure, lymphatic obstruction.
141
What is Hypokalemia?
Potassium level < 3.5 mEq/L caused by GI losses, renal losses, shift into cells, or inadequate intake.
142
What are the effects of Hypokalemia?
Hyperpolarized membranes → ↓ excitability, muscle weakness, cramps, EKG changes, cardiac arrhythmias.
143
What is Hyperkalemia?
Potassium level > 5.0 mEq/L caused by cell lysis, renal failure, or acidosis.
144
What are the effects of Hyperkalemia?
Depolarized membranes → cannot repolarize, flaccid paralysis, cardiac arrhythmias, possible arrest.
145
What is Hypomagnesemia?
Low magnesium levels caused by chronic alcoholism, diuretics, diarrhea, malnutrition.
146
What are the effects of Hypomagnesemia?
Increased ACh release → hyperexcitability, muscle twitching; often leads to hypokalemia.
147
What is Hypermagnesemia?
High magnesium levels caused by excessive intake or renal failure.
148
What are the effects of Hypermagnesemia?
Reduced ACh release → muscle weakness, lethargy, ↓ deep tendon reflexes, bradycardia, hypotension.
149
What is the normal pH range for acid-base balance?
7.35–7.45; even small deviations can have serious consequences.
150
What is acidosis?
Increased acid load (may or may not drop pH).
151
What is acidemia?
Actual decrease in blood pH (<7.35).
152
What is alkalosis?
Decreased acid or excess base.
153
What is alkalemia?
Actual increase in pH (>7.45).
154
What are buffer systems in acid-base balance?
Bicarbonate buffer (most important extracellular) and phosphate buffer (important in intracellular fluid and urine).
155
What is the role of the respiratory system in acid-base balance?
Controls CO₂ (volatile acid) and responds within minutes.
156
What is the role of the renal system in acid-base balance?
Regulates H⁺ excretion and HCO₃⁻ reabsorption; slower (hours to days), but powerful.
157
What is Metabolic Acidosis?
A condition caused by excess acid or bicarbonate loss, characterized by ↓ HCO₃⁻ and a pH that may be low or compensated.
## Footnote
Compensation occurs through hyperventilation to ↓ CO₂.
158
What is Respiratory Acidosis?
A condition caused by hypoventilation leading to CO₂ retention, characterized by ↑ PaCO₂ and ↓ pH.
## Footnote
Compensation involves renal retention of HCO₃⁻ and increased H⁺ excretion.
159
What is Metabolic Alkalosis?
A condition caused by vomiting (loss of HCl), diuretics, or antacid overuse, characterized by ↑ HCO₃⁻.
## Footnote
Compensation occurs through hypoventilation to retain CO₂.
160
What is Respiratory Alkalosis?
A condition caused by hyperventilation due to anxiety, pain, fever, or high altitude, characterized by ↓ PaCO₂ and ↑ pH.
## Footnote
Compensation involves renal excretion of HCO₃⁻.
161
What are Mixed Acid-Base Disorders?
Conditions where more than one primary disturbance occurs, such as metabolic acidosis + respiratory alkalosis, complicating ABG interpretation.
162
What is the extent and impact of Diabetes Mellitus?
The most common endocrine disorder affecting over 18 million in the U.S. and over 250 million worldwide, with rising incidence due to obesity, physical inactivity, and aging.
163
What is the general pathophysiology of Diabetes Mellitus?
A metabolic disorder involving impaired glucose uptake and utilization, resulting in hyperglycemia, abnormal lipid and protein metabolism, dehydration, acidosis, and vascular damage.
164
What is the role of insulin?
Essential for glucose uptake into most cells, especially skeletal muscle and adipose tissue, but not required for neurons and red blood cells.
## Footnote
Insulin binds to its receptor, activating intracellular signaling and triggering translocation of GLUT4 transporters to the cell membrane.
165
What are the effects of insulin?
Promotes glucose uptake and storage as glycogen, stimulates lipogenesis and protein synthesis, and inhibits glucagon effects, gluconeogenesis, and lipolysis.
166
What is Type 1 Diabetes Mellitus (T1DM)?
