B4 CPR Pulmonology Flashcards
respiratory epithelium contents
ciliated pseudostratified columnar epithelium
Goblet Cells
what structure is start of respiratory system
respiratory bronchiole
what part of nasal cavity lined with olfactory epithelium
superior conca
bronchus vs bronchiole
bronchus have cartilage
respiratory system 2 functioms
conducting
gas exchange
components of conduction portions of respiratory
seromucus & vascular network in lamina propria
vibrissae
fxn superficial vascular netwrok lamina propira
warm inspired air
fxn mucus & serous glands lamina propira
moisten inspired air
3 parts wall sx of respiratory
mucosa (epithelium & lamina propira)
submucosa (seromucous gland, smooth musc)
adventitia (outer layer)
5 cells respiratory epithelium
ciliated columnar
goblet
brush
basal
small granule
cytoskeletal structure for,s axoneme cilia
microtubules
Primary Cilia Dyskinesia/Kartagener’s syndrome
defective/absent dynein arms
prevent mucocilliary clearance
can be in all arms, outer or inner arms
Smoker respiratory epithelium changes
metaplasia to stratified squamous
decrease ciliated columnar cell
increase goblet cell
smoker melanosis
benign focal pigment of oral mucus from mutagentic chemical tobacco
Brush cells from what
microfilaments of akctin
brush cells receptor
chemosensory receptor
afferent nerve endings
basal cell fxn
undifferentiated stem cells
small granule cell names & fxn
Neuroendocrine, Kulchitsky
regulate bronchial & vascular muscle tone response to- hypoxia
what is only tissue type that increases in number as go down respiratory tract
elastic fibers (toward alveoli)
nasal cavities of lamina propira microorganisms
bind/inactivated by IgA in plasma cells
What does the nasal cavity mucosa contain to help warm, humidify, and clean inspired air
loop capillary
seromucus gland
what sx has lots of cartilage
larynx
Sx of trachea
C rings hyaline cartilage
relax in swallow
bifurcates to R & L primary bronchi
perichondrium
connective tissue layer lining both sides of the cartilage and contains its vascular supply and stem cell
major feature/fxn nasal cavity vestibules
Vibrissae
filter & humidify air
major feature/fxn nasal cavity
warm, humidify, clean air
major feature/fxn superior nasal cavity
solubize/detect odorants
major feature/fxn nasopharynx
conduct air to larynx, pharyngeal, palatine tonsils
major feature/fxn larynx
phonation
major feature/sx trachea
conduct air to primary bronchi of lung
R vs L primary bronchi
both have superior, secondary, tertiary bronchus
R bronchi has 3 lobes in R lung
L bronchi has 2 lobes in L lung
what is final part of conducting respiratory system
terminal bronchioles (from smaller generations of tertiary bronchi)
change in bronchi as they branch
progressiveky smaller
acute vs chronic bronchitits
acute = viral
chronic = smoking/pollutants, leave permanent change
subtype of non small cell lung cancer (85% all lung cancer)
Adenocarcinoma
Squamous cell carcinoma
large cell carcinoma
adeno carcinoma
non small cell, most common
from bronchiole glands & alveoli epithelial cells
well differentiated
from p53 mutate
rare metastasize, best prognosis
squamous cell carcinoma
non small cell
metaplasia of epithelium to stratified squaous epithelium (reversible)
can lead to dysplasia (irreversible)
makes keratin pearls
doesn’t spread normally
large cell carcinoma
non small cell
poorly differentiated
lack squamous/glandular morphology
grow faster/more than other nonsmall
clear in nucleus when stain
metastasize
small cell carcinoma
oat cell
smokers highly aggressive
metastasize far/wide very fast
neoplastic transformation of small granyle in bronchial respiratory epithelium
poor prognosis
bronchiole sx
no mucosal gland/cartilage
terminal bronchioles have ciiated simple columnar/simple cuboidal epithelium
start mucociliary appartays
significance mucociliary apparatus
trachea to bronchioles
inner lining of conducting airqay
parasympathetic response in terminal bronchioles
constrict
sympathetic response in terminal bronchioles
dilate
bronchiolitis
likely from RSV
very common babies/kids
old people with pre existing
inflammation of bronchial wall, epithelial necrosis
Which structures are lined by respiratory mucosa, with prominent spiraling bands of smooth
muscle and increasingly smaller pieces of hyaline cartilage?
