Exam 5 Material Flashcards

(1019 cards)

1
Q

Accessory Muscles of Inspiration

A

Sternocleidomastoid (elevates sternum)

Anterior, Posterior, Middle Scalenes (elevate and fix upper ribs)

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2
Q

Principal Muscles of Inspiration

A

External intercostals (elevate ribs, increasing width of thoracic cavity)

Interchondral part of internal intercostals (elevate ribs)

Diaphragm (domes descend, increases vertical dimension of thoracic cavity. Elevates lower ribs)

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3
Q

Quiet Breathing muscles of expiration

A

Expiration results from passive recoil of lungs and rib cage

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4
Q

Active breathing muscles of expiration

A

internal intercostals (except interchondral part)

Rectus Abdominus (depresses lower ribs, comperss abdominal contents, push up diaphragm)

External/Internal Obliques (depresses lower ribs, comperss abdominal contents, push up diaphragm)

Transversus Abdominus (depresses lower ribs, comperss abdominal contents, push up diaphragm)

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5
Q

Rib movement during respiration

  1. Pump Handle
  2. Bucket Handle
A
  1. increases Anterior Posterior (AP) dimensions
  2. increases lateral dimension
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6
Q

Where do the two layers (Mediastinal and Visceral) of the pleura meet?

A

At the root of the lung

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7
Q

Costocervical trunk

A

Supplies the first 2 posterior intercostal spaces

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8
Q

Subclavian Artery

A

Gives:

internal thoracic a.

Vertebral a.

Costocervical trunk

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9
Q

Descending Thoracic Aorta

A

Supplies posterior intercostal arteries

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10
Q

Which artery Runs in the costal groove

A

Posterior intercostal artery

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11
Q

“Internal thoracic A gives […] and terminates into […] and […]

A

“Internal thoracic A gives anterior intercostal arteries and terminates into musculophrenic and superior epigastric

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12
Q

Anterior intercostal a.

A

Follows the inferior border of the rib and anastomoses with the posterior intercostal arteries

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13
Q

Musculophrenic a.

A

continues along the costal margin supplies diaphragm, anterior and lateral walls

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14
Q

Superior epigastric a.

A

continues onto the anterior abdominal wall and anastomoses with inferior epigastric a.

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15
Q

Blood supply of Parietal pleura

A

Supplied segmentally by the vessels associated with the adjacent wall

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16
Q

Blood supply of Diaphragmatic

A

superior phrenic arteries

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17
Q

Blood supply of Mediastinal portion

A

pericardiacophrenic artery

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18
Q

Laryngotracheal groove evaginates forming _______ by the end of week ___.

A

laryngotracheal diverticulum

4

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19
Q

Anatomical location of the laryngotracheal diverticulum

A

anterior to the foregut

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20
Q

As the laryngotracheal diverticulum elongates its distal end enlarges to form the

A

Respiratory buds

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21
Q

Which mesodermal layer is surrounding the laryngotracheal diverticulum? And into what does it develop?

A

Splanchnic mesoderm develops into the cartilage, connective tissue and muscles of the trachea.

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22
Q

Tracheoesophageal septum divides the foregut into:

A

Ventral (laryngotracheal tube)

Dorsal (oropharynx and esophagus)

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23
Q

Laryngeal epithelium develops from _________ of ______ part of the Laryngotracheal tube

A

endoderm

cranial

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24
Q

Laryngeal cartilages are derived from migration of ___________ into the mesenchymal of ____ & ____ pairs of pharyngeal arches.