An autoimmune destruction of pancreatic β-cells leading to absolute insulin deficiency, accounting for ~5–10% of diabetes cases, usually with onset in childhood or adolescence.
## Footnote
Pathophysiology includes unregulated glucagon secretion, leading to hyperglycemia and diabetic ketoacidosis (DKA).
167
What is Type 2 Diabetes Mellitus (T2DM)?
Characterized by insulin resistance and eventual β-cell dysfunction, accounting for 90–95% of cases, often diagnosed years after onset.
## Footnote
Risk factors include obesity, sedentary lifestyle, aging, and family history.
168
What is Gestational Diabetes Mellitus (GDM)?
Occurs in 2–5% of pregnancies due to increased insulin demands not being met, with risks including fetal macrosomia and increased maternal risk for T2DM later in life.
169
What is Prediabetes?
Includes impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), often asymptomatic and associated with ↑ risk of T2DM and cardiovascular disease.
## Footnote
Lifestyle changes can delay or prevent progression.
170
What are the macrovascular complications of chronic hyperglycemia?
Atherosclerosis leading to increased risk for myocardial infarction (MI) and stroke (CVA).
## Footnote
Tight glucose control has limited effect on macrovascular disease.
171
What causes microvascular complications in chronic hyperglycemia?
Thickening of capillary basement membranes and endothelial dysfunction.
172
What are the symptoms of retinopathy due to chronic hyperglycemia?
Capillary hemorrhages, microaneurysms, neovascularization leading to vision loss and potential blindness.
173
What are the effects of nephropathy in chronic hyperglycemia?
Glomerulosclerosis, decreased Glomerular Filtration Rate (GFR), and proteinuria which may progress to End-Stage Renal Disease (ESRD).
174
What are the symptoms of neuropathy due to chronic hyperglycemia?
Autonomic dysfunction (GI dysmotility, bladder dysfunction, erectile dysfunction) and peripheral sensory issues (loss of protective sensation in feet, increased risk for ulcers, infections, amputations, paresthesias, burning, numbness).
175
What lifestyle modifications can help manage chronic hyperglycemia?
Exercise increases insulin sensitivity and lowers glucose without increasing insulin; weight loss improves insulin responsiveness and may delay or prevent T2DM.
176
What are the effects of sulfonylureas in T2DM treatment?
Stimulate insulin secretion from β-cells, block ATP-sensitive K⁺ channels, may decrease hepatic insulin clearance and increase insulin sensitivity in tissues.
## Footnote
Risk: Long-acting agents may cause hypoglycemia.
177
What is the role of Metformin in T2DM treatment?
Decreases hepatic glucose production, increases peripheral insulin sensitivity, does not cause hypoglycemia, and is the first-line agent in most T2DM cases.
178
What are the effects of GLP-1 Receptor Agonists in T2DM treatment?
Increase insulin secretion, decrease glucagon secretion, delay gastric emptying, and suppress appetite leading to weight loss benefit.
179
What is the requirement for insulin therapy in diabetes?
Required in all T1DM patients and often needed in advanced T2DM.
180
What are the types of insulin and their characteristics?
Rapid-acting: onset ~30 min, peak ~2h, lasts <5h; Intermediate-acting: onset ~2h, peak ~11h, lasts ~24h; Long-acting: steady 24h basal release.
181
What is the most dangerous acute side effect of insulin therapy?
Hypoglycemia.
182
What is the purpose of capillary blood glucose testing?
Uses glucose oxidase test strips for day-to-day monitoring.
183
What does HbA1c reflect in diabetes management?
Average blood glucose over the past 2–3 months, better long-term metric than random glucose levels, useful for assessing treatment effectiveness.
184
What are the functions of the kidneys?
Maintain homeostasis through excretion of metabolic wastes, regulation of electrolytes, fluid volume, acid-base balance, erythropoietin production, vitamin D activation, blood pressure regulation via RAAS, and gluconeogenesis during prolonged fasting.
185
What are common etiologies of intrarenal disorders?
Congenital anomalies, mechanical trauma, infections (e.g., pyelonephritis), urinary tract obstructions, and glomerular disorders.
186
What is the significance of urinalysis in kidney disorders?
Detects presence of proteins, blood, leukocytes, nitrites, and casts.