bronchi
What are the last bronchiole branches that lack alveoli and are lined by simple cuboidal
epithelium consisting mainly of club cells with innate immune and surfactant secretory
functions
terminal bronchioles
terminal bronchiole division
respiratory bronchioles then branch into alveolar ducts that branch into alveolar sacs
atria sx
distal terminations of alveolar ducts
give rise to alveolar sacs
what are alveolar sacs
cluster of alveoli
very thin lamina propira
differemt anout lamina propira in alveoli
thin
elastic & reticular fibers
smooth muscle
3 components blood-air barrier
thin capillary endothelial cells
two attentuated thin cells line alveolus
fused basal laminae of thin cell with capillary endothelial cells
emphysema
destruction of interalveolar wall
reduce SA for gas exchange
common froim cigarettes
why does cigarette smoke cause emphysema?
inhibit a1AT (protect lung from elastase that marophages produce)
lungs are unable to recoil due to decrease elasticity
main components COPD
emphysema
chronic bronchitis
two cells of alveoli walls
type I (squamous) alveolar cells
type II (alveolar septal) alveolar cells
Ti alveolar cells
most of surface
minimal barrier that readily permeable to gas exchange
TII alveolar cells
cuboidal where septal walls converge
foamy appearance from lamellar bodies
lamellar bodies
organelles with phospholipid, glycosaminoglycabs, proteins
continuous secrete as pulmonary surfactant
function of lamellar bodies
post translational assemply/packing surfactant components
helps decrease surface tension in alveoli
incomplete differentation of TII alveolar cells & RDS
lead cause for infant respiratory distress
difficulty expanding alveoli
hyaline membrane disease as look glassy/protein rich when collapsed alveoli
alveolar macrophages/dust cell sx/fxn
darker from iron/erythrocytes
phagocytose erythrocyte from damaged capillaries/airboene particles
migrate to bronchioles to motor removal esophagus
dust cells = heart failure cells
in congestive heart failure
lungs congest with blood & phagocytozised
hemosiderin is chem rxn see occur
major fxn/sx bronchi
repeat branching
air deeper into lungs
major fxn/sx bronchioles
air conduction
help bronchoconstrict/bronchodikate
major fxn/sx terminal bronchioles
air to respiratory area lungs
exocrine club cells with protective/surfacant
major fxn/sx respiratory bronchioles
air deeper with gas exchange, protective/surfacant club cells
major fxn/sx alveolar sac/duct
conduct air
gas exchange
major fxn/sx alveoli
all gas exchange
surfacant TII dust celkl
path of sx from terminal bronchioles
to respiratory bronchioles
to alveoli ducts
to alveoli
what structure characterize TII alveolar with surfacant synthesis
lamellar bodies
mad of multivestibular bodies
what make regenerated epithelium
TII pneumocytes
blood circulation lungs consist of
pulmonary circulation (O2 poor)
bronchial circulation (O2 rich)
what structures accompany bronchial tree pulmonary circulation
pulmonary artery branches
respiratory bronchiole arterial branches give rise capillary networks in Intraalveolar septa
venules from capillary to small pulmonary veins
bronchial circulation blood path
from thoracic artery to bronchial arteries
branch in tree to anastamose with branch pulmonary artery
mix blood with cappilary netwroks
lymph drainage of lung
superficial near lung in visceral (parallel deep network)
deep lymph in CT (hilum nodes)
where are lymph vessels not foudn
past alveolar ducts
sympathetic NS lungs
from R & L sympathetic trunks
bronchodilation
vasoconstriction (increase ventilation-perfusion)
inhibit bronchial tree glands
parasympathetic NS lungs
R/L vagus nerves
bronchoconstriction
vasodilation
pleural fluid path
produce by parietal circulation
reabsord lymph system
inspiration
active
pressure in cavity decreases
contraction of muscle move cage up
expiration
passive
muscles relax
elastic tissue retract
blood path to lungs
sternal angle at 2nd rib trachea bifurcates
aortic arch
thoracic artery
bronchial artery
trachea location (spinal levels)
c6- T4/5
end at carina
what is carina
lowest cartilage ring of trachea
area of bifurcation