A

neural crest cells

4 th & 6th

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25
Laryngeal muscles develop from
mesenchymal myoblasts from the 4th and 6th pharyngeal arches
26
Where are Arytenoid swellings-mesenchyme
at cranial end of Laryngotracheal tube
27
Epiglottal swelling derived from
caudal part of hypopharyngeal eminence (from 3rd and 4th pharyngeal arches)
28
Laryngeal ventricles- formed by
recanalization of the laryngeal lumen
29
TRACHEO-ESOPHAGEAL FISTULA (TEF)
abnormal communication between trachea & esophagus due to defective development of the tracheo-esophageal septum
30
TEF may be a component of
VACTERL – **V**ertebral anomalies, **A**nal atresia, **C**ardiac defects, **T**EF, **E**sophageal atresia, **R**enal anomalies & **L**imb defects
31
TEF may be associated with
polyhydramnios [excessive quantity of amniotic fluid]. esophageal atresia inhibits free passage to the intestines of swallowed amniotic fluid.
32
Signs & Symptoms of TEF
coughing and choking during feeding, pneumonia, pneumonitis, polyhydramnios.
33
A respiratory bud (lung bud) develops at the ______ end of the laryngotracheal diverticulum during the ____ week.
caudal 4th
34
As the lung bud develops it divides into
2 primary bronchial buds
35
The secondary and tertiary buds grow ________ from the primary buds into \_\_\_\_\_\_\_\_\_
laterally pericardioperitoneal canals.
36
Segmental bronchus with surrounding mesenchyme-
bronchopulmonary segments
37
STAGES OF LUNG DEVELOPMENT
Pseudo-glandular stage (week 5 - 17) Canalicular period (week 16 - 25) Terminal Sac period ( week 24 to birth) Alveolar period (week 32 (late fetal period) to 8-10 years)
38
Pseudo-glandular stage
(week 5 - 17) major elements of the lung are formed but no respiratory bronchioles.
39
Canalicular period
(week 16 - 25) terminal bronchiole divides into 2 or more respiratory bronchioles respiratory bronchiole divide into 3-6 alveolar ducts. Type II Alveolar cells appear which produce surfactant. (secretion in week 20)
40
Terminal Sac period
(week 24 to birth) Terminal sacs formed lined by squamous epithelium; capillaries establish close contact.
41
Alveolar period
(week 32 (late fetal period) to 8-10 years) Primitive alveoli with well developed epithelial – endothelial capillary contacts (blood – air barrier after birth)
42
Mature alveoli are formed
after birth as the lungs expand
43
alveoli formation continues up to
8-10 years
44
Function of Surfactant
reduces the surface tension and facilitates expansion of the terminal sacs
45
During which week does surfactant production begin? When is it suffieient for survival in NICU? Outside NICU?
Week 20 Week 22-26 (NICU) Week 26-28 (Not NICU)
46
Respiratory distress syndrome (RDS) 1. Causes 2. Clinical Signs 3. Cell changes 4. Symptoms
1. Surfactant deficiency 2. rapid labored breathing shortly after birth. 3. irreversible changes in type II cells rendering them incapable of producing surfactant. 4. underinflated lungs, amorphous deposits in lungs.
47
Functions of Glutocorticoids in pregnancy
accelerates fetal lung movements & surfactant production
48
Three factors that influence the normal development of lungs
1. Thoracic space for growth 2. Fetal breathing movements 3. Amniotic fluid volume
49
congenital diaphragmatic hernia
lung is unable to develop normally thoracic space is reduced due to the presence of intestinal content in the thoracic space.
50
Oligohydramnios
insufficient amount of amniotic fluid may lead to retarded development of lungs (pulmonary hypoplasia)
51
Intraembryonic coelom
primordium of future body cavities.
52
Intraembryonic coelom develops in
lateral mesoderm, and divides it into 2 layers
53
Somatopleure
- parietal layer of serous pericardium, pleura and peritoneum.
54
Splanchnopleure
visceral pericardium, pleura and peritoneum
55
Head fold function
brings heart and pericardium anterior to the foregut. septum transversum forms, and separates pericardial and abdominal cavities.
56
After the septum transversum is formed and in place, the Heart remains suspended by the
dorsal mesocardium
57
Lateral Fold Function
apposes paired heart tube primorda and brings dorsal aortae to midline heart primordia fuse to form tubular heart
58
Pericardial coeloms function
fuse to form pericardial cavity
59
Pericardial cavity
lined by visceral and parietal layer continuous with paercardioperitoneal canals
60
Closing of ventral wall separates
Intraembryonic Coelom (IEC) from Extraembryonic Coelom (EEC)
61
Pleural Cavity Formation
Bronchial buds grow into pericardioperitoneal canal Membranous ridges develop from lateral wall
62
Pleuropericardial membrane
separate pleural cavity from pericardial cavity will fuse to form fibrous pericardium
63
Cranial Membranous Ridge
from the Pleuropericardial folds
64
Caudal Membranous Ridge
from the Pleuroperitoneal folds
65
PERITONEAL CAVITY-FORMATION
Closure of pleuroperitoneal openings with septum transversum
66
Pleuroperitoneal folds
project into pleuroperitoneal cavity
67
Migration of myoblasts into the peritoneal membrane - results in
final closure of the pleuroperitoneal canal
68
COMMON SITES OF DIAPHRAGMATIC HERNIA
Anteromedial Central Posterolateral
69
Anteromedial Diaphragmatic hernia
Rare. Defect b/t costal and sternal musculature
70
Central Diaphragmatic Hernia
Esophageal hiatus may be abnormally large **congenital hiatal hernia**
71
Posterolateral Diaphragmatic Hernia
Defect of pleuroperitoneal membrane: **congential diaphragmatic hernia** Abdominal contents herniate into thorax More common on left side
72
Congenital Diaphragmatic hernia
Abdomen empty when lying flat. Contents herniate into thorax. Lung compressed & hypoplastic. High mortality rates Requires urgent surgery
73
Eventration of the Diaphragm Caused by
defective musculature in one half of diaphragm
74
defective musculature in one half of diaphragm due to
failure of the muscle tissue from body wall to extend into the pleuroperitoneal membrane.
75
Eventration of the Diaphragm Effects
The affected side moves up with the contraction of diaphragm during respiration- **paradoxical respiration.**
76
Mid-clavicular line 1. Inferior border of lung 2. Inferior border of parietal pleura
1. Rib 6 2. Rib 8
77
Mid-axillary line 1. Inferior border of lung 2. Inferior border of parietal pleura
1. Rib 8 2. Rib 10
78
Paravertebral 1. Inferior border of lung 2. Inferior border of parietal pleura
1. Rib 10 2. Rib 12
79
Spontaneous Pneumothorax
Absense of lung disease, no prior proviking event, ruptured bleb or bullae
80
Traumatic Pneumothorax
secondary to pleural injury blunt or penetrating trauma
81
Non-tension pneumothorax
no valve mechanism (unsealed opening) as a result there is no build up pressure.
82
Tension Pneumothorax
air filling the pleural cavity can not escape (forming one-way valve). visceral pleura ruptured. pressure builds. mediastinal shift SOB. Needs urgent intervention
83
Signs & Symptoms of Tension Pneumothorax
Dyspnea Chest pain Tracheal deviation Hypotension Neck vein disension Hyperresonance
84
Needle decompression Indication
Tension pneumothorax-when thoracostomy (chest tube) is not possible in prehospital setting.
85
Site of needle decompression
2nd intercostal space. Midclavicular line. Affected side.
86
Tube Thoracostomy Indication
relieve trappes collections of air or fluid in throax
87
Thoracostomy site of insertion
4th or 5th intercostal space b/t anterior axillary and midaxillary lines.
88
ENDOTRACHEAL INTUBATION Introduction laryngoscope
Moves tongue forward Exposes epiglottis and voal fold
89
Introduction of endotracheal tube: Endotracheal Intubation
Advance tube b/t vocal folds into trachea Look/Listen for correct placement Be careful! Aspirate to remove excess secretions.
90
Pancoast Tumor
Tumor limited to apical lung region. can metastasize to neighboring structures
91
Pancoast Tumor Presentations
Subclavian Vein Compression C8, T1, phrenic nerve, sympathetic chain Compression (Claude-Bernard-Horner syndrome)
92
Hilum of lung
Region where mediastinal pleura meets visceral pleura. Structures enter/leave lung here
93
Root of Lung
Attaches lung to mediastinum structures Formed by structures entering/leaving lung.
94
Structures that form lung root
Bronchi Pulmonary Artery Pulmonary Vein Bronchial Arteries Lymph vessels Nerves
95
Structures on medial surface of Right Lung
Both Vena Cava Heart Azygous Vein Esophagus
96
Structures on medial surface of Left Lung
Heart Aortic Arch Thoracic Aorta Esophagus
97
Oblique fissures of lungs
begin at spinous process of scapula. follow rib VI anteriorly
98
Horizontal fissure of Right Lung
Follows 4th intercostal Space laterally to meet oblique fissure. Left lung does not have one.
99
Bronchial Tree 1. Primary Bronchus 2. Secondary Bronchus 3. Tertiary Bronchus
1. To lung 2. To lobe 3. To lobe segment
100
Where do inhaled objects tend to impale?
wider, shorter and more vertical right bronchus and eventually in the right lower lobe
101
"Label: ![]()"
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102
Bronchopulmonary Segments
smallest functional unit conical in shape surgically resectable w/o affecting neighbors
103
What vessels travel along with the segmental bronchi?
branches of pulmonary artery
104
Pulmonary artery and veins also supply
visceral pleura
105
Pulmonary vein leaves lung in
intersegmental septa
106
Left bronchial arteries
direct branches of aorta
107
Right bronchial artery from
posterior intercostal
108
Bronchial veins drain into
Left: Hemiazygos Right: Azygos
109
Lung Lymphatic Drainage Pathway
Intrapulmonary Bronchopulmonary (hilar) Tracheobronchial (carinal) Paratracheal Bronchomediastinal trunk Right thoracic trunk/thoracic duct Systemic venous system
110
Pneumonia (consolidation)
normal air-filled spaces of alveoli become filled w/ denser material like fluid/pus
111
Pleural effusion vs edema
effusion: fluid in cavity edema: fluid in alveoli
112
Visceral Afferent lung innervation
no visceral afferents to lung or visceral pleura Visceral afferents innervate bronchi
113
Parasympathetic lung innervation
from vagus nerve. bronchoconstriction, vasodilation, incr. mucus secretion by glands
114
Sympathetic lung innervation
-from sympathetic trunks via cardiopulmonary nerves. bronchodilation (beta receptors) and vasoconstriction
115
Lung nerve distribution
along bronchial tree and pulmonary vessels
116
Lamina propria
vessels lined up parallel to the airflow→ warms the air. Clinical correlate: nasal congestion
117
Olfactory receptor cells 1. Histological Features 2. Function
1. Long cilia w/ odor receptors. Axons from olfactory nerve 2. Bipolar neurons
118
Brush cell Function
sensory cells
119
Nasal: Supporting cells 1. Histological features 2. Function
1. Apical Microvilli. Mitochndria heavy, sER/rER. Secretory vesicles→ contain odorant binding protein OBP 2. Mechanical/Metabolic Support. Helps odor perception
120
Basal Cells Function
regenerate supporting and olfactoy receptor cells
121
Serous Olfactory glands / Bowman’s glands have their secretory units in the
Lamina Propria
122
How are odors sensed?
odor present olfactory glands secrete secretions trap/dissolve odor particles particles bind to OBP OBP bring odor particles to receptors Glandular secretions wash away particles once sensed.
123
Larynx 1. Skeleton 2. Functions
1. Hyaline Cartilage 2. Air conduction and phonation
124
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125
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Larynx Tumor
126
Trachea features
1. Mucosa 2. Submucosa 3. Hyaline Cartilage (Continuous) 4. Adventitia 5. Posterior part has small Trachealis muscle
127
Trachea Hyaline Cartilage 3 C's
Continuous C-shaped Cartilagenous
128
"Identify ![]() ![]() "
Trachea
129
Bronchi an also be classified as
Extrapulmonary Intrapulmonary
130
Bronchi: Mucosa
Respiratory Epithelium
131
Bronchi: Muscular Layer
Spirally oriented smooth muscles in in→ regulates the airway diameter
132
Bronchi: Submucosa
Loose CT with sero-mucus glands (Gl) in larger bronchi
133
Bronchi: Cartilage Layer
Hyaline cartilage plates
134
Bronchi: Adventitia
Connective tissue in the extrapulmonary part then surrounded by lung tissue in intrapulmonary bronchi
135
"Identify ![]() ![]() "
Respiratory Epithelium
136
"Identify ![]() ![]() "
Bronchi. 1st: extrapulmonary 2nd: intrapulmonary
137
Respiratory Epithelial cells
Ciliated columnar Mucus Small Granue/Kulchitsky Basal Brush
138
Ciliated Columnar Cells 1. Histological Features 2. Function 3. Clinical
1. 250 cilia on surface 2. expel particles trapped in mucus 3. Primary ciliary dyskinesis: Kartegener's Syndrome
139
Mucus Cells 1. Histological Features 2. Function 3. Clinical
1. Short, bunt microvilli 2. mucin granule secretion for protection 3. Incr. in smokers/chronic inflammation
140
Small Granule/Kulchitsky 1. Histological Features 2. Function 3. Clinical
1. most numerous @ primary bifurcation. basal granules 2. Catecholamine/hormone secretion 3. small cell carcinoma affects them
141
Basal Cell 1. Histological Features 2. Function
1. Near basement membrane 2. Stem cells pluripotent
142
Brush cells 1. Histological Features 2. Function
1. columnar. extend to apical surface. short microvilli 2. Synapse w/ afferent nerves-\> sensory function
143
Chronic bronchitis 1. associated with 2. clinical 3. signs 4. Results
1. smoking, inhalation of toxic fumes and exposure to heavy air pollution 2. Chronic, productive cough. positive history 3. Wheezing, cyanosis (Blue bloater) 4. Chronic irritation → inflammatory changes → metaplasia
144
Bronchiole Epithelium
Larger: Ciliated pseudostratified columnar with goblet cells Smaller (terminal&respiratory): ciliated cuboidal with secretory (Club) cells
145
Bronchiole Histological features
no glands All smooth muscle. Replaces cartilage.
146
"Identify ![]() ![]() "
Bronchioles
147
Club cell functions:
1. Secretes Surface Active Agent & Proteins 2. Detox 3. Stem Cells
148
Bronchial Asthma 1. Describe 2. Pathophysiology 3. Symptoms 4. Treatment
1. Inflammatory Airway Disease 2. Airway Obstruction: incr. mucus, incr. SM, wall inflammation. 3. SOB, wheexing, coughing 4. Albuterol (B2 agonist), anticholinergics. Corticosteroids (antiinflammatory).
149
First sites where gaseous exchange take place.
Respiratory Bronchiole
150
Alveolar ducts terminate in
alveolar sacs
151
Alveoli
thin walled sacs where gaseous exchange takes place.
152
Alveoli shape
polyhedral
153
Alveoli cell types
Macrophages Type I Pneumocytes Type II Pneumocytes
154
Alveolar Macrophages
Dust Cells phagocytosis of inhaled particles degrade surfactant
155
What are Dust Cells loaded with in heart failure?
RBC's.
156
Type I pneumocytes
Squamous cells which line 95% of alveolar surface Terminal cells not capable of mitosis. Surface is covered by surfactant
157
Type II Pneumocytes P2
Cuboidal cells which secrete surfactant Found at the septal junctions→ AKA septal cells Most numerous but cover only 5% of alveolar surface Apical lamellar bodies→ foamy appearance
158
Surfactant Protein SP-A
regulates synthesis and secretion of surfactant and modulates immune response . regulates airborne allergic response w/ SP-D
159
SP-B and SP-C
regulate surfactant spreading
160
After what week of gestation is adequate surfactant produced?
35
161
Interalveolar Septu contains
collagen fibers Elastic fibers continuous capillaries permanent and transient cells
162
Adjacent alveoli communicate through
alveolar pores (of Kohn)
163
Adjacent alveoli communicate through alveolar pores (of Kohn) which allows
collateral airflow → spread of Pneumonia
164
Components of Thin portion of blood gas barrier
Surfactant Type I pneumocyte Basal lamina of P1 Capillary endothelium Endothelial cells
165
Components of Thick portion of blood gas barrier
Surfactant Type I Pneumocyte w/ basal lamina Connective Tissue Capillary Endothelium Endothelial cells
166
Most effective portion of blood-air barrier
Thin portion
167
Emphysema
permanent enlargement of respiratory spaces affecting airways distal to the terminal bronchioles
168
Emphysema Pathways 1. Neutrophils 2. Smoking Treatment:
1. Neutrophils release proteases including elastase→ breaks down elastic fibers 2. Smoking elevates neutrophils activity→ elevated elastase→ destruction of elastic fibers → permanent dilation of airways Treatment: Serum Alpha 1 antitrypsin (AAT) counteracts elastase activity
169
"Identify the disease: ![]() "
Emphysema
170
"Identify the disease: ![]()"
Pneumonia
171
Emphysema 1. PMHx 2. Symptoms 3. Alveoli
