Flashcards in Respiratpry Deck (186):
What is responsible for sigmoidal curve of Hb?
Increase slope due to cooperative binding
decrease slope due to saturation
in anemia:and in CO, cooperativity is maintained or lost?
High temp shift the curve to the (L/R)? What does it mean?
to the right
Low temp, low metabolism, hang on to O2
3 forms that CO2 is transported?
Dissolved CO2 (5%)
Bicarbonate (HCO3) (90%)
Total contain CO2 include 3 forms
Ez that catalyzes Co2 hydration
What is carbamino compound?
CO2 bind to terminal amine group, especially of Hb
RXN is facilitated in low O2 tissue
at any PCO2, decreasing PO2 will increase CO2 content
Role of lipid
mmb, energy, hormone
Muscle in respiratory and their innervation
Diaphragm - phrenic nerve
Intercostal muscle: intercostal nerve
Upper airway muscle: vagus
> Upper airway
> Lower airway an lungs
Upper airway: nose, larynx, pharynx, trachea: cough, sneeze
Lower airway and lungs:
> Pulmonary stretch R
> Pulmonary irritant receptors
> J (juxtacapillary) receptors
Pulmonary stretch R (location, stim, afferent pathway, response, note)
Location: smooth muscle of large and small airways
Stimulus: lung distention, discharge during inflation
Afferent path: vagus nerve
Response: inhibit respiration, terminate inspiration, allow expiration, decrease HR
Note: Hering-Breuer Reflex
Pulmonary irritant R (location, stim, afferent pathway, response, note)
Location: epithelium of large airways
Stim: irritant, smoke, dust, histamine
Afferent airways: Vagus X
Response: cough, bronchoconstriction (reflex)
Note; asthma (histamine)
J (Juxtacapillary) R (location, stim, afferent pathway, response, note)
location: near walls of pulmonary capillaries
Stim: pulmonary edema
Afferent pathway: vagus
Response: rapid, shadow breathing
common afferent pathway of lung mechanoR - lower airway and lung?
Vagus Nerve X
Peripheral chemoreceptor of the respiratory system? (2) each stimulated by what?
which one is more effective
Carotid bodies: decrease PaO2, increase PaCO2, decrease pH
Aortic bodies : stim by decrease PaO2, increase PaCO2
Carotid is more effective
Carotid body chemoR: pH and CO2, which one has higher effect? MOA of both?
Effect of pH is smaller than that of CO2
both act via inhibition K channel
central chemoreceptors: location, afferent to where? response to what stim?
on the ventrolateral surface of the medulla
afferent to medullary respiratory center
- response to H+ and (PCO2) of local interstitial fluid and cerebral spinal fluid (CSF), not affected by PO2
Ventilation response to hypoxia
Hypercapnia (too much CO2) increase ventilation rate
- Effect of hypoxia is minimal until PO2 <60 mmHg
Ventilation response to Hypercapnia.
Hypoxia potentiates the effect of PCO2 on ventilation rate.
a chronic inflammatory disorder of the airways characterized by episodes of wheezing, shortness of breathm chest tightness, and cough
causes of asthma
irreversible airflow obstruction
smooth muscle consttraction
thick mucus plug
not reversible by bronchodilators
Asthma treatment: 2 approaches
Managing symptoms: bronchodilators:
> beta 2 agonist
> muscarinic antagonist
Managing disease: anti- inflammatory agents
> mast cell antagonist
> Anti IgE Ab
Inhibitor of LT synth and LT Receptor antagonist
Beta Agonist in asthma
Salmeterol (long acting 12h)
Toxicity: Tachyphylaxis is common with overuse( rapid loss of effect)
skeletal muscle tremor
Tachycardia and arrythmia (rare)
Muscarinic R Antagonist
relax smooth muscle by antagonizing Ach released at post -ganglionic nerve ending
Ipratropium (Atrovent): short term (4-6h)
Titropium (Spirive) long term 24h
block M R, relax smooth muscle and decrease glandular secretion
Adjunctive to Beta agonist in severe cases
Atropine life side effects (minor)
Effect of leukotrienes in Asthma.