tracheal disorders & dyspnea
tracheal stenosis, tracheomalacia, foreign body aspiration
structural difference between R & L bronchi
R main bronchi is shorter, wider and vertical
L main bronchi is longer, narrower and horizontal
what bronchi most objects get stuck in
R bronchi almost always
lay Left recumbant as aspirate if on R
difference in lobes on Left side
cardiac notch for L side of heart
lingua
apex of lung location
2-3 cm above medial third of clavicle
anterior border lungs
behind sternum @ 2 costal cartilage then diverge @ 4 costal cartilage
lower border of lung location
6th rib midclavicular line
8th rib midaxillary line
10th rib paravertebra line
(chest tube 2 down from 10)
where does oblique fissure run
T4 posteriorly to 6th rib anteriorly
where does horizontal fissure run
around 4th intercostal
4 parts of parietal pleura
cervical
costal
diaphragmatic
mediastinal
innervation visceral pleura
vagus
insensitive pain
parietal pleura innervation
somatic nerevs
sensitive to pain
cupola
in pleural recess
@lung apex
vulnerable injury neck trauma
pancoast tumors
apical lung tumors in cupola
lay supine foreign body enters
the superior portion of right lower lobe
superior, posterior, medial
lay on R side foreign body enters
Right upper lobe
apical, posterior, anterior
upright, foreign body enters
lower portion of right lower lobe
medial basal, anterior basal, lateral basal, posterior basal
pulmonary vein clinical
need for afib treatment
diagnosing pulmonary veno-occlusive disease
bronchial circulation clinical
bronchial arteries enlarge in chronic lung disease
targets for embolism in sever hemoptysis
lymphatic drainage & lung cancer
carinal nodes enlargements
located in inferior tract of bronchiole, which makes this enlarged
when enlarged likely metastasized
pulmonary plexus
sympa & parasympa
@ root each lung
sympathetic lung nerve supply
upper thoracic sympa ganglia
T1-4
bronchodilator
vasoconstrictor
visceral afferent nerve lung
info about inflation & chemical irritation
send to central NS
doesn’t do pain
costal pleura innervation
supply by intercostal nerves
diapragmatic/mediastinal pleura innervation
phrenic nerve
auscultation upper lobes
anteriorly above 4th (R lung)
above 6th (L lung)
auscultation middle lobe/lingua
anterior between 4-6ribs
auscultation lower lobes
posterior below scapular spine
percussion thorax sounds
should be resonant, cardiac/liver dullness
hyperresonace is overinflation (emphysema/pneumothorax)
dullness (consolidation, pleural effusion, tumor)
types pneumothorax
primary - spontaneous in healthy people
secondary - occur in people with underlying lung disease
presentation of pneumothorax
chest pain, decreased sound, hyperresonance of percussion
what can pneumothorax lead to
lung collapse
COPD level of diagnosis
see 7th rib on xray
active expiration muscles
contract abdomen to reduce vertical dimension
contract internal intercostal to decrease transver & anteroposterior dimension
intrapleural pressure
made of parietal & visceral pleura pressures
should always be negative
only forced expiration makes positive pressure
transpulmonary pressure
difference alveolar & intrapleural pressure
elastic nature
great pressure this is, larger lungs
relationship of resistance, diameter, lymph, volume, pressure lungs
Resistance is proportional to lymph
Resistance & lymph inversely proportional to diameter
as diameter increases, velocity decreases
volume decreases, pressure increases + resistance increases
decrease in lung volume causes
increase in resistance
increase in pressure
resistance change of lungs to asthmatics
increase resistance due to increase muscle spasm this decreases volume
ressitance change of lungs to bronchitis
increase resistance due to increase of mucus
air can’t move in or out
intrapleural pressure change in exercise
heavy breathing out and faster
intrapleural pressure elevated
intraalveolar pressure elevated
resistance low
pressure change in forced expiration
airway collapse, from constipation strain
both intraalveolar & intrapleural pressures increased
blocks air from expiring
COPD airway collapse forced expiration