1. smoking, liver disease etc 2. Cough, dyspnea Dilated
172
Pneumonia 1. PMHx 2. Symptoms 3. Alveoli
1. elderly, children, immuno-compromised etc. high risk. 2. Fever, chills, cough with sputum, chest pain 3. constricted alveoli. large capillaries
173
Adenocarcinoma
Most common in non-smoking women Peripheral mass
174
"Identify the Cancer: ![]() "
Small Cell Lung Cancer
175
"Identify the Cancer ![]() "
Squamous Cell Carcinoma
176
"Identify the Cancer: ![]()"
Adenocarcinoma
177
Type of epithelium in vocal folds
stratified squamous
178
Respiratory Zone of Lung
End of respiratory tree Gas exchange surface Epithelial layer and an extracellular matrix Surrounded by capillaries
179
Conducting Zone of Lung
Air flow into/ out of lung heat, hydrate, clean Heat exchange, water vapor pressure equilibriation, remove particulate load Mucociliary clearance
180
Gas moves from the trachea to the alveoli via
bulk flow
181
In the alveoli gas moves across the alveolarcapillary membrane by
diffusion
182
Fick's Law
Vgas= D(A/T)(P1-P2) V=rate of diffusion D=diffusion coefficient T=diffusion barrier thickness A=surface area available for gas exchange
183
Normal Alveoli surface area
75m2 (300 million alveoli)
184
Most extensive capillary network in Body
Pulmonary Circulation
185
Respiratory System Functions
Gas exchange Acid-Base balance Phonation Pulmonary Defense Metabolism
186
Activation of metabolic Functions
Angiotensis I --\> Angiotensin II
187
Inactivation of Metabolic Function
Bradykinin Serotonin Prostaglandin E1, E2, F2
188
Diffusion barrier thickness
blood-gas interphase 0.5μm thick
189
Pulmonary blood-gas interphase formed by
alveolar-capillary membrane of terminal respiratory unit
190
Pulmonary blood-gas interphase consists of
Thin layer of surface liquid Alveolar epithelium cells (Type 1 Pneumocytes) Associated Basement Membrane Thin layer of interstitial fluid Pulmonry capillary endothelial cells, plus associated basement membrane
191
Two types of cells in Alveolar epithelium
Type I pneumocytes Type II pneumocytes
192
Type I pneumocytes and Type II pneumocytes ratio
1:, but Type 1 pneumocytes occupy most of the surface area
193
Surfactant functions
Stabalizes alveolar size Increases compliance Keeps lung dry
194
Conducting Zone 1. Functions 2. Structures 3. Pathology 4. Diseases
1. Airflow 2. Trachea, Bronchi, Bronchioles 3. Flow Velocity (Ventilation) 4. Asthma, COPD, Bronchitis, Bronchiectasis, cystic fibrosis
195
Respiratory Zone 1. Functions 2. Structures 3. Pathology 4. Diseases
1. Gas Exchange 2. Resp. Bronchioles Alveolar Ducts, Alveoli 3. Gas Exchange. Maybe Volume problems 4. Pul. Fibrosis (incl. pneumoconiosis), Hypersensitivity pneumonitis, pneumonia
196
Function of Cilia lining airway
Beat the mucus covering them away from alveoli, towards pharynx. Function can be inhibited by cigarette smoke.
197
What is another name for mucus movement toward pharynx by cilia?
mucociliary escalator
198
Chronic Bronchitis 1. Definition 2. Caused by 3. Effects on Goblet cells 4. Effects on Cilia 5. Effects on Mucus glands
1. Inflammation of Bronchi 2. Cigarette smoke 3. Goblet cells may incr. in number 4. Cilia movement often impeded 5. Mucus gland incr. secretion and viscosity of mucus. Glands may hypertrophy. Leads to coughing/obstruction.
199
When can Chronic Bronchitis be confirmed as the diagnosis
Cough w/ sputum for at least 3 months a year for 2 consecutive years.
200
What makes air move in lungs?
Pressure gradients
201
Charles's Law
@ constant Pressure, Volume is directly proportional to temperature. (V1/T1)=(V2/T2)
202
Airtight chest wall allows for creation of pressure changes that
facilitate the movement of air on inspiration and expiration.
203
When does air flow into the lung?
When Alveolar pressure is less than atmospheric pressure
204
When does air flow out of the lung?
When alveolar pressure is higher than atmospheric pressure
205
What are the 2 phases of respiration
Inspiration Expiration
206
Muscles involved with inspiration
Diaphragm External Intercostals Scalene Sternocleidomastoid Pectoralis Serratus Anterior Latissimus Dorsi
207
Muscles involved with Expiration
Internal Intercostals Innermost Intercostals Rectus Abdominus Obliques
208
What is Boyle's Law?
@ Constant temperature Volume is inversely proportional to Pressure. P1V1=P2V2
209
How is alveolar pressure determined?
Air particles collide with wall. Each colision applies force. Pressure =Force/Area. Increasing surface area = drop in pressure.
210
Transpulmonary Pressure (Lung Elastic Recoil Pressure)
Alveolar Pressure-Intrapleural Pressure
211
Chest Wall Recoil Pressure
Intrapleural Pressure - Atmospheric Pressure
212
Why is expiration slower than inspiration and why is a greater DPA required to drive expiration than inspiration?
Incr. Airway Resistance during expiration make for larger pressure gradients that dissipate more slowly.
213
Lung Compliance formula
C=ΔVL/ΔPTP C=1/E
214
forces the lung needds To overcome
1. Airway resistance 2. Frictional forces 3. Inertia of air + tissues 4. Elasticity of lung
215
Pressure volume relationship is termed
hysteresis
216
If lung is filled with saline so that There is no surface tension
hysteresis not present
217
Pressure Tension mathematical relationship (formula)
P=2T/r (4T if 2 surfaces like a bubble)
218
Surfactant Constituents
90% Phospholipids 10% Protein
219
Surfactant Phospholipids
60% phosphatidycholine 7-15% phosphatidylglycerol Remainder: The rest of the membrane phospholipids
220
SP-A and SP-D
large hydrophilic collagen-like lectin superfamily (collectins) – lung defense
221
SP-B and SP-C.
hydrophobic – facilitates surfactant monolayer formation
222
At low lung volumes, the smaller alveoli tend to collapse, a phenomenon known as
atelectasis
223
Compliance too high
lung inflates easily and has little elastic recoil Emphysema COPD
224
Compliance too low
lung inflates with difficulty due to large elastic recoil Pulmonary fibrosis Respiratory distress syndrome
225
On which chromosomes are the α-like and β-like globin genes clustered?
Chromosomes 16 and 11.
226
What are the specific locations of the α-globin and β-globin genes?
2 α-globin genes on Chromosome 16. (α1, α2) --making there 4 in total per person. 1 β-globin genes on Chromosome 11--making there 2 in total per person.
227
The myoglobin protein monomer is mostly composed of which secondary structure?
Alpha helix. Actually devoid of beta sheet.
228
What are the 6 coordinate covalent bonds that can be formed by Fe2+?
* *Four** bonds ro nitrogen in porphyrin ring * *One** bond to amino acid of globin protein **One** bond free to reversibly bond Oxygen
229
Where in the globin protein is Iron located, and why?
Deep inside. Ensures Oxygen release in the molecular form Oxygen entrance/exit is in a defined path.
230
Hemoglobin A
pair of identical αβ dimers (α2β2 tetramer) with widely spaced heme groups.
231
What types of interactions exist between subunits of Hemoglobin A?
Hydrophobic Ionic Hydrogen bonds
232
How many O2 molecules can be carried on a single Hb monomer?
One.
233
Methemoglobin
Basically O2- gets released instead of O2. This leaves Fe3+ instead of Fe2+. This form of iron cannot bind Oxygen. Also, the other 3 monomers can no longer release oxygen. So this is not an oxygen carrier. Heme binding pocket structured so this can rarely happen, and when it does, it is enzymatically fixed.
234
Describe the conformational change in hemoglobin when O2 binds.
out of plane shifts to in pane.
235
2,3-BPG
forms taught state of Hb. Decreases Hb O2 affinity. allows formation of additional salt bridges between αβ / αβ dimers creates driving force for Hb to assume deoxyHb structure (taut).
236
How do Hydrogen ions affect hemoglobin?
They reduce the pH of the environment, and they promote O2 release.
237
Carbonic anhydrase in hemoglobin
promotes formation of carbonic acid from CO2 H+ ions protonate Hb, forming positive charges Salt bridges form Taut form stabalized. O2 delivered to tissues.
238
Quarternary Hb structures Fetus
2γ2 ~1% "
239
Quarternary Hb structures Adult HbA
α2β2 ~90%
240
Quarternary Hb structures Adult HbA2
α2δ2 ~2%
241
"Quarternary Hb structures Adult HbA1C"
α2β2 -glycated ~5%
242
Which hemoglobin has highest O2 affinity?
Fetal. α2 γ2
243
Glycation
non-enzymatic, spontaneous reaction. does not interfere with normal function of HbA1C.
244
HbA1C levels may be useful to
monitor blood glucose levels over the previous three months
245
Hemoglobinopathies Thalassemia
Qualitative change in Hb Quantitative change in Hb
246
Amino Acid substitution in HbS
Glutamic Acid is substituted by Valine at position 6 of the B-globin chain
247
How much HbA is there in Sickle Cell Disease
No HbA exists at all.
248
Drugs that increase expression of fetal globins
5-azacytidine (Decitabine; demethylating agent) Hydroxyurea Butyrate compounds (inhibit histone deacetylation)
249
Drugs that increase expression of fetal globins mechanism of action
alter epigenetic gene regulatory mechanisms may change acetylation of chromatin proteins Alter gene silencing patterns, Derepression of γ-globin gene
250
Hemoglobin C
point mutation at the 6 th codon position of the β-globin gene missense mutation (Glu→Lys) moves toward anode @ slowest pace. mild hemolysis. tends to crystalize n RBC b/c less soluble than HbA.
251
HbSC disease
episodes of sickling that are similar to sickle cell disease (but milder)
252
Other DNA diagnostic tests for HbS, HbAS and HbSC
ASO, RFLP
253
a-Thalassemia
Common in South east Asia, Africa and the Mediterranean deficiency in a-globin chain synthesis
254
a-globin gene deletion can be caused by
unequal crossing over during homologous recombination
255
Genetic basis of a-thalassemia Los of 1 gene 2 genes 3 genes 4 genes
Loss of one gene (aa/a-) is a silent carrier with no clinical problems Loss of two genes (a-/a-) or (aa/- -) results in mild anemia. Loss of three genes (a-/- -) cause β4 tetramers referred to as HbH, which causes moderate hemolytic anemia. Loss of all a globin genes is lethal (- -/- -) and is known as hydrops fetalis
256
Hemoglobin Bart hydrops fetalis
most severe form of α-thalassemia aggregation of γ4 tetramers (as there is absence of a-globin chains) fetal onset of generalized edema, ascites, pleural and pericardial effusions, and severe hypochromic anemia Stillbirth or death as neonate. No HbF or HbA.
257
Hemoglobin H (HbH) disease
infancy or childhood with mild-to-moderate hemolytic anemia and hepatosplenomegaly Mild thalassemia-like bone changes Deletion of 3/4 alleles. HbA low to low normal.
258
β-thalassemia
Autosomal recessive disorder Allelic Heterogeneity Excessive a-globin chains precipitate and result in severe hemolytic anemia
259
β-thalassemia major
‘Cooley's Anemia’ and ‘Mediterranean Anemia’ Very low or absent HbA levels – Absent or very little β globin synthesis High HbA2 and HbF levels (Compensatory)
260
β-thalassemia intermedia
Mostly homozygotes or compound heterozygotes one severe mutation, second mutation is less severe or two less severe mutations Low HbA levels High HbA2 and HbF levels (Compensatory)
261
β-thalassemia minor
"""β-thalassemia carrier"", ""β-thalassemia trait"" or ""heterozygous β-thalassemia"" Are mostly heterozygotes Almost normal HbA levels "
262
Bone changes in thalassemia
Frontal bossing, malar prominence – indicative of extramedullary erythropoiesis Bone marrow tries to compensate and expands to perform erythropoiesis and this leads to bone deformity and fractures
263
Treatment of β-thalassemia
**Regular transfusions** **Iron chelation** and **dietary control** **bone marrow transplantation** from an HLA-identical sibling.
264
Genetics of Hemophilia A and B
A: 40% of cases of severe Factor VIII deficiency arise from a large inversion. Deletions, insertions, and point mutations account for the remaining 50-60% B: Point mutations and deletions in the Factor IX gene
265
Phenotype of Hemophilia carrier females
usually asymptomatic some carrier females have increased bleeding tendency from skewed X-inactivation
266
Treatment for Hemophilia
Recombinant factor VIII (or IX) replacement therapy
267
Preinspiration
Airway pressure everywhere is 0 (no flow) Intrapleural pressure -5 PIP, there is a +5 cm H2O holding airways open.
268
During inspiration
Chest wall expands, diaphragm flattens. Intrapleura PIP and alveolar pressure PA fall by 2, and air flows into the lungs. at a point further it is -1. +6 holding airway open
269
End inspiration
Flow is 0. Slightly higher intrapleural pressure PIP. airflow driven by PA and PATM gradient
270
Forced expiration
Intrapleural pressure increases to +30 (diaphragm and thorax).
271
Dynamic compression of the airway
process that results in effort independence of the flow-volume loop.
272
Effort independence region of flow volume loop
dynamic compression results in resistance to air flow as intrapleural pressure increases extra effort not result in increased air flow due to this "valve".
273
EPP- Equal pressure point
point at which pressure inside the airway equals pressure outside (intrapleural pressure).
274
When does Dynamic airway compression start?
after the equal-pressure point (EPP).
275
Tidal Volume
the volume of air inhaled or exhaled with each normal breath
276
Inspiratory Reserve Volume
the volume of air that can be inhaled at the end of a normal tidal inspiration
277
Expiratory Reserve Volume
the volume of air within the lungs that can be exhaled after the end of a tidal exhalation
278
Residual Volume
the air remaining in the lungs after a maximal expiration (this volume of gas cannot be expelled, and cannot be measured by spirometry)
279
Functional Residual Capacity
the total volume of air remaining in the lungs at the end of a tidal exhalation
280
Total Lung Capacity
the volume of air in the lungs at the end of a maximal inspiration
281
Vital Capacity
the volume of air exhaled from maximal inspiration to maximal exhalation; maximum expiration. When done with force this volume is termed the forced vital capacity
282
Forced Expiratory Volume in 1 second
the volume of air exhaled in the first second of a FVC test
283
Ranges for: 1. Inspiratory Reserve Volume 2. Tidal Volume 3. Expiratory Reserve Volume 4. Residual Volume 5. Total Lung Capacity 6. Inspiratory Capacity 7. Functional Residual Capacity 8. Vital Capacity
1. 1.9 – 2.5 L 2. 0.4 – 0.5 L 3. 1.1 – 1.5 L 4. 1.5 – 1.9 L 5. 4.9 – 6.4 L 6. 2.3 – 3.0 L 7. 2.6 – 3.4 L 8. 3.4 – 4.5 L
284
Formulas for 1. Total Lung Capacity 2. Inspiratory Capacity 3. Functional Residual Capacity 4. Vital Capacity
1. (TLC = IRV+VT+ERV+RV) 2. (IC = VT + IRV) 3. (FRC = ERV + RV) 4. (VC = IRV + ERV + VT)
285
Obstructive Lung disorder
Expiratory flow rate is significantly decreased decreased FEV1 and FVC FEV1/FVC ratio is low.
286
Restrictive lung disorder
Lung inflation is decreased decreased FEV1 and FVC FEV1/FVC ratio is normal or increased
287
Spirometry- Use of FEF25-75
Represents the expiratory flow rate over the middle half of the FVC (between 25% and 75%).
288
Small airway obstruction may be present even when
FEV1/FVC% is above the lower limit of normal.
289
What has the greatest sensitivity for the detection of early airflow obstruction?
FEF25-75
290
Obstructive lung disease impact 1. FVC 2. FEV1 3. FEV1/FVC 4. TLC 5. RV 6. FRC
1. decr. 2. very decr. 3. \<0.8 4. incr. 5. incr. 6. incr.
291
Restrictive lung disease impact 1. FVC 2. FEV1 3. FEV1/FVC 4. TLC 5. RV 6. FRC
1. very decr. 2. decr. 3. \>0.8 4. decr. 5. decr. 6. decr.
292
Examples of Obstructive lung disorders
Chronic Bronchitis Emphysema Asthma
293
Examples of Restrictive Lung Disorders
Pulmonary Fibrosis IRDS Scholiosis
294
Emphysema Obstruction
Disintegration of the lung’s elastic framework and destruction of alveolar walls Enlargement of air spaces distal to the terminal bronchioles air trapping – prolonged expiratory phase, barrel chest, flat diaphragm caused by cigarette smoking Genetic risk factor - alpha-1-antitrypsin (AAT) deficiency
295
Helium dilution Technique
Known concentration of helium in a known volume of gas (oxygen) in spirometer Person is asked to breathe until the gas equilibrates between the spirometer & the lungs Useful in healthy individuals with no lung obstruction Helium does not get beyond obstruction, thus yielding a false FRC Body plethysmography can overcome this problem
296
EPP
when pleural pressures = airway pressures
297
Dynamic airway compression