187
What are the characteristics of Autosomal Recessive PKD (ARPKD)?
Onset in infants and children, cysts in collecting ducts, often associated with hepatic fibrosis, prognosis is poor.
188
What are the characteristics of Autosomal Dominant PKD (ADPKD)?
Onset in adulthood (30s–40s), more common than ARPKD, cysts develop in all parts of the nephron, often asymptomatic until renal failure occurs.
189
What are the symptoms of ADPKD when present?
Hypertension, hematuria, flank pain.
190
What is the etiology of pyelonephritis?
Ascending bacterial infection from the lower urinary tract.
191
What are common pathogens causing pyelonephritis?
E. coli, Proteus, Enterobacter.
192
What are the symptoms of pyelonephritis?
Flank pain, fever, chills, dysuria, urgency, frequency.
193
What is the treatment for pyelonephritis?
Antibiotics and addressing underlying urinary obstruction if present.
194
What are the types of obstructive kidney disorders?
Hydroureter (dilation from complete ureteral obstruction) and hydronephrosis (swelling of the kidney due to urine buildup).
195
What are the consequences of obstructive kidney disorders?
Increased pressure upstream leading to ischemia and atrophy, increased risk of infection and further renal injury.
196
What is nephrolithiasis?
Crystallized solutes (e.g., calcium oxalate, uric acid) in the renal pelvis, often asymptomatic until the stone enters the ureter.
197
What are the symptoms of nephrolithiasis?
Severe, colicky flank pain, hematuria, nausea, vomiting.
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What is the treatment for nephrolithiasis?
Hydration, pain management, lithotripsy to break up stones, and surgery for large or impacted stones.
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What are benign renal tumors?
Usually asymptomatic and slow-growing; may be discovered incidentally.
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What is Renal Cell Carcinoma (RCC)?
Arises from proximal tubule epithelium; most common adult kidney cancer; can invade renal vein or metastasize.
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What are secondary renal tumors?
Spread to the kidney from adrenal gland, GI tract, or hematologic malignancies.
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What are glomerulopathies?
Diseases affecting the glomerular capillaries.
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What are key signs of glomerulopathies?
Hematuria, proteinuria, decreased glomerular filtration rate (GFR), hypertension.
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What is Acute Glomerulonephritis (AGN)?
Immune-mediated condition with immune complex deposition in glomeruli, leading to increased glomerular permeability.
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What are clinical features of Acute Glomerulonephritis?
Edema (often periorbital), hematuria ('cola-colored urine'), proteinuria, hypertension.
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What are complications of Acute Glomerulonephritis?
Azotemia (↑ BUN, creatinine), decreased urine output (oliguria).
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What is the treatment for Acute Glomerulonephritis?
Supportive care, immunosuppression if autoimmune, treat underlying infection.
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What is Rapidly Progressive Glomerulonephritis (RPGN)?
Aggressive immune injury to glomeruli with rapid loss of renal function over weeks/months.
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What are lab findings in Rapidly Progressive Glomerulonephritis?
↑ Serum creatinine, hematuria, proteinuria.
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What may be required for Rapidly Progressive Glomerulonephritis?
Dialysis, immunosuppressive therapy.
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What is Chronic Glomerulonephritis?
Slow progression of glomerular injury leading to progressive scarring and renal failure.
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What are the etiologies of Chronic Glomerulonephritis?
Uncontrolled or undiagnosed GN, repeated infections.
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What is the treatment for Chronic Glomerulonephritis?
Control hypertension, manage fluid volume, address proteinuria, delay ESRD progression.
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What is the normal Glomerular Filtration Rate (GFR)?
~125 mL/min in men, ~115 mL/min in women.
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How is GFR regulated?
Autoregulation (myogenic constriction, tubuloglomerular feedback), renin release from juxtaglomerular (JG) cells.
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What triggers renin release from JG cells?
↓ perfusion pressure or ↓ NaCl delivery.
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What is the countercurrent system?
Involves Loop of Henle and vasa recta; maintains medullary osmotic gradient essential for concentrated urine production.
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What is Acute Tubular Necrosis (ATN)?
Most common cause of intrarenal AKI, caused by ischemia or nephrotoxins.