pressure drop magnified as increase resistance
intrapleural pressure higher due to emphysema as recoil decreased
pursed lip breathing creates
high resistance @ mouth
raise airway pressure
FEV1
forced expiratory volume in 1 second
FVC
forced vital cpacity
tidal volume
volume air in inhalation or exhalation
functional residual capacity
expiratory reverse volume + residual volume
residual volume
volume air in lung after forceful expiration
total lung capacity
maximum volume lungs can expand with greatest effort
vital capacity + residual volume
what would happen if puncture parietal pleura and cause pneumothorax
interpleural pressure no longer 0
collapsed lung as no P hold to chest wall
present with chest pain, SOB, tachycardia, cyanosis
puncture acts as a valve where air can only come in, nowhere for air to escape
dead space
no gas exchange occurs here, about 150mls of air
alveolar ventilation & dead space
when inhale always 150mL of dead air first
then come in fresh air
exhale out the old 150 first and new 150 stays stuck in dead space
breathing pattern in exercise
deep, fast breaths
increased amplitude of breath
increased frequency of breath
don’t keep reserve air
surface tension & pressure
increase pressure leads to increase of surface tension, decrease radius
smaller alveoli have greater surface tension (surfactant)
law of laplace
collapsing pressure is directly proportional to surface tension & inversely proportional to radius of alveolus
what phase of breathing are lungs more compliant
exhalation
decreasing the amount ofpressure change needed to move volume
lung wants to recoil and is getting to
what phase of breathing are lungs less compliant
inhalation
need more pressure to move volume
lung wnats to recoil but forcing to expand
excess H2O in lung causes
collapsed lung
if person has decreases in surfactant, this will occur as surface tension remains high (premie)
saline filled vs air filled lung compliance
air filed lungs have larger increase of surface tension, which decreases compliance and need more pressure to fill
lung compliance & emphysema
increased compliance
loss of elasticity means it is easier to stretch the lung and it doesn’t want to recoil
lung compliance & fibrotic disease
reduce compliance
fibers want to stay close together & recoil which requires more pressure ot overcome and fill lungs
components of compliance
lung compliance (alveolar-intrepleural pressure),, positive
chest wall compliance (intrapleural-atmospheric pressure),, negative
these pressures when balanced lead to good compliance as large volume changes will occur with small pressure changes
passive resting point
balanced point of recoil and expansion forces
FEV1 and normal parameters
forced expiratory volume in 1 second
80% of vital capacity
obstructive lung diseases measure/character
partial/complete obstruct
normal TLC (tot lung capacity)
normal FVC (forced vital capacity)
Decrease FEV1 (forced expiratory volume 1 sec)
restrictive lung diseases measure/character
decreased TLC (total lung capacity)
reduced FVC (forced vital capacity)
reduced/normal FEV1
when to measure peak expiratory flow
maximally forceful & rapid exhalation that immediately follows maximal inhalation
where in flow volume loop would you see if there’s an obstruction
at the peak wxpiration flow rate
should be rapid rise then linear fall in flow
obstructive pattern flow-volume loop
scoop out of expiration
increased lung volumes (take longeras increased resistance)
restrictive pattern
witches hat
refduced flow rate
reduced lung volume
humid air effect partial pressures
decrease partial pressures
3 reasons alveolar gas pressures differ from atmospheric pressures
alveoli air saturatted with water vapor (decrease partial pressure)
mix of fresh air with high CO2/low O2 air from dead space
continual exchange of gases continually between alveolar air and capillary blood
Why is hypoxia likely to occur faster than blood alkalosis
CO2 twenty times more soluble in blood than O2
likely to have higher partial pressure of CO2 as higher concentration
henry law
concentration of gas in liquid is proportional to partial pressure