Above EPP, upstream towards mouth, there is dynamic airway compression. - decr. radius, decr. resistance. - Thus restricts airflow - lower lung volumes - Results in effort independent portion of the flow-volume loop
298
Poiseuille’s Law Formulas
R=8nl/r4 V=ΔPπr4/8nl V=ΔP/R
299
If flow is turbulent – the airflow is proportionate to
sq.root(ΔP)
300
Extra-alveolar blood vessels
radial traction forces keep them open Pulled open as alveoli expand their resistance falls as the lung inflates.
301
Alveolar vessels
Stretching of the alveolar walls leads to stretching and pulls vessels closed
302
Zone 1
(PA \> Pa \> Pv ) * Flow is limited by compressive force of alveoli along length of pulm. capillary. * No flow & inc in zone 1 may occur with blood loss, positive pressure ventilation (Low Pa or high PA )
303
Zone 2
(Pa \> PA \> Pv ) * Initial part of the capillary is patent. * As capillary pressure falls below alveolar pressure along the length of the vessel compression occurs and increases capillary resistance.
304
Zone 3
(Pa \> Pv \> PA) Normal flow, arterial and venous pressure exceed alveolar so no compression along the length of the vessel.
305
Zone 4
Very base of lung, where the lung structures are subject to small transpulmonary pressure gradient. extra-alveolar vessels have increased resistance and flow is reduced overall.
306
Which part of the brain contains the generator of respiratory rhythm
Medulla Oblongata
307
Which neural structures have neurons that drive respiration
Dorsal Root Ganglion and parts of the rostral ventral root ganglion
308
Pontine Nuclei function
act as a switch b/t inspiration and expiration
309
What is the most important part of the medulla oblongata for rhesiratory rhythm generation?
preBötzinger complex
310
What is the function of non-rhythmic pontine areas like the pneumotaxix center and apneustic center?
Sends input to Medulla oblongata to control smooth respiratory rhythm.
311
What feeds signal to the Medulla Oblongata and Pons?
Cerebrum Mechanoreceptors Chemoreceptors (Both kinds) Proprioceptors
312
What is the pathway of respiratory muscle stimulation by pons/medulla?
1. Cerebrum, Chemoreceptors, Mechanoreceptors, Proprioceptors 2. Pons/Medulla 3. Spinal Motor Neurons 4. Respiratory Muscles
313
What is the Pons?
contains apneuistic and pneumotaxic centers that can modulate the basic pattern of the medulla.
314
What type of breathing control is signaled by the cerebrum?
Voluntary control
315
What controls emotional responses that affect breathing patterns?
limbic system and hypothalamus
316
What types of receptors are involved with reflex pathways of breathing?
Pulmonary Stretch Receptors Irritant Receptors J Receptors Proprioceptors
317
Pulmonary Stretch Receptors 1. Location 2. Firing pattern
lie in smooth muscle layer of airways fire in proportionate response to transmural pressure
318
Irritant Receptors 1. Loction 2. Respond to 3. Also Stimulated By 4. Stimulation results in
1. in airway epithelium 2. touch, noxious substances (smoke/particle deposition), Inflammatory histamines, serotonins, prostaglandins activated during inflammation 3. Lung edema 4. Coughing/gasping
319
Proprioceptors 1. Present in 2. Function 3. Signal
1. Tendons, joints, muscles. 2. Inform the brain of body position 3. The ones in the chest wall signal the breathing effort.
320
J Receptors
Juxtapulmonary capillary receptors (C-fiber endings) in Alveolar and bronchial groups Fire in response to lung injury, overinflation, pulmonary edema, pulmonary embolism. Not sensitive to inflammatory mediators Bronchial C-Fibers sensitive to inflammatory mediators Results in rapid, shallow breathing, bronchoconstriction, airway secretion
321
Cough 1. Stimulus 2. Receptor 3. Afferent Path 4. Effect
1. Mechanical/Chemical irritation 2. Upper Airway Irritant receptors 3. Vagus Nerve 4. Bronchoconstriction
322
Sneeze 1. Stimulus 2. Receptor 3. Afferent Path 4. Effect
1. Mechanical/chemical irritation 2. Nasal irritant receptors 3. Trigeminal, olfactory 4. Sneeze
323
Hering-Bruer Inflation Reflex 1. Stimulus 2. Receptor 3. Afferent Path 4. Effect
1. Lung inflation 2. Airway smooth muscle stretch receptor 3. Vagus Nerve 4. Stops Inspiration
324
Hering-Breuer deflation reflex 1. Stimulus 2. Receptor 3. Afferent Path 4. Effect
1. Lung deflation 2. Possible J, irritant, or stretch receptors 3. Vagus Nerve 4. starts inspiration
325
Positional Perception 1. Stimulus 2. Receptor 3. Afferent Path 4. Effect
1. Stretch of muscle or tendons 2. Proprioceptors 3. Spinal nerve pathways 4. Allows fine control of muscle groups
326
Pulmonary Vascular Congestion 1. Stimulus 2. Receptor 3. Afferent Path 4. Effect
1. Edema 2. J receptors 3. Vagus nerve 4. Tachypnea, sensation of dyspnea
327
Central Chemoreceptors
- Detect changes in PCO2 and pH - Located on ventral surface of medulla oblongata
328
Distinguishing Characteristics of CSF
- Separated from blood by Blood-brain-barier - Has little protein, so very limited buffer capacity - Sensitive to changes in PCO2. Incr. PCO2=decr pH
329
How does blood pH relate to CSF pH
They are directly proportional in the Respiratory circulation. In Metabolic circulation, there is little effect.
330
How does CSF pH affect ventillation?
Incr. pH, decr. ventillation.
331
Peripheral Chemo Receptors
- Located at carotid bifurcation and along aorta - Detect changes in pH, PCO2, and PO2. - Contain Glomus cells
332
Peripheral Chemo-receptors: Carotid bodies
- 2mm sensory organ - afferents feed CNS via glosso-pharyngeal nerve - sense changes in pH and decr. in PO2
333
Peripheral Chemo-receptors: Aortic bodies
- feed CNS via vagus nerve - sense decr. PO2
334
What are the glomus cells?
Sites of chemoreception
335
What changes allow the glomus cell to be depolarized?
decr. PO2 incr. PCO2 incr. H+
336
In what range of normal should PCO2 of arterial blood be held?
3mmHg
337
How does PACO2 affect Ventillation?
Increase in PACO2 increases VE.
338
How does PAO2 affect hypercarbic drive?
Low PAO2 increases hypercarbic drive High PAO2 only slightly decreases hypercarbic drive.
339
What is the most important stimulus to ventilatory drive
Arterial PCO2
340
Which types of chemoreceptors are the primary ones, and which ones respond fastest?
Central: Primary Peripheral: Quick Response
341
The response to PCO2 is potentiated by
low PO2
342
Describe the exception for PCO2 and pH in chronic disease.
In chronic disease, when PCO2 is high, but pH is compensated, then the hypoxic drive becomes more important. This is because PCO2 is only changed due to the change in pH.
343
What is partial pressure?
"The pressure exerted by a gas in a mixture of known gasses. Expressed in terms of ""dry gas"" concentration "
344
What is Functional Concentration?
The percentage or concentration of a known gas in a mixture of known gasses
345
Air pressure formula
Pg=PB x Fg
346
What is the standard Fractional Concentration of Oxygen? What is standard Barometric pressure?
21% 760 mmHg
347
What is the standard Fractional Concentration of H2O? What is the standard partial pressure of H2O?
6% 47mmHg
348
Minute Ventillation Formula
VE = VT × *f*
349
Minute Ventilation Definition
Amount of air entering the lung in one minute
350
What is standard Anatomic dead space?
150mL
351
Dead Space/Tidal Volume radio in healthy humans
0.25-0.35
352
Anatomic Dead Space Definition
Volume of air not participating in gas exchange. Volume lost to Conducting airway.
353
What is the result of alveloi with no perfusion?
Alveolar dead space. In health, value negligible.
354
Physiological dead space formula
Anatomical dead space + Alveolar dead space
355
Where is tidal volume distributed?
dead space alveoli
356
Alveolar ventilation formula
V\*A = (VT x *f*) - (VD x *f*) V\*A = (VT - VD) *f* V\*A = (VT -VD) x (breaths/min)
357
Which method should be used to measure Anatomical Dead Space?
Fowler's Method
358
Which method should be use to measure Physiological Dead Space?
Bohr's Method
359
How does a person's adult weight correspond to anatomic dead space?
1ml/pound. so 150lb adult woud have VD/t = 150mL/breath\*(12breath/min) = 1800mL/min
360
Describe the Fowler Method of Anatomic Dead Space measurement
- Inspire 100% O2 after tidal expiration - Exhale to maximum (RV) This will enable you to expire also air that was in the dead space as pure O2. This is exhaled along with alveolar dead space O2 and N2. The N2 volume and concentration in expired air is measured.
361
Bohr Method of Measurng Physiological Dead Space
VD/VT = 1-(PECO2/PaCO2)
362
Continuing Ventilation ensures that alveolar air is kept
high in PO2 and low in PCO2
363
Alveolar ventilation is dependent on:
Depth and Rate of breathing
364
The Alveolar Ventilation Equation based on PA/aCO2
VA = (VECO2 X 0.863)/ PACO2
365
VECO2 represents
expired volume of CO2 in 1 minute
366
Calculates global alveolar partial pressure of oxygen
PAO2 = PIO2 - (PACO2/R) Healthy person @ sea level: PAO2 = 150 - (PACO2/R) R=Resp. Quotient=0.8 (usually)
367
Factors that can affect PAO2
PB FIO2 Metabolic Activity Ventilation
368
"FIO2 – is **[...]** in ambient air"
FIO2 – is 21% in ambient air
369
What is the A-a O2 Gradient?
difference between the alveolar oxygen gas tension and the arterial oxygen tension
370
The A-a O2 Gradient when PAO2 is calculated from the alveolar gas equation and PaO2 is measured in arterial blood.
[PIO2 − (PACO2/R)] − PaO2
371
Normal values of the A-a O2 gradient are between
5-15mmHg
372
The A-a O2 Gradient • A value of more than 15 is usually associated with
hypoxemia
373
True or false: Low oxygenation due to hypoventilation (i.e. extrapulmonary source of hypoxemia) would not affect A-a gradient
True!!
374
pnea vs. ventilation
pnea = metabolic changes ventilation = respiratory pressure changes
375
What are the 3 phases of glycolysis?
ATP Investment 6C -\> 3C sugar ATP Generation
376
Irriversible enzymes of glycolysis
hexokinase PFK-1 pyruvate kinase
377
Which enzymes of glycolysis produce ATP? How many molecules?
1. Phosphoglycerate Kinase 2. Pyeuvate Kinase
378
Which enzymes of Glycolysis require ATP?
Hexokinase PFK-1
379
Which enzyme of Glycolysis produces NADH?
Glucose-3-Phosphate Dehydrogenase
380
GLUT transporters use what type of transport?
Facilitated diffusion
381
Locations of GLUT transporters
GLUT 1: Neurons, Brain, Erythrocytes GLUT 2: Liver GLUT 3: Neurons/Brain GLUT 4: Muscle/adipose
382
What is the most important regulated step of glycolysis. Why?
PFK-1 allosteric regulation.
383
"Lactate (lactic acid) accumulation in muscle causes **[...]** and may manifest as **[...]** during intense exercise"
a drop in pH cramps
384
Arsenate Inhibitor
Inhibits G3PD in glycolysis
385
Fluoride Inhibitor
Inhibits Enolase. Used in lab to test glucose levels.
386
Cori Cycle
Takes lactate, and transports from blood to liver. Used for Gluconeogenesis
387
Warburg Effect
Most cancer cells use glycolysis as main source of ATP.
388
Glucokinase
in liver has a high Km for glucose (more active when the blood glucose is elevated). It is also present in B-cells of the pancreas.
389
What is normal resting Alveolar Ventilation (VA)?
4L/min
390
What is normal Perfusion (Q)?
Relates to Cardiac Output. 5L/min
391
What is the ideal VA/Q ratio?
4/5 0.8
392
Alveolar- arterial oxygen (A-a O2) gradient – 5 to 15 mm Hg is due to
venous admixture
393
Increased venous admixture results in
low O2 tension in blood. (hypoxemia)
394
Total venous admixture is called
Physiological shunt
395
2 causes for physiological shunt
50% comes from anatomic shunt (right-to-left shunt) 50% from low VA/Q at base of lung
396
Wasted blood
All of the blood entering the lung is not fully oxygenated, leading to some “wasted blood.”- physiologic shunt.
397
Shunt calculate
Anatomic + low VA/Q = Physiological Shunt (Wasted blood)
398
Dead Space Calculate
Anatomic + Alveolar = Physiological Dead Space (Wasted air)
399
"At rest the lung apex is approximately **[...]** distended."
70%
400
"At rest the lung base is **[...]** distended."
15%
401
"Pulmonary circulation is a **[...]**-flow, **[...]**-pressure, **[...]**-resistance system."
high low low
402
"Since upward flow runs **[...]** hydrostatic pressure there is **[...]** resistance to blood flow toward the apex of the lung"
against more
403
how does the ventilation-perfusion ration change as you go down the lung?
decreases
404
Ventilation vs. Perfusion @ 1. Apex 2. Base
1. Apex: P \< V 2. Base: P \> V
405
Hypoxic vasoconstriction For low V/Q ratio (lots of blood or too little ventilation)
causes the blood coming into the area to be directed to other parts of the lung.
406
Bronchoconstriction: for high V/Q ratio
bronchi constrict slightly. resistance incr. and ventilation decr. in area w/ not enough perfusion limits alveolar dead space
407
How does Reginal low VA/Q ratio (90%) affect A-a O2 Gradient?
Increase
408
How does Anatomic shunt affect A-a O2 Gradient?
Increase
409
How does Generalized Hypoventilation affect A-a O2 Gradient?
No change
410
How does diffusion block affect A-a O2 Gradient?
Increase
411
Hypoxemia: Hypoventillation 1. A-a gradient 2. O2 therapy 3. DLCO
1. Normal 2. N/A 3. N/A
412
Hypoxemia: Shunt 1. A-a gradient 2. O2 therapy 3. DLCO
1. Abnormal 2. Not effective 3. N/A
413
Hypoxemia: V/Q Mismatch 1. A-a gradient 2. O2 therapy 3. DLCO
1. Abnormal 2. Effective 3. Normal
414
Hypoxemia: Diffusion Problem 1. A-a gradient 2. O2 therapy 3. DLCO
1. Abnormal 2. Effective 3. Abnormal
415
V/Q = 0
perfusion of an area with no ventilation i.e. a shunt
416
V/Q = infinity
dead space – ventilation with no perfusion
417
2 Forms of O2 Transport
Dissolved in Plasma Bound to Hemoglobin
418
Solubility of Oxygen
0.003mL O2/ dL Plasma
419
Dissolved Oxygen formula
Dissolved O2 = PO2 x solubility. =100 x 0.003 = 0.3mL/dL
420
What is the primary means for transporting Oxygen? Why?
Hemoglobin. Because in the soluble state, we would need to pump 83L/min to supply our body's need of 250mL/min.
421
Saturation Curve: Why is this sigmoid curve significant?
- Plateau portion of the curve is also known as loading phase - Steep portion of the curve known as unloading phase
422
Loading phase of hemoglobin
O2 content & O2 saturation remain fairly constant over a wide range of partial pressures – occurs in lungs
423
unloading phase of hemoglobin
allows release of O2 at tissue level where there is low PO2
424
Bohr effect
The effect of pH & PCO2 on Hb’s affinity to bind O2 high PCO2 and low pH = low binding affinity
425
Anemia: O2 Pressure O2 Saturation O2 Binding sites
normal. normal. fewer.
426
Polycythemia – does it improve tissue Oxygenation?
↑in the concentration of RBC’s more Hb per 100 ml blood Increased oxygen carrying capacity of blood No change in the affinity – just more binding sites for O2
427
Carbon Monoxide Hb changes
Has 210 x the affinity of O2 to Hb - PaO2 is normal but O2 content low No physical signs to indicate O2 content is low, when CO binds Hb – blood is cherry red & not cyanotic
428
First organ affected w/ carbon monoxide poisoning
brain
429
Carbon Monoxide symptoms
slowed reaction time blurred vision coma
430
2 types of gas movements in lungs
Bulk Flow Diffusion
431
Bulk Flow
all molecules move as one unit
432
Bulk Flow: Driving pressure
pressure gradient b/t Patm(at the mouth) - PA
433
Diffusion
Movement from alveoli -\> blood or blood -\> tissues
434
Gas diffusion depends on
pressure gradient membrane thickness surface area diffusion coefficient
435
Fick's Law
Vgas= D(A/T)(P1-P2) V=rate of diffusion D=diffusion coefficient T=diffusion barrier thickness A=surface area available for gas exchange
436
"If you double the thickness the rate of diffusion would be **[...]**"
halved
437
Diffusion coefficient formula
Diffusion coefficient (D) = solubility/√Mol wt
438
Normal Rate of O2 diffusion
250ml/min
439
Normal Rate of CO2 diffusion
200ml/min
440
R- respiratory exchange ratio
R = VCO2 / VO2 = 0.8
441
"Time required for RBC to move in the alveolar capillary is **[...]** at rest"
0.75 secs
442
Amount of O2 uptake is limited by
pulmonary capillary blood flow
443
Effect of blood flow on uptake different Gases: Equilibration times N2O O2 CO
0. 1 sec 0. 25 sec does not equilibriate
444
How long does it take for Hb to be fully saturated with CO?
0.75 seconds
445
O2 Diffusion Limited
increase barrier thickness - Pulmonary edema - Pulmonary fibrosis
446
To measure Diffusion Capacity
single breath test with carbon monoxide (CO)
447
Carbon monoxide is chosen To measure Diffusion Capacity because
PCO is diffusion limited only none in venous blood avidity to binding Hb maintains PaCO near zero
448