Mucin secretion (submucosal gland)
chemotactic (esinophil and neutrophil)
Vasoactive (blood vessel)
Bronchioconstriction (smooth muscle)
Leukotriene Antagonists (think lukast)
how many types? list nams of each, use, toxicity
- LT4 Receptor blockers:
> Zafirlukast, montelukast used orally
> Toxic:GI distress, increase liver transaminases
5-lipoxygenase inhibitor: Zileuton inhibits enzyme that form intermediates in synthesis of LT
> Toxicity: as above, monitor liver ez
Corticosteroids (MOA, net effect) asthma
bind to intracellular glucocorticoid R
> direct activiation of gene expression (upregulate anti inflam gene)
>interference with transcription factors (down regulating of pro-inflam genes)
>inhibition of production of cytokines
> reduce activity of mast cell and eosinophils
> stabilize microvascular permeability
> increase expression of beta receptor
Corticosteroid list of drugs
Systemic: prednisone, methhylprednisone
> acute severe asthma
> chronic asthma
> toxicity: severe for long term use: weght gain , cataract, osteoporosis, glucose intolerance, growth inhibition
Topical: Beclomethazone, triamcinolone. budesonide, fluticasone
> persistent asthma
> minimal toxicity at low -moderate dose
>Oropharyngeal candidiasis (thrush)
>inhibition of growth
Use and eliminate
MOA: inhibit phosphodiesterase (PDE)( increase cAMP) and increase adenosine bronchioconstriction
Oral absorption, eliminate via hepatic P450
Toxic: narrow theurapeutic window, GI distress, tremor and insomnia are common, hypotension, arrythmias, seisure
Cromolyn and Nedocromil (MOA)
Mast cell stabilizer: block histamine and LT from mast cells
Use: mild, persistent asthma, throat irritation and cough, hay fever, food allergy
Immuno-moduatory Therapy (MOA), ex
Anti IgE block mast cell binding
Omalizumab (sub Q)
Patient with asthma: what kind of dental problem?
xerostomia, halitogis, gingivitis, cavities,
Oral infection from steroid
two types of nephron?
Juxtamedulallary (15%) deep into medulla: water balance
What affects the filtration of substance in kidney?
1. Size: macromolecules >70kDa dont pass
2. Charge basement mmb and coast of the podocytes are negatively charged
Three functions of the kidney:
endocrine (production and secretion of hormone)
metabolic wastes in urine
urea (from protein metabolism)
uric acid ( from Nucleic acid )
creatinine ( from muscle creatine)
bilirubin ( from Hb)
Drug Filtration in kidney
- are all drugs metabolized in liver before excreted ?
- how do they gte in the tubule?
- does reabsorption happen?
- what does affect the excretion of drug
- most drugs are metabolized in the liver before being excreted, but not all
- many drugs do not traverse the filtration barrier. but enter the kidnet tubule by secretion
- some drugs may be reabsorbed
- excretion of drugs is affected by urine pH
endocrine function of the kidney: what hormones?
Renin and erythropoietin
- released by ...
- is it a hormone or ez?
- what does it do
released by granular cells od kidney
- an ez with hormone -like actions
- convert angiotensinogen >> angiotensin I
- required for the generation of the powerful vasoconstrictor angiotenosin II
- what kind of hormmone?
required for what ?
- required for erythropoiesis
- 80% comes from a group of cell in the interstitium of the renal cortex and outer medulla of the kidney
- hypoxia and several hormones (prostagglandin) stim secretion
renal corpuscle: mesangial cells
location, what they do?
locate between and within capillary loops
Support glomerular capillary
phagocytes: keep filtration barrier clean
contraction: contain myofibrils
> contraction cause decrease in filtration area
> contraction is regulated sympathetic activity and angiotensin II
Proximal tubule: how many sections? structure, number of mitochondria, role ?
what is special about apical and basolateral mmb?
Proximal convoluted tubule
proximal straight tubule
Very prominent brush border > large SA
Large number of mitochondria provide energy for active transport
Important site of secretion
Both apical and basolateral mmb are extensively amplified (connect to each other via tight junction
Two route of reabsoption and secretion
Paracellular Route : diffuse across tight junctions down an electrochemical gradient between the lumen ans blood
Transcellular route: pass across the cell by active or passive processes
3 forms of acwtive transport
1. primary active transport: directly ATP hydrolysis (Na-K ATPase)
2. secondary active transport: indirect involves ATP hydrolysis (glucose - Naa symport)
3. endocytosis: mmb invaginate and pinches off a vesicle
in micropuncture experiment in the proximal tubule to measure reabsoption and secretion: [inulin] is increased 3X, but [Na] unchanged. Why? what does it mean?
inulin is neither secreted or reabsorbed
Na reabsorbed to maintain the conc.
This is that 2/3 of filtered water has been reabsorbed , 2/3 filtered Na must also have been reabsorbed.
Changes in tubular fluid to plasma ratio (TF/P): >3 or <3, what does it mean
TF/P >3: net secretion (PAH, penicillin)
TF/P < 3: net reabsoprtion (Cl, NA, Glu, amino acids , HCO3)
what is the TF/P of bownman's space
By the end of the proximal tubule: what is the osmolarity and Na conc compared to arterial blood?
- Cl, Na, glu, aminoacid ?
- most filtered Na reabsorbed
- Most filtered Glu, La, amino acid, HCO3 follow Na to reabsorbed
- Transepithelial voltage is positive
T/F : the secretion of H in linked to the reabsorption of HCO3-
what is the enzyme involved ?
If TF/P for H increase, how is TF/P for HCO3
what drives Na reabsorption via extracellular (paracellular route?