Determinants of Diffusion/Fick’s Law
pressure gradient
surface area
distance
fixed solubility
why does blood CO2 levels reach equilibrium faster than O2
20x more soluble
dfiffusion only occures until reach equilibrium
PIO2
pressure of Inspired Oxygen
3 factors affect gas exchangne
partial pressure gradients/gas solubility
alveolar ventilation/pulmonary blood perfusion match
presentation of pathological changes respiratory membrane
what pathological changes can affect gas exchange
fibrosis (decrease in surface area, restrict from exchanging gas)
emphysema (decrease in surface area, volume incerase)
Diffuse alveolar hemorrhage/ goodpasture synfrome (decrease surface area in basement membrane)
high altitude affect gas exchange
decreased partial pressure of O2
low pulmonary alveolar pressure of O2
decrease gradient
decrease diffusion
decrease gas exchange
what is carbon monoxide diffusing capacity clinically useful for
test TLC, RV, FRC which can’t be tested by spirometry
help distinguisb between emphysema & asthma
A-a gradient
from Alveolar to arterial difference of O2
5 mmHg normal
PAO2
alveoli end of capillary blood
PaO2
arterial end of capillary blood
FiO2
fraction of inspired oxygen
% of oxygen in the inspired air
D-O
oxygen diffusing capacity
when is there reduced oxygen diffusing capcity in lung
pulmonary edema
pneumonia
fibrosis pulmonary fibers
less O2 in the alveoli than in blood as less time to equilibriate with capillaries
common pathologies fro R to L shunt
patent foramen ovale
atrial nseptal defect
ventricular septal defect
PE
congenital heart disease
pericardial tamponade
what do R to L shunts cause
hypoxia
skip capillary so not exchange of gasses
infinite V/Q
dead space
no gas exchange occurs here (PE)
Ventilation occurs
blood perfusion not occurring
hypoxia
0 V/Q
R-L shunt
only perfusion (blood)
no ventilation
hypoxemia (low PaO2)
PCO2 and PO2 in R-L shunting
high PCO2
low PO2
PCO2 and PO2 in dead space
high PO2
low PCO2
what does PACO2 come from
tissue metabolism
ventilation match metabolism, PA CO2 is constant
in nornmal person what is alveolar PO2 equal to
pulmonary arterial PO2
in normal person what is alveolar PCO2 equal to
pulmonary arterial PCO2
systemic arterial PCO2
hyperventilation PACO2
PACO2 < 40
hypoventilation PACO2
PACO2 > 40
relationship alveolar PO2 & PCO2
inversely related
Very low pressures in pulmonary circulation due to
low resistance
increased surface area
hypoxic vasoconstriction
not to perfuse non-ventilated alveolus
body need oxygen, won’t perfuse an area that has no oxygen
zone 1 blood flow & driving pressure
lowest blood flow
alveolar (PA) > arterial (Pa) > venous (PV)
capillaries collapse
zone 2 blood flow & driving pressure
medium blood flow
arterial (Pa) > alveolar (PA) > venous (PV)
in systole capillaries are open
in diastole capillaries are closed
zone 3 blood flow & driving pressure
highest blood flow
partially due to gravity
arterial (Pa) > venous (PV) > alveolar (PA)
diastolic pressure greater than alveolar so continuous flow
ventilation/perfusion ratio
gravity make intrapleural pressure less negative @ base
greater complinace
more ventilation so smaller ratio
less oxygenated blood
local controls of CO2 & O2
CO2 is bronchiolar smooth muscle regulator
O2 is arteriolar smooth muscle regulator
blood flow & exercise
increase blood flow all areas
bottom lung more perfusion still
CaO2
arterial oxygen content
how long does it take for oxygen to equilibriate across capillary
0.75s
what is tissue PO2 determined by
rate of O2 transport to tissues in blood
rate of O2 use by tissues
what happens to flow if hemoglobin present
the Oxygen binds to heme first and then will go into the alveolar flow
change of tissue PO2 with normla metabolism, increase flow
higher PO2 at eqilbm
change of tissue PO2 with increased metabolism, normal flow
decreased PO2
consume oxygen faster
change in metabolism affect carbon dioxide diffusion
increase metabolism increase CO2
decrease metabolism decrease CO2
what type of gas causes partial pressure
free, dissolved gas
what does CaO2 represent
absolute quantity of blood
content of arterial with both the free disolved oxygen & molecular