Since Diffusion Capacity (DL) is hard to measure you can use rearrange equation the below for measuring for DL
P2 = PaCO which is near 0 therefore DL = VCO/PACO
449
Forms of CO2 in the Blood in order of decreasing frequency (most-\>least)
Bicarbonate Dissolved Carbamino Compounds
450
Fate of tissue CO2
↑ PCO2 in tissues drives CO2 into blood only small portion dissolves the bulk of it diffuses into RBC’s
451
"in RBC’s CO2 is converted to **[...]** by enzyme: **[...]**"
HCO3 - + H+ carbonic anhydrase (CA)
452
In the tissues CO2 reacts with
free amine groups NH2
453
Total CO2 Arterial Blood PCO2 Bicarbonate Form Concentration
40mmHg 24 mM
454
Total CO2 Venous Blood PCO2 Bicarbonate
45mmHg 25.6 mM
455
Total arterial CO2 volume
0.48mL
456
Total venous CO2 volume
0.52 mL
457
How is incremental CO2 carried?
Carbamino Bicarbonate Free CO2
458
Haldane effect: CO2 dissociation curve
The inverse relationship between CO2 & PO2
459
Bohr effect: CO2 dissociation curve
Shift in curve in either direction 2o to PCO2 changes
460
Haldane Effect allows
more CO2 to load in tissues unload more CO2 load in lungs
461
"CO2 content much **[...]** than O2 content"
higher
462
Carbon Dioxide Diffusion
perfusion limited. 0.25 secs to equilibrate which same as O2, even though it is more soluble P is only 5-6 mmHg
463
Effects of Mild to moderate CO2 Diffusion Impairment
Can still equilibrate due to 0.5 reserve time.
464
Spinal level of superior pole of Left kidney
T11
465
Spinal level of superior pole of Right kidney
T12
466
The Rt. kidney is separated from the liver by
hepatorenal recess
467
Contents of renal hilum from anterior to posterior
Renal Vein Renal Artery Renal Plevis
468
Spinal level of renal hilum
L1/L2
469
"The kidney is surrounded by connective tissue forming the **[...]**."
renal capsule
470
"Outside of the renal capsule is the **[...]**, then the **[...]**, and lastly the **[...]**."
perirenal (perinephric) fat renal fascia (Gerota’s fascia) pararenal (paranephric) fat
471
Right Kidney Anterior Relationships
Liver (superior) Adrenal Gland (superior) Descending Duodnum (Medially) Colic/hepatic flexure (Inferior)
472
Right Kidney Posterior Relationships
Diaphragm (Superior) Rib 12 (Superior) Post. abdomen muscles (inferior)
473
Left Kidney Anterior Relationships
Stomach(superior) Adrenal Gland (superior) Spleen (Superior) Pancreas tail (Medially) Peritoneum covering small intestine (Inferior)
474
Left Kidney Posterior Relationships
Diaphragm (Superior) Rib 11 & 12 (Superior) Post. abdomen muscles (inferior)
475
The outermost part of the kidney is the
cortex
476
The renal cortex contains
glomeruli and convoluted tubules.
477
The innermostpart of the kidney is the
Medulla
478
The renal medulla contains
renal pyramids with straight tubules
479
Arcuate vessels
demarcate the renal cortex from the renal medulla
480
Flow of urine in the kidneys is from:
Glomerulus -\> tubular system -\> collecting ducts -\> minor calyces -\> mjor calyces -\> renal pelvis -\> ureter -\> bladder -\> urethra -\> toilet
481
Parts of the Nephron
Renal Corpuscle Tubular System
482
Renal corpuscle
* Glomerulus * Bowman’s capsule
483
Tubular system
P. Convoluted Loop of Henle D. Cnvoluted
484
Nephron and Collecting ducts together form a
Uriniferous Tubule
485
Left renal vein drains the:
Left kidney Left suprarenal gland Left gonads (testicular/ovarian)
486
Right renal vein drains
Right kidney
487
Right suprarenal vein and Right gonadal vein drain
directly into the IVC
488
Lt renal venous thrombosis can cause
stasis of blood in the Lt. testicle
489
stasis of blood in the Lt. testicle can lead to
varicocele
490
varicocele
a condition where veins in the scrotum become dilated, incompetent and cause retention of blood in the testicle. dilated veins can be felt as a ‘bag of worms’ on physical examination
491
Lymphatic drainage of Kidney
Left/Right lumbar (aortic/caval)
492
Lymphatic drainage of Upper ureter
Kidney lymphatics or lumbar lymph nodes
493
Lymphatic drainage of Middle ureter
common iliac
494
Lymphatic drainage of lower ureter
common, external, internal iliac
495
Lymphatic drainage of pelvic ureter nd bladder
internal iliac
496
Bladder Trigone
smooth area of the bladder in the non-distended state, bounded by 2 Ureteral orifices and Urethra
497
Ureteral orifices
open into the posterolateral aspect of the bladder
498
Urethra
commences at the neck of the bladder as the internal urethral orifice
499
Embryology of Adrenal Medulla
Neural crest cells -\> coelomic cavity wall. NCC also called chromaffin (chromaphil) cells due to their staining (yellow) with chromium salts
500
Embryology of Adrenal Cortex 1. Week 4 2. Week 6
1. celomic epithelium (mesothelium) cells proliferate. Initially form buds that separate from epithelium 2. small buds are now mesenchymal cells that form the fetal cortex.
501
What three arteries supply adrenal glands?
superior suprarenal (inf. phrenic) middle suprarenal (aorta) inferior suprarenal (renal)
502
Adrenal gland venous drainage
One suprarenal vein on each side. Left: drains to left renal vein Right: drains into IVC
503
"Preganglionic sympathetic innervation to medulla from **[...]** spinal segment"
T10- L1
504
Lymphatic drainage of adrenal glands
Lumbar lymph nodes
505
What cells in adrenal gland secrete cathecholamines? What part of the gland are they in?
chromaffin cells in the adrenal medulla
506
Most of the Urinary System develops from the
Intermediate mesoderm & Urogenital sinus
507
Intermediate mesoderm
between paraxial and lateral mesoderm; extends along dorsal body wall of the embryo
508
Development of the kidneys and ureters are closely related to that of the
genital system
509
2 portions of Urogenital ridge
nephrogenic cord: urinary system gonadal ridge: genital system
510
3 sequential systems of kidney development
**Pronephros**-rutimentary/nonfunctional **Mesonephros**-brief function in early fetal period **Metanephros**-will form permanent kidney
511
Pronephros Begins Cell groups Forms: Regression? Disappears by?
Begin week 4 7-10 cell groups in cervical region forms vestigial excretory units: nephrotomes Regress before the next system is formed more caudally disappears by end of week 4.
512
Mesonephros Starts? What happens? Degenerates by?
Starts week 4 w/ pronephros Excretory tubules appear Degenerates by end of 1st trimester
513
Excretory (mesonephric) tubules appear, method:
lengthen gradually. Form S-shaped loop Acquires tuft of blood forming primitive glomerulus Tubules elongate laterally. Join w/ mesonephric duct mesonephric duct opens into cloaca
514
mesonephric duct becomes
longitudinal collecting duct
515
"Mesonephros degenerates by the end of 1st trimester, but their excretory tubules and duct become the **[...]** of the genital system"
ductus deferens, duct of epididymis and efferent ductules
516
Metanephros
Appears in 5th week Excretory ducts develop from the metanephric mesoderm Ureteric bud grows Ureteric bud penetrates the metanephric tissue
517
Ureteric bud
outgrowth from mesonephric duct close to cloaca attachment
518
metanephric tissue
molded over by a cap from the surrounding mesoderm (metanephric blastema)
519
Development of the permanent kidneys
bud dilates to form the primitive renal pelvis splits into a caudal stalk (ureter)and cranial portion (collecting tubules) The metanephric diverticulum (ureteric bud) in its cranial part undergoes successive branching First divides into two to form the major calyces Continues to divide to form the minor calyces and collecting tubules The end of each collecting tubule divides and become arched
520
"The collecting tubules induce clusters of mesenchymal cells from **[...]** to form small **[...]**."
" The collecting tubules induce clusters of mesenchymal cells from **Metanephric Blastema** to form small **Metanephric Vesicles**. "
521
"Metanephric vesicles elongate to form S-shaped **[...]**."
metanephric (renal) tubules
522
The proximal ends of the renal tubules are invaginated by
glomeruli( tuft of capillaries)
523
The metanephric tubules differentiate into structures forming the
nephron
524
"Nephron formation is complete **[...]**, with **[...]** nephrons in each kidney"
at birth 1-2 million
525
What develops from the mesenchyme of the metanephric blastema
Excretory part Bowman’s capsule, Proximal Convoluted Tubules (PCT), Loop of Henle Distal Convoluted Tubules (DCT)
526
What develops from the ureteric bud?
Conducting part - Collecting tubules, minor calyces, major calyces, pelvis ureter
527
Metanephric tubules become continuous with the ends of arched collecting tubules to form
functional uriniferous tubules
528
"Initially, the kidney hilum faces **[...]** and receive branches from the **[...]**."
ventrally common iliac arteries
529
"By week **[...]**, the kidneys are in contact with the suprarenal glands and reach their adult position"
Nine
530
"Normally the primordial **[...]** arterial branches disappear and only the **[...]** arteries persist"
caudal final renal
531
Accessory Renal Arteries
Arise from Aorta above or below main artery
532
Accessory arteries that enter the lower pole
cross over the ureter and can cause obstruction (leading to hydronephrosis)
533
Renal segmental arteries are end arteries, so injury or ligation of an accessory artery leads to
ischemia of the segment of the kidney supplied
534
Unilateral Renal Agenesis
More common in boys Usually left absent Asymptomatic if other kidney is normal (compensatory hypertrophy)
535
Bilateral Renal Agenesis
can result in: Oligohydramnios Pulmonary hypoplasia POTTER sequence Incompatible with post-natal life
536
When there are separate ureters, one may have a fistulous opening into
urethra, vagina or vestibule
537
If the supernumerary kidney has its own separate ureter probably.....
2 separate ureteric buds developed on that side
538
Bifid Ureter:
One ureteric bud divide and induce the formation of an extra kidney Due to early, incomplete division of the ureteric bud
539
Horseshoe Kidney
Fusion of lower poles while still in pelvis Ascent interrupted by the inferior mesenteric artery
540
deep to superficial renal coverings
Renal Capsule (lines inside too) Perirenal Fat (Extraperitoneal fat) Renal Fascia (lines adrenal too) Pararenal Fat
541
Hepatorenal recess anatomical location
Superior to right kidney posterior to liver
542
How does body position affect Hepatorenal recess
Fluid in the abdomen will accumulate in this space when the body is supine
543
Hepatorenal recess also known as
pouch of Morrison
544
Hepatorenal recess one of the locations investigated during a FAST (focused assessment with sonography for trauma) exam
TRUE
545
The sympathetic innervation to the kidneys, ureters and bladder are derived from Ureters receive their innervation
lesser and least thoracic splanchnics and lumbar splanchnic nerves segmentally
546
"The renal plexus is formed by rami from sympathetics from **[...]** spinal roots"
T11-L2
547
rami from sympathetics from T11-L2 found in:
* The celiac ganglion and plexus * The aorticorenal ganglion * The lower (least) thoracic splanchnic nerves * The 1st lumbar splanchnic nerve
548
The renal plexus gives rise to the
ureteric and gonadal plexuses
549
Most renal nerves are
vasomotor
550
Sensory nerves(visceral afferent) go back to the CNS with the
thoracic splanchnic nerves
551
Pain from kidney stones, (pain from ureters mainly) is commonly referred to
flanks inguinal groin genitals upper thigh basically: loin-\>groin
552
Higher levels of T11-L2 will radiate near the Lower levels near the
ureteropelvic junction (UPJ) ureterovesical junction (UVJ)
553
Referred pain along, the distribution of the ilioinguinal
(skin over upper medial thigh, upper scrotal and labial areas)
554
Referred pain along, the distribution of the iliohypogastric
(skin over the anterior abdominal muscles, pubic symphysis)
555
Referred pain can also be along, the distribution of
subcostal nerves
556
Male and female pelvis: ureter location
"Water under the bridge" ureter being crossed over by the uterine vessels or ductus deferens
557
Urinary Bladder location
Just posterior to pubic symphyses area
558
Urinary Bladder apex attached to the umbilicus by
median umbilical fold (remnant of the urachus)
559
Urinary Bladder base
shaped like an inverted triangle and faces posteroinferiorly.
560
"The ureters enter bladder at the **[...]** and the urethra drains from **[...]**."
upper corners of the base lower corner of the base
561
Trigone of bladder
smooth triangular area on the internal surface between the openings of the ureters and the urethra
562
Urinary Bladder Blood supply
superior and inferior vesicle artery
563
Urinary Bladder Lymphatic drainage
external iliac nodes
564
If the urachus lumen of partially disintegrates it can form
urachal cyst urachal sinus urachal fistula (if it remains completely patent)
565
LIGAMENTOUS SUPPORT to URINARY BLADDER
- Pubovesical (♀) or puboprostatic (♂) - Rectovesical/cardinal(transverse cervical) - Perineal membrane, and muscles of the pelvic floor
566
Functions of ligaments supporting the urinary bladder
hold the neck of the bladder in place and help support/suspend the bladder
567
"**[...]** divides the cloaca into ventral primitive urogenital sinus and dorsal primitive rectum"
Urorectal septum
568
Three portions of urogenital sinus
Upper Middle Phallic
569
Upper portion of urogenital sinus
Vesical part. Largest portion Forms bladder.
570
Upper portion of urogenital sinus continuous with
allantois
571
allantois function
connect the developing bladder to the yolk sac through the umbilicus. soon constricts to form the urachus, which eventually obliterates and becomes the median umbilical ligament
572
Middle portion of urogenital sinus
thin pelvic part give rise to the urethra at the neck of bladder
573
Middle portion of urogenital sinus: males vs females
males: prostatic and membranous portions of urethra females: entire urethra
574
Phallic portion of urogenital sinus
forms most of the penile urethra in males
575
Bladder development occurs during weeks
7-Apr
576
"During development, the caudal portion of the mesonephric ducts are absorbed into the **[...]** and form the **[...]**"
wall of the urinary bladder trigone
577
As a result of the absorption of the caudal portion of the mesonephric ducts
the ureters enter the bladder
578
How do the ureteric orifices move and why?
They move superiorly and posteriorly due to the migration of the kidneys
579
How does body position affect Functional Residual Capacity?
Increases when standing over supine. Abdominal contents push into thoracic cavity when lying, but are suspended and pull down on diaphragm when standing. change in shape of lung compliance curve and increase in FRC.
580
Radial Traction/Tension
The pull on the alveoli. more pull=more diameter=more tension
581
radial traction
diminishing stretch of lung as you exhale
582
Retrosternal translucency
sign of lung hyperextension. Flat diaphragm especially evident in lateral view.
583
Pulmonary edema – causes in COPD
loss of lung tissue = loss of vascular tissue = poor ventillation = sm contract hypoxic vasoconstriction = vsm hypertrophy = incr. afterload on right heart
584
Acidemia – increased PCO2 and normal bicarbonate
pure respiratory acidosis.
585
Acidemia – increased PCO2 and raised bicarbonate
respiratory acidosis with metabolic compensatory alkalosis and increased bicarbonate reabsorption.
586
alkalosis
increased renal proton secretion
587
Innervation of bladder 1. Parasympathetic 2. Sympathetic
1. S2-4 (Pelvic Splanchnic) through inf. hypogastric to bladder 2. T10-12 (lesser and least splanchnics), L1&2 (lumbar splanchnics) reach the bladder through the Hypogastric plexuses
588
Visceral afferents for bladder pain travels with
sympathetic/Parasympathetic nerves
589
somatic motor neuron to the external urethral sphincter
Pudendal (S2- S4)
590
Pain from the bladder refers to
perineum
591
Referred pain from bladder may also involve
an increase in urinary frequency due to increased urinary urge
592
Ascending UTI more in women common because:
- Short urethra - Proximity to vagina and anus - Intercourse
593
Membranous urethra
located within the deep perineal pouch
594
Penile/spongy urethra
– its proximal portion contains openings for the bulbourethral glands
595
Urinary tract stones • More common in
men • Age range 20-60 years
596
Urinary tract stones composition
Aggregates of calcium, phosphate, oxalate, urate and other soluble salts
597
Urinary tract stones effect on urine