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What happens to tubular epithelial cells in ATN?
They die and slough into the lumen.
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What is Chronic Kidney Disease (CKD)?
Defined as GFR <60 mL/min for ≥3 months; may also be diagnosed based on structural damage or persistent proteinuria.
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What are common causes of CKD?
Diabetes, hypertension.
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What are the stages of CKD?
1. Decreased Renal Reserve: 50–80% nephron loss, no symptoms. 2. Renal Insufficiency: 80–90% nephron loss, azotemia, electrolyte imbalance. 3. ESRD: >90% nephron loss, uremia, requires dialysis or transplant.
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What are complications of CKD?
Anemia, hyperkalemia, acidosis, bone disease (↓ vitamin D activation).
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What is the management for CKD?
Blood pressure and blood glucose control, diet modification, erythropoietin, vitamin D, phosphate binders, dialysis or renal transplant.
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What is Acute Renal Failure (ARF)?
Sudden ↓ GFR, oliguria/anuria, ↑ BUN/creatinine
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What is the mortality rate of Acute Renal Failure (ARF)?
40–60%
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What are the causes of Acute Renal Failure (ARF)?
Prerenal: ↓ perfusion (e.g., hypotension, shock); Postrenal: Obstruction (must be bilateral); Intrarenal: Tubular/glomerular damage (e.g., ATN)
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What is Chronic Renal Failure (CRF)?
Often due to diabetes or HTN
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What are the stages of progression in Chronic Renal Failure (CRF)?
1. ↓ Renal Reserve (silent) 2. Renal Insufficiency (azotemia, mild symptoms) 3. ESRD (>90% loss)
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What are the treatments for Chronic Renal Failure (CRF)?
Symptom management, Dialysis, Transplantation, Nutritional/vitamin support (e.g., vitamin D)
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What are lipid-soluble hormones?
Include steroid hormones and thyroid hormones. They bind to intracellular (often nuclear) receptors and act directly on gene expression.
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How do lipid-soluble hormones transport in the bloodstream?
Require carrier proteins (globulins) in the bloodstream for transport.
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What are water-soluble hormones?
Include peptides and catecholamines (e.g., epinephrine). They bind to cell surface receptors and activate second messenger systems (e.g., cAMP, IP₃).
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What hormones does the anterior pituitary produce?
Growth hormone (GH), Adrenocorticotropic hormone (ACTH), Thyroid-stimulating hormone (TSH), Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), Prolactin (PRL)
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What does the posterior pituitary store and release?
Antidiuretic hormone (ADH) and Oxytocin
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What is the primary regulatory mechanism in endocrine regulation?
Negative feedback
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What are the types of feedback loops in endocrine regulation?
1. Ultra-short loop: within hypothalamus 2. Short loop: pituitary hormone → hypothalamus 3. Long loop: target organ hormone → hypothalamus and pituitary
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What are the types of endocrine disorders?
Primary: Dysfunction of the target gland; Secondary: Dysfunction of the pituitary gland; Tertiary: Hypothalamic dysfunction; Hyporesponsiveness: Target tissues resistant to hormone (e.g., Type 2 diabetes mellitus)
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What is the difference between tropic and trophic hormones?
Tropic: Hormone that stimulates another endocrine gland; Trophic: Hormone that promotes growth and nourishment of tissues
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What are the effects of excess Growth Hormone (GH) in children?
Causes gigantism
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What are the effects of excess Growth Hormone (GH) in adults?
Causes acromegaly, often due to a pituitary adenoma
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What are the treatments for excess Growth Hormone (GH)?
Surgical removal (hypophysectomy), Radiation, Somatostatin analogs (GH-inhibiting hormone)
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What are the effects of Growth Hormone (GH) deficiency in children?
Causes short stature
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What are the effects of Growth Hormone (GH) deficiency in adults?
↓ muscle mass, decreased quality of life
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What is hyperthyroidism?
Graves’ disease: Autoimmune stimulation of TSH receptors by TSI antibodies, resulting in excess T₄ and T₃ production.
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What is a thyroid storm?
Life-threatening hyperthyroid crisis (high fever, tachycardia, delirium)
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What are the symptoms of hyperthyroidism?