oxygen cooperativity
more O2 binds, O2 affinity increases
more O2 releases, O2 affinity decrease
hemoglobin & pulmonary capillaries
Hb almost fully saturated
O2 binds to Hb before dissolve in fluid
hemoglobin & systemic capillaries
Hb has increased unloading
small decline of blood PO2
how does CaO2 change with increase RBC
increases
increase in hemoglobin causes increase O2
(polycythemia)
Bohr Effect
how CO2 and pH affect O2 affinity
oxygen dissociation curve right to unload oxygen into tissue
decrease pH/increase CO2 causes more offload
temperature & O2 affinity
increase temperature increases pH. forcing offload
shift oxygen dissociation curve lung vs tissue
are opposites
right shift @ tissue = left shift @ lung
hypoventilation changes PACO2, A-aO2, FIO2 response
PACO2 increase
A-aO2 gradient normal
FIO2 response increases
decrease barometric pressure changes PACO2, A-aO2, FIO2 response
PACO2 decreases
A-aO2 gradient normal
FIO2 response increases
R-L shunt changes PACO2, A-aO2, FIO2 response
PACO2 normal
A-aO2 gradient increases
FIO2 decreases
V/Q mismatch changes PACO2, A-aO2, FIO2 response
PACO2 normal
A-aO2 gradient increases
FIO2 increases
diffusion limitation changes PACO2, A-aO2, FIO2 response
PACO2 normal
A-aO2 gradient increases
FIO2 increases
high altitude affect alveolar PO2
decrease
high altitude affect ventilation
causes hyperventilation
decrease PaCO2
high altitude affect arterial blood
increase pH causing respiratory alkalosis
decrease PaCO2
high altitude affect pulmonary blood flow
increase pulmonary resistance (low PO2 leads to constriction)
increase pulmonary artery pressure
high altitude affect O2 hemoglobin curve
shift curve to R as increase RBC
decrease affinity for O2
high altitude affect erythropoietin
a kidney hormone in hypoxemia
decrease PaO2
hypoxia
CO poisoning change dissociation curve
CO bind to hemoglobin and causes a lack of oxygen in the tissue
this increases oxygen affinity for hemoglobin further limiting O2 tissue
Haldane effect
removing O2 from Hb increases Hb able pick up CO2
Bohr effect
influence of CO2and H+ on release O2
diffusion limited gas exchange
total amount of gas transported limited by the partial pressure gradient
CO don’t equilibriate at end of capillary
perfusion limited gas exchange
partial pressure not maintained
regulated by blood flow
not much perfusion occur
what type of limit on N2O
perfusion limited
partial pressure equilibriate with alveolar pressure
what type of limit CO2 and O2
perfusion limited
low PO2 gradient
what type of limit CO
diffusion limited
PCO don’t equilibriate with alveolar pressure
type of limit on O2 in fibrosis
alveolar wall thickens
increase diffusion distance so diffusion limited
type of limit of O2 in strenuous exercise
diffusion limited as less O2 going to pulmonary more in tissues
type of limit of O2 in high altitude
diffusion limited
reduced partial pressure gradient for O2 mean equilibriate slower
What is unilateral renal agenesis?
Failure of the Ureteric Bud and Metanephric Blastema to produce a kidney on one side. The intact kidney typically undergoes hypertrophy as a compensatory mechanism.
What is bilateral renal agenesis?
Generally not seen congenitally as it is lethal in utero.
What is renal dysplasia?
The kidney develops but there is malformation of the nephrons due to genetic mutations disrupting molecular signaling mechanisms.
What are Congenital Polycystic Kidney Diseases?
Genetic mutations, either autosomal dominant or recessive, disrupt nephron structural development or cellular functions (e.g. ion channels, cilia in epithelial cells).
What are Wilm’s tumors?
A spectrum of nephroblastoma tumor types that appear by age 4, involving defects in nephron development and mutations in tumor suppressor genes.
What are renal tumors?
Various types can originate from different cell types.
What is a double-ureter?
A condition where either complete or partial duplications of ureters are possible.
What is the primary functional problem associated with double-ureter?
One of the ureters can have an ectopic distal drainage point, leading to improper waste drainage.