Urine becomes saturated and a small change in pH can cause precipitation of these salts
598
Effects of Urinary tract stones
Pain usually radiates from the infrascapular region into the groin or scrotum hematuria
599
Cause of Urinary tract stones
bacteria, maybe
600
Complications of Urinary tract stones
infection urinary obstruction renal failure
601
Polycystic kidney
Inherited disorder that can be AD or AR
602
AD Polycystic kidney
super rare. cycts on all nephron segments renal failure usually only until adulthood
603
AR Polycystic kidney
cysts progressively form from collecting duct kidneys become large. renal failure in infancy or childhood
604
Layers from skin to kidney
1. Skin 2. Subcutaneous tissue 3. Latissimus dorsi 4. Serratus posterior inferior 5. Thoracolumbar fascia posterior layer 6.Sacrospinalis 7. Thoracolumbar fascia middle layer 8.Quadratus lumborum 9. Thoracolumbar fascia anterior layer 10.Pararenal fat 11. Renal Fascia 12. Gerota’s fascia (Perirenal fat)
605
Renal transplant location
placed and attached in the region of the iliac fossa
606
Suprapubic catheterization location
inserted through the skin about 1 inch above the symphysis pubis.
607
Suprapubic catheterization 1. insertion conditions 2. use
1. general or local anesthesia 2. closed drainage. may be left in place for a time, sutured to the abdominal skin.
608
Benefits of urinary bladder catheter
Lower incidence of urinary tract infection ease of voiding naturally when the catheter is clamped ease of ambulation
609
Problems of urinary bladder catheter
A physician has to insert it. Cleaning is a pain in the butt at home. Cleaning needs to be sterine in hospital
610
Urethral catheterization male: 2 bends
first bend is in the spongy urethra and can easily be manipulated second bend is located at the membranous urethra and is fixed
611
Urethral catheterization male: risk of not inserting carefully
damage to bulb of penis -just deep to the first bend
612
How does stress (ie: laughing/coughing) cause incontinence
Stres (like from laughing or coughing) increases intra-abdominal pressure/ Sphincters become weak, so they do not close, and urine leaks.
613
Cystocele definition
Prolapse of the bladder into the vaginal canal
614
Cystocele Causes
repetitive straining of bowel movements constipation chronic or violent coughing heavy lifting being overweight or obese
615
Kidney – functions
Regulate acid-base balance Maintain extracellular fluid volume Excretion BP Regulation Endocrine
616
Renal sinus
Space around hilar structures, filled w/ loose conn. tissue
617
Renal Cortex
Granular in appearence consists most of nephron components\ extends b/t medulary pyramids as renal columns (bertin)
618
Renal Medulla
Pyramid arrangement Apical portion of pyramid: renal papilla. Projects into minor calyx Striated appearence: straight portions of tubules and straight blood vessels.
619
Three types of nephrons
Cortical: Short LOH Intermediate: mid cortical Juxtamedullary: long loops of Henle, these are crucial for concentrating urine
620
Renal Lobe
Medulla and associated cortex
621
Medullary Ray: Pars Recta
straight tubules
622
Cortical Labyrinth (Pars convoluta)
renal corpuscle and convoluted tubules
623
Renal lobule
Med. Ray in middle w/ areas of cort. laby on either side collecting duct and the nephrons it drains bounded by interlobular arteries
624
"Identify: ![]() "
Medullary Rays. Pars Recta
625
Blood supply to kidneys Cortico-medullary junction
arcuate arteries
626
Ultra-filtrate collects in {{c1::urinary space}} and is directed to the {{c2::PCT}} at the {{c3::Urinary Pole}}
thank you
627
Renal corpuscle – Bowman’s capsule Visceral Layer
Podocytes modified squamous cells invests glomerular capillaries
628
Renal corpuscle – Bowman’s capsule Parietal layer
outer layer simple squamous epithelium contin. w/ PCT
629
Renal corpuscle – Bowman’s capsule: Urinary Space
Bowman's space lies b/t 2 layers collects ultrafiltrate
630
Slit diaphragm (FS)
– covers pedicles of visceral layer of BC – zipper like thin sheet with a dense center containing nephrin – Anchored to actin filaments within pedicels of podocytes
631
Endothelium of glomerular capillaries
- numerous fenstrations - no diaphragms - produces NO and PGE2 - Abundant aquaporin-1 receptors
632
Glomerular basement membrane (GBM)
Thick Fused basal lamina of endothelial cells and podocytes Type IV collagen Heparan Sulfate
633
Structural arrangement of Glomerular basement membrane
Lamina Rara Interna (of capillary) Lamina Densa: Type IV collagen - physical barrier Lamina Rara Externa (of podocyte): haparan sulphate to repel negatively charged molecules
634
Factors Affecting Filtration
charge size shape
635
Clinical correlate: Goodpasture's Syndrome
IgG against Type IV collagen of basement membrane -\> glomerulonephritis: hematuria and proteinuria
636
Renal corpuscle - Mesangium Components:
Mesangial cells (contain actin filaments) Matrix
637
Two types of mesangial cells
At vascular pole (Lacis cells, extraglomerular mesangial cells) Within the corpuscle enclosed by the GBM
638
Mesangium Functions
Phagocytosis of residue along the GBM Structural support: Secrete ECM Secretion of inflammatory substances – interleukin-1, prostaglandin E2, PDGF Contractile cells
639
How do Renal tubules modify glomerular ultrafiltrate
reabsorption secretion reduce urine volume hyperosmotic fluid
640
"Identify: ![]() "
Proximal Convoluted Tubule
641
Proximal convoluted tubule type of epithelium cell description
simple cuboidal epithelium -\> absorption Large cells -\> large spaces b/t adjacent nuclei
642
Proximal convoluted tubule: Functions
receive ultra-filtrate from glomerulus. Reabsorbs 65% of it. 100% glucose 98% amino acids, small polypeptides Some protein and large peptides are returned to the blood via endocytosis
643
Proximal convoluted tubules: Basic histology: Apical surface
microvilli form brush border
644
Proximal convoluted tubules: Basic histology: Lateral Surface
Tight junctions and Zona Adherens Pilcae Basal interdigitations Basal striations associated with elongated mitochondria
645
Plicae
folds in lateral PCT which interdigitate with adjacent cellular processes
646
PCT: water reabsorption
Na + / K+ pumps : on lateral folds, creates osmotic gradient
647
PCT: Endocytic complex
apical tubular pits b/t microvilli, endocytotic vesicles, endosomes, lysosomes -\> protein absorption and recycling (image A)
648
PCT: Glycoalyx
Contains enzymes for absorption of glucose, peptides, etc. -\> stain w/ PAS Extensive Brush Border
649
How do Renal Tubules modify glomerular ultrafiltrate?
Reabsorption Secretion Reducing Urine Volume Create Hyperosmotic Fluid
650
Proximal straight tubule also called
Thick descending Loop of Henle
651
Cells of the Proximal Straight Tubule
Short cells. Poorly developed brush border. Less complex basolateral/lateral interdigitations than PCT Fewer/smaller mitochondria
652
" ![]() "
Proximal Straight Tubule
653
Thin Segment of the Loop of Henle
Longer in juxtamedullary nephrons and are found in the medulla
654
The Thin Segment of the Loop of Henle has four distinct segment based on
shape of cells, their content of organelles, the depth of their tight junctions, and their water permeability
655
Thin segment of Loop of Henle Epithelium
thin simple squamous in both ascending and descending limbs in short nephrons Squamous cells –modified in various parts of loop of Henle
656
" ![]()"
Thin Segment of Loop of Henle
657
Vasa Recta function
Help maintain osmotic gradient in the interstitium
658
Hypertonic interstitium
causes loss of water from the arterioles as they descend into medulla Movement of water into the venules as they ascend
659
" ![]()"
Vasa Recta
660
Distal straight tubule Found in
Found in the medullary ray of the cortex. Also found in outer medulla.
661
Cells of the Distal Straight Tubule
Short cells Blunted Brush Border Less complex basolateral/lateral interdigitations Smaller cells w/ less mitochondria in cytoplasm
662
Distal straight tubule of loop of Henle Also called
Thick Ascending Limb
663
Cortical Part of Distal straight tubule of loop of Henle found in
medullary rays
664
Distal straight tubule of loop of Henle function
Transport ions from lumen of tubule to interstitium via. active transport. Reabsorption of other ions: Ca2+ and Mg2+
665
" ![]()"
Top line: Straight descending Yellow Circle: Straight ascending
666
Distal convoluted tubule Epithelium
Simple Cuboidal
667
Distal convoluted tubule cells
Smaller cells therefore more nuclei visible
668
Distal convoluted tubule cytoplasm
less acidophilic
669
" ![]()"
Arrows: Distal Convoluted Tubule
670
Distal Convoluted Tubule Functions
Reabsorb Na+, Bicarbonate, Ca2+ (PTH) Secrete K+, H+, Ammonium Na/K-ATPase activity Water impermeable
671
PCT nuclei location
basally
672
DCT nuclei location
apically
673
Which has more microvilli? Which has more basal folds? PCT DCT
PCT: more microvilli DCT: more basal folds
674
Macula Densa
Modified cells of the distal straight tubule
675
Macula densa located at
vascular pole
676
Cells of the Macula Densa Shape
Narrow and taller
677
Macula Densa Functions
Senses changes in Na+ concentration within the lumen of the distal tubule sends signals to the juxtaglomerular cells in afferent arteriole
678
Juxtamedullary Cells type
modified smooth muscle cells
679
" ![]()"
Macula Densa
680
How do Juxtaglomerular cells regulate BP?
Produce renin → cleaves angiotensinogen to angiotensin I
681
aldosterone function
stimulates reabsorption of Na+ and secretion of K+ by connecting tubules and collecting ducts
682
Connecting tubules
Connects DCT to cortical collecting duct
683
Connecting tubules epithelium
Gradual transition of epithelium from DCT to collecting duct
684
Connecting tubules secretion/reabsorption function
Secretes of K+ into lumen→ partly regulated by aldosterone.
685
Cortical collecting duct found in
medullary ray of the cortex.
686
Cortical collecting duct epithelium
Lined by simple cuboidal epithelium with prominent cell boundaries
687
Medullary collecting ducts epithelium
simple cuboidal transitions to simple columnar epithelium
688
Collecting ducts: Light/Principal Cells
- Most abundant: Pale staining - Single primary cilium: short scattered microvilli - Abundant ADH regulated Aquaporins (AQP- 2) channels - true basal infoldings
689
Collecting ducts: Dark/Intercalated Cells
- Fewer - Not present in the inner medulla - Microvilli and microplicae at apical cytoplasm - Secretion of H+ or bicarbonate - Only found in outer medulla
690
Ducts of Bellini
- 200 to 300 µm in diameter. - Empties at the area cribrosa at the apex of a renal papilla.
691
Renal interstitium cell types
fibroblasts mononuclear cells
692
Medullary interstitium appearance
resemble myofibroblasts present along the descending vasa recta
693
Excretory Passages Function
transit and storage of urine
694
Excretory Passages Structures
minor and major calices renal pelvis ureter urinary bladder urethra
695
Excretory Passages have the following features
a) mucosa b) muscularis c) adventitia
696
" ![]()"
" ![]()"
697
Urothelial plaques
on the apical surface of urothelium contains crystalline uroplakin which contributes to the permeability barrier
698
Apical scalloped surface of urothelium covered by
uroplakin
699
elliptical vesicles of urothelium surface
Flattened also called fusiform vesicles
700
Ureter Mucosa
Urothelium + lamina propria
701
Ureter Muscularis→ 3 layers of smooth muscle
inner longitudinal middle circular outer longitudinal (only present in distal end)
702
Contraction of Ureter Muscularis layers produces
peristaltic waves
703
" ![]()"
" ![]()"
704
Urinary bladder General organization
Mucosa Muscularis Adventitia/serosa
705
Bladder Mucosa
Epithelium + fibroelastic CT
706
Bladder Muscularis
thick and consists of smooth muscle arranged in an inner longitudinal, middle circular and outer longitudinal layer oblique orientation of muscles
707
" ![]()"
Urinary Bladder. Arrow: ureter entering bladder
708
Function of slow flow through vasa recta
preserve the osmolar gradient of the interstitium keeps the pO2 of the medulla lower than that in the cortex
709
99% reabsorption takes place at the
proximal tubule into the peritubular capillaries entering into the renal vein
710
Macula densa cells
specialized chemoreceptors cells in the walls of the distal convoluted tubule, which respond to changes in solute concentration (especially Na)
711
Juxtaglomerular cells
modified smooth muscle cells located in the walls of the afferent arteriole immediately proximal to the glomeruli
712
3 elements of glomerular filtration barrier
1. Entothelium of glomerular capillaries 2. Glomerular basement embrane 3. Podocyte layer
713
Endothelium of the glomerular capillaries
numerous fenstrations no diaphragm
714
Glomerular basement membrane
Fused basal lamina of the endothelial cells and podocytes Rich in heparin sulphate to repel negatively charged molecules
715
Podocyte layer of glomerular filtration barrier
visceral layer of the Bowman ’s capsule Modified highly ramified epithelial called podocytes Primary processes Secondary processes Teritary processes Filtration slits between pedicels (~40 nm)
716
How is filterability of solutes related to their size
inversely
717
Order by decreasing filterability Inulin Albumin Sodium Myoglobin Water Glucose
Water Sodium Glucose Inulin Myoglobin Albumin
718
When molecular size is equal, filtration favors {{c1::positively}} charged molecules.
That's why Ablumin isn't well filtered, even though it's small enough for the membrane pores. negative charge and the electrostatic repulsion exerted by negative charges on the glomerular capillary wall proteoglycans.
719
Net Filtration Pressure Formula
∆P= (PGC + πBS) – (PBS + πGC)
720
Glomerular Capillary Filtration Coefficient (Kf )
product of hydraulic conductivity and surface area of the glomerular capillaries directly proportional to GFR Not primary mechanism for impacting GFR
721
Chronic, uncontrolled hypertension and diabetes mellitus gradually reduce Kf by
increasing thickness of the glomerular capillary basement membrane and eventually by damaging capillaries
722
Nephrotic Syndrome
kidney disorder that causes your body to excrete too much protein in your urine. Increase in onocotic pressure in the bowman’s space. Favors filtration
723
Urinary cholelithasis
Kidney stone causing obstruction and dilation of urinary system. Increase in hydrostatic pressure within the bowman space Opposes filtration
724
What fraction of the fluid in the glomerular capillaries filters into Bowman's Capsule?
5-Jan
725
What is the implication of 1/5 of the fluid in the capillaries filtering into the Bowman’s capsule
glomerular plasma proteins that are not filtered get concentrated.
726
Filtration fraction
The 1/5 of protein-free fluid that filters into the Bowman’s capsule
727
How does FF affect oncotic pressure in peritubular capillaries?
The greater the FF, the higher the oncotic pressure in the peritubular capillaries.
728
What is the driving force for reabsorption?
Oncotic pressure
729
Filtration Fraction Formula
GFR/RPF
730
Filtration Fraction Normal Value
120/600 = 0.2 = 20%
731
Blood info for Vasoconstriction 1. Flow 2. Pressure upstream 3. Pressure downstream
1. Flow decreases 2. Pressure upstream increases 3. Pressure downstream decreases
732
Blood info for Vasodilation 1. Flow 2. Pressure upstream 3. Pressure downstream
1. Flow increases 2. Pressure upstream decreases 3. Pressure downstream increases
733
The major function of autoregulation in the kidneys is to
maintain a relatively constant GFR allow for precise control of renal excretion of water and solutes.
734
If GFR too high
Needed substances cannot be reabsorbed quickly enough and is lost in the urine
735
If GFR too low
Too much reabsorption occurs inclusive of waste products such as Urea
736
Autoregulation is primarily accomplished due to
changes in the resistance of the afferent arteriole
737
2 mechanisms of changes in the resistance of the afferent arteriole
Myogenic Responses Tubuloglomerular feedback (TGF)
738
Myogenic response
intrinsic property of smooth muscle is to contract when stretched
739
Tubuloglomerular feedback: Increased MAP leads to
increase in RBF and GFR
740
Effects of Decreased delivery of sodium to the macula densa
dilates the arteriole increase in renal blood flow and GFR
741
High delivery of sodium ions to the macula densa
Triggers adenosine and ATP secretion Leads to vasoconstriction of the afferent arteriole decrease renal blood flow and GFR
742