Weight loss, tachycardia, heat intolerance, Exophthalmos, goiter, nervousness, tremor
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What are the treatments for hyperthyroidism?
β-blockers (e.g., propranolol) for symptom control, Antithyroid drugs (e.g., PTU – propylthiouracil), Radioactive iodine (RAI) ablation
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What is hypothyroidism?
Hashimoto’s thyroiditis: Autoimmune destruction of the thyroid gland.
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What is cretinism?
Congenital hypothyroidism that results in mental impairment and growth delay.
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What is myxedema?
Severe, chronic hypothyroidism in adults → coma if untreated.
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What are the symptoms of hypothyroidism?
Weight gain, cold intolerance, bradycardia, Dry, coarse skin, hoarseness, decreased DTRs
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What is the thyroid hormone dynamics?
Mostly T₄ is released; converted to T₃ in peripheral tissues by iodinase. T₃ is the active form.
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How can T₄ be displaced from transport proteins?
By NSAIDs (e.g., aspirin)
255
What is the function of Parathyroid Hormone (PTH)?
Secreted in response to low serum calcium (Ca²⁺), ↑ GI absorption of calcium, ↑ Bone resorption, ↑ Renal Ca²⁺ reabsorption, ↑ Phosphate excretion.
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What is Vitamin D (Calcitriol)?
Fat-soluble vitamin necessary for intestinal calcium absorption, synthesized in the skin (via UV), activated in liver and kidney.
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What is the role of Calcitonin?
Secreted by thyroid C (parafollicular) cells, inhibits osteoclasts, leading to net bone deposition.
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What are the causes of Hyperparathyroidism?
Parathyroid adenoma (primary) and secondary to chronic renal failure.
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What are the effects of Hyperparathyroidism?
Increased bone resorption leading to osteoporosis, increased serum calcium causing kidney stones, dehydration, and polyuria.
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What is the treatment for Hyperparathyroidism?
Parathyroidectomy.
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What are the etiologies of Hypoparathyroidism?
Surgical removal (e.g., post-thyroidectomy) and congenital absence.
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What are the symptoms of Hypoparathyroidism?
Neuromuscular irritability (e.g., tetany, paresthesias) and hypocalcemia.
263
What is the treatment for Hypoparathyroidism?
Calcium and vitamin D supplementation.
264
What is cortisol and where is it secreted?
Cortisol is a glucocorticoid secreted by the adrenal cortex.
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What regulates cortisol secretion?
ACTH from the anterior pituitary.
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What are the functions of cortisol?
Increases gluconeogenesis, protein catabolism, appetite, and fat redistribution; decreases inflammation; supports vascular tone and blood pressure; modulates immune response, mood, and memory.
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What is aldosterone and its role?
Aldosterone is a mineralocorticoid that regulates Na⁺/K⁺ exchange in the distal nephron.
268
What are the functions of aldosterone?
Promotes sodium reabsorption and potassium excretion, supports blood volume and blood pressure.
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What is Addison’s Disease?
Adrenal insufficiency due to autoimmune destruction of the adrenal cortex (primary) or decreased ACTH (secondary).
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What are the symptoms of Addison’s Disease?
Hypoglycemia, hypotension, hyperkalemia, fatigue, weight loss, salt craving, and skin hyperpigmentation (primary only).
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What is the treatment for Addison’s Disease?
Hormone replacement with glucocorticoids (e.g., hydrocortisone) and mineralocorticoids (e.g., fludrocortisone).
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What is Cushing’s Syndrome?
Any cause of excess cortisol, including exogenous steroids, adrenal adenoma/carcinoma, and ectopic ACTH production (e.g., small cell lung cancer).
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What is Cushing’s Disease?
Pituitary adenoma secreting excess ACTH.
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What are the symptoms of Cushing’s Syndrome?
Central obesity, moon face, buffalo hump, striae, hypertension, hyperglycemia, osteoporosis, muscle wasting, and psychiatric disturbances.
275
What is the treatment for Cushing’s Syndrome?
Surgery (e.g., adrenalectomy, hypophysectomy), radiation, and medications to block cortisol synthesis (e.g., mitotane).