What are potential fistula sites in double-ureter?
Fistula sites can be the urethra, vagina, or vestibule (also in females).
Relationships right and left kidneys
right more inferior than left
Move rhythmically with breathing
Posterior position kidney significance
Allow for posterior surgical access
Hard to approach anterior due to fat
3 most likely locations for constriction/lodge kidney stones
Renal pelvis
Cross iliac arteries
Piece wall bladder
Blood flow through nephron
Filtered at glomerulus into glomerular capsule
Fluid move from capsule into proximal convuluted tubule, defend limb, ascend limb, distal convuluted tubule, collecting duct, papillary duct, minor calyx, major calyx, renal pelvis, ureter
Blood flow through kidney
Start I. Afferent arteriole
Goes to capillaries in glomerular
Flows out of efferent arteriole
Blood supply for adrenal areteries
Superior and middle suprarenal arteries from aorta
Inferior renal artery from renal artery
Sympathetic innervation kidney arteries
Mostly lesser sphlancnic nerve from T10-12
Parasympathetic innervation kidney artery
None from vagus
All indirect
Dermatome pain kidney
L1-2 and T11-12
Low back pain
Adrenal medulla cells
Act as post ganglionic sympathetic neurons
Release NE/E
Innervated by pre-ganglionic via greater splanchnic nerve
Adrenalblood vessel innervation
Sympathetic via greater sphlancnic to celiac ganglion
Post ganglionic neurons from celiac to blood vessels (in smooth muscle)
What is antibody-mediated glomerulonephritis?
It is an autoimmune attack against an antigen in the basement membrane.
What happens if antibodies cross-react with antigens in the alveolar basement membrane?
It leads to Goodpasture Syndrome.
What is the consequence of inflammatory damage to the glomerulus?
It impairs filtration.
What is Diabetic Nephropathy?
Thickening of basement membrane and arteriosclerosis, progressive failure of renal function.
What causes Sickle Cell Nephropathy?
Due to reduced oxygen in vasa recta of renal medulla, normal erythrocytes convert to sickle shape, occlude blood flow, induces ischemic damage.
What is Pyelonephritis?
Inflammation and neutrophil accumulation in collecting ducts.
Secondary to bacterial infection via urinary tract.
What is Cystitis?
Inflammation of bladder mucosa due to infection.
What is Bladder cancer?
Proliferation or instability of urothelium.
What is Urethritis?
Inflammation due to infection, typically Chlamydia.
Where does each collecting duct of kidney drain into
Papillary duct, minor calyx, major calyx, renal pelvis, ureter
Contents of renal corpuscle
Glomerulus (capillary)
Capsular space (bow,an space where form urine)
Contents of glomerular capsule
Bowman capsule & epithelial celss
Contents of glomerular capsule
Bowman capsule & epithelial cells
Blood filtration through glomerulus
Lumen of capillary to Bowman space to proximal convoluted tube through me[horn to urine
Structural elements of blood filtration
Fenestrated glomerular capillary, basement membrane, podocytes
Structural elements of blood filtration
Fenestrated glomerular capillary, basement membrane, podocytes
Filtration step nephron
Basal laminate traps substances, prevent into capsular space
Podocytes (become pedicles) surround capillary to further fikter
Normal urine content
Low protein concentration, no cells
If high protein shows problem with filtration
What is first structure affected by low BP in kidneys
Afferent arterioles
Justaglomerular cells
Sensory cells that detect arterial blood pressure
Response to deceased BP in kidney
JG cells detect change
Secrete renin which activates forming angiotensin
Angiotensin is vasoconstrictor to increase BP
Macula Densa job
In distal convoluted tubule (near afferent arteriole)
Monitors Na and regulate it through transporters
Macula Densa in reduced BP
Detects lack of Na
Releases chemical signals to JG
Activate renin release to increase BP
Mesangial cells locations and function
Inside glomerulus
Phagocytosis and endocytic between extraglomerular arteriole and intreaglomerukar
Helps increase pressure by contraction and structure repair in capillary
Functions of intraglomerular mesangial cell
Surround capillary
Phagocytose
Repair
Constriction