Autoregulatory range values
90-180
743
Net Transport: Filtration
Nephron starts in corpuscle (glomerulus and Bowman's) Ultrafiltrate enters capsule Passed through tubules to collecting ducts, gets filtered. Forms urine
744
Filtration is driven by
starling forces
745
Net Transport: Reabsorption
process by which solutes and water are removed from tubular fluid, and moved into blood.
746
Net Transport: Secretion
Transfer of materials from peritubular capillaries to renal tubular lumen
747
Net Transport: Excretion
Substances not filtered and not completely reabsorbed are excreted in urine Substance that is filtered and then secreted is excreted in large amounts in the urine b/c it comes from 2 places in nephron
748
Net Tubular Modification
Filtered Load = Excretion rate Amount filtered and amount excreted per unit time are always the same. There is no net tubular modification.
749
Filtered Load Formula
Filtered Load = GFR x Px
Amount/time = (volume/time) x (amount/volume)
750
Excretion Formula
Excretion = Ux x V
Amount/time = (amount/volume) x (volume/time)
751
Net Tubule Reabsorption
Filtered Load \> Excretion. always. glucose, sodium, urea
752
"If a substance is completely reabsorbed in the nephron, the rate of filtration and the rate of reabsorption are **[...]**, and the excretion rate is **[...]**."
" If a substance is completely reabsorbed in the nephron, the rate of filtration and the rate of reabsorption are **equal**, and the excretion rate is **zero**. "
753
If a substance is partially reabsorbed in the nephron, how does excretion compare to filtration
excretion is less than filtration
754
Net Glomerular Secretion
Filtered Load \< Secretion. always. PAH, creatinine
755
Creatinine filtration
freely filtered. very small amount secreted.
756
Net Transport Rate formula
Filtered Load - Excretion (GFR x Px) - (Ux x V) (Kf x ∆P x Px) - (Ux x V)
757
Filtered fraction (FF)
percent of plasma being filtered
758
Filtered fraction formula
FF= GFR/RPF
759
Renal plasma flow (RPF)
volume of plasma that enters the kidney in a minute
760
Renal plasma flow (RPF) normal value
600mL/min
761
GFR normal value
120mL/min
762
Normal Filtered fraction
FF=120/600 FF= 0.2
763
Renal Blood Flow equation
RBF= RPF/(1-HCT)
764
Renal Plasma Flow formula
RPF= RBF x (1-HCT)
765
What are the three main nephron transport mechanisms
Simple diffusion Facilitated diffusion Active Transport
766
"PCT- Sodium (Na+) 1. Reabsorption proportion 2. Na/K-ATPase, stimulated by **[...]** and **[...]**. facilitates [...]. "
"2/3 gets reabsorbed Na/K-ATPase, stimulated by **Catecholamines** and **angiotensin II**. facilitates **reabsorption** "
767
PCT-Water and Electrolytes Solutes and their proportions/paths chloride concentration rises slightly through the proximal tubule because
2/3 of the filtered water, potassium and almost 2/3 of the filtered chloride follow the sodium (leaky system to these substances) of the large percentage of bicarbonate reabsorbed here
768
"PCT- Urea As water is reabsorbed from tubule, urea concentration in the tubular lumen **[...]** This creates **[...]** "
"As water is reabsorbed from tubule, urea concentration in the tubular lumen **increases** This increase creates **a concentration gradient favoring the reabsorption of urea**. "
769
"PCT- Metabolites 1. Filtered glucose: reabsorbed via 2. Proteins, peptides, amino acids, ketone bodies: reabsorbed via 3. Metabolite concentration should be **[...]** in tubular fluid "
"1. 2o Active Transport linked to sodium 2. 2o Active Transport 3. Metabolite concentration should be **zero** in tubular fluid "
770
PCT-Bicrbonate pathway
Combines with Free H+ in lumen and is converted to CO2 and H2O H+ is pumped into lumen. Exchange with Na+. (H+ ATPase) CO2 crosses luminal membrane. Combines w/ H2O. Reforms H+ and Bicarbonate H+ pumped back into the lumen while bicarbonate pumped through basolateral membrane
771
Bicarbonate reabsorption is dependent upon
H+ secretion and the activity of CA
772
Na+/H+ antiport is stimulated by
Angiotensin II
773
In volume depleted states, the amount of bicarbonate reabsorption in the PCT
increases
774
Diuretics
medications designed to increase the amount of water and salt expelled from the body as urine.
775
Which part of the Nephron is the primary active site of carbonic anhydrase inhibitors?
Proximal Convoluted Tubule
776
What effect does Blocking carbonic anhydrase have?
reduces bicarbonate reabsorption and the activity of the Na+/H+ antiport. Sodium remains in the lumen and therefore water remains in the lumen. They get excreted by urine
777
"PCT recaptures **[...]** of filtered sodium"
PCT recaptures 2/3 of filtered sodium
778
Benefits of Glomerulotubular Balance
helps protect extracellular volume despite any GFR changes
779
Thin Descending Segemnt of the LofH
Permeable to water (20% of filtered water) Impermeable to solute
780
Thin Ascending Segemnt of the LofH
Impermeable to water
781
Thick Ascending Segemnt of the LofH
Impermeable to water solutes transported out (25% of the filtered load of sodium, potassium and chloride absorbed here)
782
Transport in the Loop of Henle- Thick Ascending Segment
Na/k+- ATPase pump creates a relative sodium deficiency intracellular, which provides a favorable gradient for the movement of sodium across the luminal surface into the cell via Na/Cl/K+ cotransporter and drives the Na/H+ antiport, which allows more H+ secretion, which leads to more bicarbonate absorption
783
Loop of Henle- Thick Ascending Segment: Potassium
K+ channel in lumen membrane. Allows for diffusion of ino back to lumen. Positive lumen potential promotes sodium, calcium, and magnesium reabsorption via a paracellular pathway
784
Pharmacology Diuretics (Loop Diuretics)
blocking Na/CL/K+ co-transporter in the luminal membrane = increase urine output of sodium, chloride, potassium and other electrolytes as well as water
785
Pharmacology Diuretics (Loop Diuretics): Why excrete water?
1. incr. soulte quantity. decr. osmotic gradient. prevent water reabsorption 2. Disrupt countercurrent multipler system. decr. ion absorption, which impair ability of kidney to concentrate or dilute urine
786
Early DCT: General. and Na and Cl
Reabsorbs Na Cl Ca Na/K+-ATPase creates a low intracellular concentration allowing NaCl to cross apical membrane via Na/Cl- symporter impermeable to water. osmolality decreases. Lowest of the whole nephron.
787
Early DCT: Calcium
Enters cell from luminal fluid passively through Ca channels. PTH regulated Actively extruded into the peritubular fluid via Ca2+-ATPase or 3Na/Ca2+ antiporter Cells have calcium binding protein calbindin. Facilitates reabsorption. Incr. by Vit.D. Enhance PTH action on DCT.
788
Pharmacology- Diuretics (Thiazide Diuretics)
block NaCl symporter in DCT. this enhances Ca reabsorptionin DCT, and can lead to hypercalcemia.
789
Tubuloglomerular FeedBack
Macula densa cellssense tubular flow and GFR. Send signals back to afferent/efferent arteriole to constrict/dilate to keep GFR normal.
790
Tubuloglomerular Feedback: Decr. GFR
" ![]()"
791
Tubuloglomerular Feedback: Incr. GFR
" ![]()"
792
Late DCA & Collecting Duct -- Principal Cells
Luminal Membrne contains eNaC. Influx of Na down concentration gradient (created by Na/k+-ATPase) Some chloride does not follow sodium, creating a negative luminal potential causing potassium secretion Aldosterone activates the mineralcorticoid receptor on these cells
793
Aldosterone activates the mineralcorticoid receptor on these cells, having the following effects
1. Increasing luminal ENaC channels 2. Increase ENaC opening time 3. Stimulates/Augments Na/K+-ATPase
794
"Late Distal Tubule & Collecting Duct- Principal cells express **[...]** which are regulated by **[...]**."
aquaporins ADH
795
Late Distal Tubule & Collecting Duct Intercalated cells 1. Luminal membrane contains a H+-ATPase, which 2. Most of the H+ is eliminated from the body via 3. H+ can combine with ammonia to form ammonium, which is 4. For every H+ excreted by the above buffers 5. Aldosterone stimulates H+-ATPase of intercalated cells. THUS,
1. pumps H+ into the lumen. 2. buffers, phosphate and ammonia 3. poorly reabsorbed and is thus excreted 4. bicarbonate is added to the body (new bicarbonate) 5. excess aldosterone causes Metabolic Alkalosis
796
Pharmacology- Diuretics (K-sparing diuretics) Potassium sparing diuretics work by
1. Blocking ENaC channels 2. Blocking aldosterone receptors 3. Blocking the production of aldosterone e
797
Normally, Intake of water = output of water through various sources - If this balance is disrupted:
it could result in dehydration or overhydration
798
What is the major regulator of fluid & electrolyte balance.
Kidneys
799
How do kidneys regulate fluid and electrolyte balance?
reabsorption or secretion through the tubules This occurs under the influence of hormonal control: ADH & aldosterone.
800
Blood Volume (BV) formula
Blood Volume (BV) = PV/(1 – Hct)
801
ISW =
75% ECF
802
ECF(extracellular water) =
1/3rds TBW OR Interstitial fluid (ISF)+ Plasma volume(PV)
803
Plasma =
25% ECF
804
ICF (intracellular water) =
2/3rds TBW OR TBW - ECF
805
Males: TBW =
60% weight in kg
806
Females: TBW =
55% weight in kg
807
1 kg =
2.2 lbs 1L of water
808
Volumes of fluids can also be measured by using
dilution technique
809
Isotopic water(D2O) Titrated water(THO) Antipyrine
Distributes across all body compartments Useful for measuring TBW
810
- Radioactive albumin - Evans Blue
Remain in plasma Too large to cross capillary walls Useful for measuring plasma volume(PV)
811
Sulfate, mannitol & inulin
Remain in ECF & can’t cross cell membranes Useful for measuring ECF ECF=amount of mannitol in plasma/Plasma [mannitol].
812
Dye techniques to measure TBW & fluids in other compartments The marker substance is measured in (units)
- millimoles(mmol) - milligrams(mg) - units of radioactivity-millicuries(mCi)
813
Dye techniques to measure TBW & fluids in other compartments Process
known quantity dye is injected & allowed to equilibrate. Then the concentration of dye is measured in plasma Then the volumes are calculated
814
Compartment volume formula
(amount injected - amount excreted)/concentration in plasma V = Q/C
815
Use of Darrow-Yannet diagram
assess compartmental fluid balance
816
Any changes in the volume will 1 st affect
the ECF volume. may or may not alter ICF
817
The change in volume of ICF occurs only by
changes in ECF osmolarity
818
"Identify the problem: ![]() "
Isosmotic Isotonic NaCl
819
"Identify the Problem: ![]() "
Hyperosmotic High intake of NaCl
820
"Identify the Problem: ![]() "
Hyposmotic SIADH
821
"Identify the Problem: ![]() "
Isosmotic Diarrhea
822
"Identify the Problem: ![]() "
Hyperosmotic Water depravation
823
"Identify the Problem: ![]() "
Hyposmotic Adrenal Insufficiency
824
Blood Plasma Definition
non-cellular liquid layer of the blood obtained by sedimentation and centrifugation.
825
Blood Serum definition
Prepared in laborotory whole blood coagulates, is centrifuged, and coagulation factors removed. the serum is plasma minus coagulation factors.
826
How are serum proteins separated
Charge (Serum Protein Electrophoresis) Density (Densitometry)
827
Globulin types
alpha beta gamma
828
Alpha globulins
a1: Antitrypsin, a Fetoprotein, Transcortin, Retinol binding protein a2: Macroglobulin, Ceruloplasmin, Hepatoglobin
829
Beta Globulins
Transferrin Hemopexin LDL
830
Gamma Globulins
Immunoglobulins. IgG, IgM, IgA, IgD, IgE
831
Albumin Maintenance Function
maintains osmotic pressure
832
Albumin Transport Function
Calcium ions Free Fatty Acids Bilirubin hormones drugs
833
alpha and beta globulin functions
Enzymes Transport Inhibitor Proteins
834
Gamma Globulin functions
Immune response (Immunoglobulins)
835
Normal serum range
3.5-5 g/dL
836
Main functions of albumin
Maintain osmotic pressure Prevent edema Transport of lipids Bind and transport Calcium ions
837
congenital analbuminemia
appear normal. do not show edema. Other serum proteins regulate the osmotic pressure early on.
838
Different causes of hypoalbuminemia
Decreased albumin synthesis Increased albumin loss
839
Kwashiorkor disease
Dietary deficiency of proteins. Frequent Infections. Decreased albumin synthesis
840
Liver Cirrhosis
Severe liver damage impairs albumin synthesis
841
Kidney Disease
Glomerulus Basement Membrane gets damaged Albumin gets lost in urine.
842
Severe burns
Blood vessels get damaged There is a huge serum loss. There is increased albumin loss (because albumin is in serum)
843
The a1 globulin fraction
a1 antitrypsin: \>90%
844
a1 Antitrypsin (a1-AT)
serum protein released by liver inhibits neutrophil elastase in lung alveoli
845
Hereditary deficiency of a1-AT can lead to
pulmonary and liver disease
846
By what mechanism can smoking lead to emphysema
Neutrophils activated Release neutrophil elastase Reactive Oxygen Species modify the structure of a1-AT reduce binding to neutrophil elastase Elavated neutrophil elastase destroys alveoli elastin
847
alpha fetoprotein
a1 globulin. abundant in fetal plasma. low albumin levels. Functions similar to albumin later in fetal life.
848
Maternal serum AFP is used as
marker for possible fetal abnormalities.
849
AFP is mostly found in the
amniotic fluid
850
If AFP is in amniotic fluid, how can it be measured?
A small amount of amnoitic fluid can cross the placenta, allowing AFP to be measured in maternal serum.
851
High maternal serum AFP level can be an indicator of
neural tube defects
852
Low maternal serum AFP level can be an indicator of
Down Syndrome
853
Transcortin
transports 75% of cortisol in blood.
854
Retinol-binding protein
Transports retinol from liver to peripheral tissues
855
a2 Macroglobulin (A2M) functions
inhibits plasmin and thrombin
856
Nephrotic Syndrome
damage to GBM yields a greater than 10 fold increase in a2 Macroglobulin (A2M) A2M excess can't get lost in urine because it is too big. Albumin is tiny, so that one gets lost in this disease.
857
Ceruloplasmin functions
Copper Transport in blood Ferroxidase activity
858
Wilson disease
very low blood levels of ceruloplasmin hepatic copper binding is deficient Apoceruloplasmin (without copper) is released into the blood where it is degraded.
859
Ferroxidase forms
Ferric Iron
860
Explain the need for Ceruloplasmin
Macrohages degrade heme, release ferrous iron. Ferrous iron can cause free radicals. Ceruloplasmin oxidizes ferrous iron, forming ferric iron. Ferric iron bound to transferrin and transported in blood.
861
Haptoglobin
binds to free hemoglobin dimers in the blood and prevents loss of Hb in urine.
862
Why does acute hemolysis lead to a low serum level of free haptoglobin?
Haptoglobin-hemoglobin complex is taken up by macrophages.
863
Transferrin
b-globulin which transports ferric iron in blood especially between: intestine, liver, bone marrow and spleen.
864
Low transferrin saturation
found in patients with iron deficiency as fewer sites of transferrin are filled.
865
High transferrin saturation
found in patients with iron overload (High serum iron leads to increased binding).
866
Hemopexin
B-globulin that binds to free heme in the blood Prevents the loss of heme-iron
867
Hemopexin prevents:
A. Heme-induced damage of plasma membranes B. Heme usage by microbes
868
Low-density lipoproteins (LDL) separate in SPEP together with
b-globulins
869
The g globulin fraction is synthesized by
plasma cells (Activated B-lymphocytes)
870
IgM
found in blood and lymph first antibody to be produced in response to an antigen (infection).
871
IgG
(smallest and most common) found in all body fluids produced by repeated exposure to the same antigen cross the placenta giving passive immunity to the fetus and newborn
872
IgE
found in the lung, skin, mucous membranes secreted in allergic reactions.
873
IgA
found in body secretions protects body surfaces. main antibody found in human milk.
874
IgD
role in serum is uncertain.
875
Multiple myeloma
tumor of the plasma cells example of monoclonal gammopathy
876
Multiple myeloma is characterized by
presence of high amounts of a single type of immunoglobulin produced by a malignant clone of the cell.
877
Acute phase reaction of the liver leads to
changes in the synthesis of serum proteins.
878
The hepatic acute phase reaction is
overall positive response to prevent damage following an injury
879
Positive acute-phase reactants
Serum proteins that are synthesized in larger amount as they reduce inflammation and deprive microbes of iron.
880
Positive acute-phase reactants examples
a1 -Antitrypsin Ceruloplasmin Haptoglobin Hemopexin
881
Negative acute-phase reactants
Serum proteins that are synthesized in smaller amount in order to preserve amino acids for the increased synthesis of positive acute phase reactants.
882
Negative acute-phase reactants examples
Albumin Transcortin Retinol-binding protein Transferrin
883
C-reactive protein
acute phase reactant does not lead to a peak in SPEP
884
If normal Plasma & Urine osmolarity changes
kidneys can either retain or excrete water by osmoregulation
885
Urine osmolarity can vary across the range:
30 – 1200mOsm/L
886
How does the kidney dilute or concentrate the urine?
Solute wastes – 600mOsm/day must be excreted in urine.
887
obligatory volume.
minimum urine volume that needs to be excreted /day
888
3 processes that contribute to corticopapillary osmotic gradient
1. Countercurrent multiplication 2. Urea recycling 3. Slow rates flow
889
Which portion of the nephron does most of the diluting?
Ascendng limb of loop of henle.
890
Salt vs Water in Loop of Henle
The loop of Henle deposits more salt than water in the intersitium
891
The loop of Henle deposits more salt than water in the intersitium, so:
Medullary interstitium becomes hypertonic – potential for urine concentration! Tubular fluid becomes hypotonic – potential for urine dilution!
892
How Does The Medullary Interstitium Get So Concentrated?
- Descending LH is water permeable - Ascending LH is impermeable to water, & also transports Na+ & Cl actively into the interstitium
893
Generation & maintenance of osmotic gradient is due to
- ATP dependent solute transport - Increase in medullary osmolarity - Slow tubular fluid flow
894
How Does The Counter-current Multiplier Work?
- Urea is necessary for increasing osmolarity of Inner medulla - Urea Contributes to half the hyperosmotic gradient - Urea is passively reabsorbed from the tubule( MCD) - Requires ADH
895
Counter-current Multiplier Low protein states
urea is by product of protein metabolism
896
Sites Of Tubular Urea Transport
In presence of ADH As H2O is reabsorbed from Collecting Duct, Urea concentration rises ADH upregulates transporters (UTA1 and UTA3) Urea diffuses passively via transporters into the interstitium Some of it is secreted into both thin & thick LoH
897
urea recycling.
50 % is absorbed in proximal tubule. Of the 50% in the lumen after recycling 20% is excreted
898
Low ADH
Collecting duct is impermeable to water No Urea reabsorption Medulla slightly hyperosmotic
899
High ADH
Collecting duct permeable to water (AQP2) Urea reabsorption (MCD) Medulla highly hyperosmotic
900
Nephrogenic Diabetes Insipidus (DI)
V2 receptor mutations, AQP2 mutations acquired eg. Lithium therapy
901
Central Diabetes Insipidus (DI)
congenital lack of ADH production acquired e.g. Head trauma
902
"Fill chart: ![]() "
" ![]()"
903
Total clearances of solutes can be expressed as
osmolar clearance (Cosm ).
904
Cosm Formula
Cosm = (Uosm x V)/Posm
Uosm - urine osmolarity Posm - plasma osmolarity V - flow rate
905
CH2O
The volume of free water cleared from plasma, & excreted in urine per unit time
906
CH2O of water excreted in urine does not contain any solutes. This portion is additional to obligatory urine volume that contains solutes
True
907
CH2O indicates the ability of the kidney to
concentrate or dilute urine
908
CH2O Formula
CH2O =V - ((Uosm x V)/Posm)
909
rate of free water clearance represents
that rate at which solute free water is being excreted
910
CH20 = 0
urine is iso-osmotic to plasma
911
CH20 = positive
hypo-osmotic urine produced
912
CH20 = negative
hyperosmotic urine produced
913
Amount of Na+ in the body depends on
sodium intake & excretion
914
Mechanisms that regulate your Effective circulating volume (ECV)
- Renin Angiotensin Aldosterone System (RAAS) - Sympathetic NS - Starlings forces - Atrial Natriuretic Peptide (ANP)
915
What Are The Volume Sensors?
Baroreceptors Renin Release Starlings Forces Macula Densa
916
How does Angiotensin II defend The Effective Circulating Volume
Promotes ADH release Evokes thirst Promotes vasoconstriction: systemic arterioles, intrarenal afferent & efferent arterioles incr. Proximal tubule Na+ reabsorption incr. Distal tubule Na+ reabsorption via Aldosterone
917
Angiotensis II vasoconstricst efferent or afferent more?
Efferent. Incr. Filtration Fraction
918
Baroreceptor Reflex for Renal
incr: - afferent arteriole resistance - renin release - proximal tubule Na+ reabsorption
919
Mechanisms evoked in response to increased ECV
"Atrial Natriuretic Peptide ANP Starlings Forces ![]() "
920
Atrial Natriuretic Peptide (ANP) Released by: Receptors located in:
Released by cardiac Atrial myocytes Receptors located in the venous system
921
Atrial Natriuretic Peptide Secretion stimulated by:
Atrial stretch from excess blood volume (BV or PV)
922
Atrial Natriuretic Peptide Actions
Vasodilate afferent arterioles & constricts efferent arterioles thereby ↑ GFR Inhibits Na+ reabsorption directly at the medullary CD
923
50% Mg2+ is in 1% is in Rest is in
bone ECF intracellular
924
-Daily Mg2+ requirement is
300mg
925
Mg2+ is absorbed in
ileum
926
Mg2+ deficiency affects
cardiovascular, gastrointestinal & neuromuscular function Reduces PTH effectiveness leading to hypocalcemia.
927
Renal handling of Magnesium
25% is reabsorbed in proximal tubule 65% is reabsorbed around loop of Henle A small amount in distal tubule through magnesium ion channel on the luminal side
928
Decrease in free ionized calcium is sensed by
extracellular calcium sensing receptor (CaR).
929
Ca2+ is actively extruded out of the cell into the interstitial fluid, either via a
Ca2+ ATPase pump or Na+ -Ca2+ exchanger
930
Most Ca2+ is absorbed in Some in Ca2+ reabsorption in ____ under control of \_\_\_
proximal tubule ThALH via para cellular route distal tubule PTH
931
Insulin and Potassium
Insulin accelerates K+ uptake into cells Insulin/glucose used clinically in treatment of hyperkalemia
932
Exercise and Potassium
Intense exercise releases K+ . High levels of epinephrine is also released during exercise which promotes K + entry into cells
933
Potassium nephron absorption
70% is reabsorbed in PCT 20% Is reabsorbed in ThALH Rest is regulated in DCT & CCD & is secreted into the lumen
934
"Describe the genotype of each lane on the electrophoresis ![]() "
" 1: Homozygous Normal MM 2: Heterozygous MZ 3: Compound Heterozygous SZ 4: Homozygous ZZ ![]()"
935
Hepatocyte With PiMM genotype
AAT is synthesized into ER through secretory pathway Released into circulation
936
Hepatocyte With PiZZ genotype
AAT is Synthesized into ER Sometimes leads to formation of AAT polymers ER retention causes cellular stress Chronic hepatocellular injury
937
Treatment of AATD
‒Advise patients not to smoke ‒Avoidance of second-hand smoke Intravenous administration of A1AT protein Slows progression of COPD
938
AATD Genetic Liver Pathology
Gain of Function
939
AATD Genetic Lung Pathology
Loss of Function
940
"Identify the Disease ![]() "
Acute Inflammation
941
"Identify the Disease: ![]() "
Prolonged Inflammation
942
"Identify the Disease ![]() "
No Disease. Normal Serum Protein Electrophoresis
943
"Identify the Disease ![]() "
Multiple Myeloma (Monoclonal Gammopathy)
944
"Identify the Disease ![]() "
Nephrotic Syndrome
945
"Identify the Disease ![]() "
Hypogammaglobulinemia
946
"Identify the Disease ![]() "
a1-Antitrypsin deficiency
947
Describe the SPEP graph for Acute Inflammation
1. Albumin peak is reduced due to less hepatic synthesis 2. a1-peak is elevated due to positive acute phase reactant: a1-antitrypsin. 3. a2-peak is elevated due to positive acute phase reactants: haptoglobin, ceruloplasmin and a2- macroglobulin. 4. b-globulin peak: although hemopexin (positive acute phase reactant) is released, it does not lead to an elevated b-peak because at the same time there is less transferrin released by the liver (transferrin is a negative phase reactant). ? SOM.1
948
Normal Serum Protein Electrophoresis vs. Prolonged Inflammation
1. Albumin peak reduced to a much greater degree than acute inflammation 2. a1-peak is elevated due to positive acute phase reactant: a1-antitrypsin 3. a 2-peak is elevated due to positive acute phase reactants: haptoglobin, ceruloplasmin, a2-macroglobulin 4. . b-globulin peak is elevated due to even more hemopexin release than in acute inflammation 5. g-globulin peak is strongly increased, all immunoglobulins but mainly IgG.
949
Liver cirrhosis (polyclonal Gammopathy) SPEP
1. Reduced Albumin Peak 2. a1 peak not elevated 3. a2 peak reduced 4. B-globulins and gamma globulins form B-g bridge All immunoglobulins elevated. Incr. IgA found in a specific liver disease
950
Multiple Myeloma (Monoclonal Gammopathy) SPEP
All peaks normal except elevated gamma due to presence of a high amount of one single immunoglobulin.
951
Nephrotic Syndrome SPEP
1. Albumin peak reduced due to urine loss 2. a1 peak reduced 3. a2 sharp increase due to 10 fold incr. of macroglobulin 4. B globulin peak decreased
952
Damage of the basement membrane of the glomerulus in the kidney results in
loss of proteins with exceptions of a2-macroglobulin.
953
Hypogamma globulinemia SPEP
All peaks normak. Gamma peak absent.
954
a1-Antitrypsin deficiency SPEP
All peaks normal. a1 peak absent
955
Normal Albumin level
3.8-5.0
956
normal a1-globulin level
0.1-0.3
957
Normal a2-globulin level
0.6-1.0
958
Normal B-globulin level
0.7-1.2
959
Normal g-globulin level
0.7-1.5
960
Albumin 1. Increased 2. Decreased
1. Severe dehydration. 2. : Liver damage, Nephrotic syndrome, severe protein malnutrition and Acute phase response.
961
a1-globulin 1. Increased 2. Decreased
1. Acute and chronic inflammatory diseases, liver cancer (AFP). 2. a1-AT deficiency, Nephrotic syndrome.
962
a2-globulin 1. Increased 2. Decreased
1. Acute and chronic inflammatory diseases, Nephrotic syndrome (macroglobulin). 2. Wilson disease (ceruloplasmin)
963
B-globulin 1. Increased 2. Decreased
1. Hypercholesterolemia (LDL), Prolonged inflammation (hemopexin). 2. Nephrotic syndrome.
964
Gamma Globulin 1. Increased 2. Decreased
1. acute and chronic inflammatory diseases, acute infections, liver cirrhosis, multiple myeloma, and lymphoma 2. Hypogammaglobulinemia
965
TF/P Ratio: Proximal Tubule Sodium Reabsorption
remains at 1.0 because equal amount of sodium and water reabsorbed here.
966
TF/P Ratio: Proximal Tubule Glucose/Amino Acid Reabsorption
Completely reabsorbed. therefore there TF/P approaches zero.
967
TF/P Ratio: Proximal Tubule Bicrabonate Reabsorption
more avidly reabsorbed compared to water but the reabsorption is not complete
968
[sound:rec1575599427.mp3] Why Na conc. = 1 but Cl conc. slightly exceed 1?
first 1/2 of tubule: sodium is reabsorbed with co-transport with amino acids, glucose and other solutes second 1/2 of tubule: little glucose and amino acids . Therefore sodium is not reabsorbed with chloride ions first half Cl conc around 105 mEq/L vs the second half conc around 140 mEq/L
969
Why does Urea TF/P go above 1?
it is reabsorbed from the tubule but to a much lesser extent than chloride ions, therefore the concentration increases ore greatly
970
Why does Creatinine TF/P go above 1?
it is filtered into the proximal tubule, NOT reabsorbed and is SECRETED. Hence the rapid rise in TF/P of Creatinine.
971
Loop of Henle Permeability:
Descending: Water permeable Ascending: Solute Permeable
972
Principal Cells Function
reabsorb Sodium and water, but secrete potassium. TF/P curve more steep than Na and Cl in the Distal Convoluted Tubule
973
Intercalated cells function
Secrete Hydrogen into tubular lumen. Hydrogen combines w/ bicarbonate to form CO2 CO2 diffuses across luminal membrane CO2 dissociates and forms H+ and HCO3. H+ gets secreted and HCO3 gets reabsorbed.
974
Collecting Tubule
mainly concerned with water reabsorption All solutes except Bicarbonate increase conc. Also has capacity for urea reabsorption
975
Inulin in nephron
Freely filtered not secreted or reabsorbed TF/P increases moving along nephron
976
Creatinine in nephron TF/P
Freely filtered not reabsorbed. very little secreted. TF/P increases moving along nephron, close to inulin but slightly more.
977
PAH in nephron
Very step curve. Filtered Highly secreted.
978
Use for Renal Clearance
Measure GFR & RPF determine renal handling of different substances
979
Renal Clearance Definition
Volume of plasma cleared of a substance per unit time
980
Renal Clearance formula
Cx = (Ux x V)/Px
Ux = Urine Concentration Px =Plasma Concentration V = urine flow rate (mL/min)
981
If the substance is not excreted in the urine, its clearance is
ZERO
982
If the substance is filtered and not reabsorbed or secreted in the urine, its clearance =
GFR like inulin
983
If the substance undergoes net reabsorption, its clearance will be
less than that of inulin ex.(Na+, Urea, Cl- )
984
If the substance undergoes net secretion, its clearance will be
greater than that of inulin ex.(PAH)
985
If there is net reabsorption of a substance, how do excretion and filtered load compare?
excretion \< filtered load
986
If there is net secretion of a substance, how do excretion and filtered load compare?
excretion \> filtered load
987
Creatinine
Endogenous (by-product of muscle metabolism) Released into blood at relatively constant rate plasma concentration is fairly stable; therefore only need one blood sample * Freely filtered ✓ * Not reabsorbed ✓ * Is secreted in small amounts (true Ccr normally overestimates GFR by ~10-20%)
988
2 drawbacks of Creatinine
it is also secreted & this incr urinary excretion by 20%, in the numerator of the clearance formula the colorimetric method measures other substances such as glucose leading to  20% incr in the denominator in the clearance formula But since they cancel each other, no biggie.
989
Clearance of inulin =
GFR
990
• Clearance of creatinine =
~ GFR
991
•Clearance of PAH =
RPF
992
Fractional excretion
Proportion of the filtered load that was excreted
993
Fractional excretion formula
Fractional excretion of Z (FEZ ) = rate of excretion of Z/rate of filtration of Z Clearance/GFR
994
Aspirin
Acidic drug pKa = 3.5
995
Morphine
Basic Drug pK 7.9
996
Three systems to regulate [H+]
– Buffers (First line) – Respiratory system (Second line) – Regulates PCO2 – Renal system (Third line) – Regulates HCO3 levels
997
Carbon dioxide (CO2 )
Volatile acid major metabolic acid handled by lungs
998
Nonvolatile acids
Handled by the kidneys
999
"Buffering systems of body fluids (ECFand ICF) immediately combine with **[...]** to prevent large changes in **[...]**."
"Buffering systems of body fluids (ECFand ICF) immediately combine with **acid/base** to prevent large changes in **[H+]**."
1000
Respiratory Response: pH
Within minutes to eliminate CO2 (H2CO3 ) from body
1001
Renal Response: pH
Slowest - hours/days to eliminate excess acid/base Most powerful
1002
Normal Plasma pH
7.36-7.44
1003
Normal [HCO3 -]
22-25 mEq/L (24mEq/L)
1004
Normal Arterial PCO2
38-42mmHg (40 mmHg)
1005
Kidneys regulate the
plasma [HCO3 -]
1006
urine pH range
5.8-6
1007
H+ secretion in the collecting duct
H+ ATPase K + -H+ ATPase secreted protons are buffered by HPO4 - and NH3 to form Acid Phosphate (NaH2PO4 - ) and NH4 + Cl
1008
hyperkalemia
Acidosis
1009
hypokalemia
alkalosis
1010
Primary Hyperaldosteronism
Aldosterone stimulates reabsorption of Na+ Stimulates K+ excretion in urine Stimulates renal tubular H+ ATPase--alkalosis
1011
Respiratory acidosis 1. pH 2. CO2 3. HCO3-
1. low 2. high 3. normal (Acute) high (Chronic)
1012
Respiratory alkalosis 1. pH 2. CO2 3. HCO3-
1. high 2. very low 3. almost normal (acute) low (chronic)
1013
Metabloic Acidosis 1. pH 2. CO2 3. HCO3-
1. low 2. low 3. low
1014
Anion gap formula normal
Na-Cl-HCO3 8-16
1015
Serum K+ and diabetic ketoacidosis
Serum K+ is increased Plasma glucose: 500mg/dL Insulin deficiency in type I diabetes mellitus prevents K+ entry into ICF (K+ levels in ECF increase) – Remember, Insulin activates the Na-K ATPase
1016
Metabolic alkalois 1. pH 2. CO2 3. HCO3
1. high 2. high 3. high
1017
Metabolic alkalosis – compensation by kidneys
Renal system compensates, if it is functioning normally, by excreting more HCO3
1018
Salicylate poisoning
Acute salicylate poisoning → stimulation of respiratory center Chronic salicylate poisoning results in metabolic acidosis – as a result of formation of weak acids
1019
Mixed acid-base disorders
Patient has more than one acid-base disorder PCO2 and HCO3 move in opposite directions If the pH is normal and HCO3 and PCO2 are abnormal