TF Cl > PCl
> concentration gradient
Cl reabsorbed via paracellulaar route
lumen turns positive
drive Na reabsorption
the main driving force of H2O reabsorption ?
reabsorption of Kreb's cycle intermediates and glucose?
sencondary active co-transport with Na
driving force of K reabsorption?
2 ways reabosption of protein and peptide
Protein: by endocytosis, degraded in lysosomes to aa, then enters the peritubular capillary
peptide: are degraded by ez in brush border to aa, which then are reabsorbed
Passice reabsorption of weak organic acids and bases
the conc of weak acid and base in TF increases as H2) reabsorbed . only unionized form will pass the epithelium.
theh extent to which an organic acid or base is ionized in the TF depends on the pH of the TF ( and the pKA of the substance)
many drugs are weak acids or bases
if TF becomes alkaline, what happens to reabsorption of weak acids ?
more inonized, reabsorption is diminished
(treat aspirin overdose)
drugs that ncrease renal excretion of salt and water
Na handling in the kidney
Proximal: 60% - NAHCO3 form
Thick ascending loop: 20-40% - Na -
Distal tubule: 10-12% - NaCl - Thiazide
Collecting duct: 2-4% Nacl - Aldosterone antagonist
Loop of henle: The Na/K/2Cl transporter
transport Na, K and 2 Cl from the lumen into the cell. Na/K pump pump
bronchiole attaches to what?
> what population of patients?
inflammation of the lungs: pneumonitis or pneumonia
occurs in 1/3 of immuno compresses patients
lobar pneumonia: location, consequence
in 1 lobe, Strep Pneumonia
red hepatization (neutrophill)> gray hepatization (break down of PMN)> resolution
inflammatory consolidation around small bronchi and bronchiole
everywhere in the airway to lung
communicable disease resulting in necrotizign granulomatous inflammatory reactions
a visceral or deep mycosis leading to pneumonitis
What types of fungal pneumonia found in Immunocompromised induviduals?
Viral pneumonia: population
infants, elderly, immunocompromised individuals
diffuse infiltrative lung disease
activate MO>recruit others
Pulmonary Interstitial fibrosis:
thickening: collagen and scar tissue
right heart is bigger than left: work hard
Origins of Pulmonary Emboli
most frequently from deep leg venous thrombi
air, amniotic fluid, right sided infective endocarditis
Etiology of primary Pulmonary hypertension
Causes of secondary pulmonary hypertension
chronic pulmonary emboli
congenital heart disease
Morphology of pulmonary hypertension
pulmonary arteries: atheromas, thickening/ fibrosis/hypertrophy
Obstructive lung disease
a decreased abilit to expired
Def: abnormal enlargement of air spaces distal to the terminal bronchioles
> classification: centriacinar, panacinar, paraseptal
chronic excessive mucus production in the airways
chronic necrotizing infection of the bronchi and bronchioles leading to dilation
> common in ?
> major cause
dilation of the proximal portions of the acini and distal portions of the acini are spared
> upper lobes
> associated with ?
uniform dilation of the acini at the level of respiratory bronchioles to the terminal alveoli.
- lesions are more frequent in the lower zones of the lungs
- associated with alpha- l-antitrypsin deficiency
> common in?
> def: productive cough for 3 consecutive months for 2 or more years
> skoker or dwellers living in smog
> inhale substances lead to activation of neurohormonal pathways that stimulate airway secretory cells to release chemical mediators
> attract inflammatory cells and stimulate airway mucous secretion
- reversible bronchocontriction in response to varied stimuli
> extrincsic (immunologic or allergic)
> intrinsic (non-immunologic or idiosyncratic)
obstruction of airways impaired mucocillary clearance and persistent infection due to dilated airways
> most common cause is inflection
major types of lung cancer
squamous cell carcinoma
small cell carcinoma
common disorders in lipid metabolism
2 ways of naming FA
C system COO = C1
omega system, start at the other end, only define the first double bond of the system
C system C X:Y; A,B....what does it mean
X : length
Y # double bonds
A, B position of double bonds (between n , n+1)
> why essential
precursor of ?
in human, double bonds cannot be inserted beyond C9-10
>precursors of Eicosanoids (regulatory molecule)
> deficiency: skin leison, kidney damage, weight loss
What is the major storage and transport form of FA?
one end is hydrophobic, one is hydrophilic
> accumulation will cause?
> transport formr?
structural component of mmb (stiffener)
precursor for steroid hormone
abnormal accuulation: atherosclerosis
> cholesterol ester
digestion of dietary lipids
in intestine, bile acid - glycocholate
cholecystokinin (CCK) secreted by upper part of small intestine triigers gall bladder to release bile salt, emulsifies TG, CE
CCk also triggers pancreas to elease lipases and cholesterol esterase: emulsified TG/CE >>> 2-monoglycerides FA cholesterol which then transferred to intestinal cell. Here there are 2 options:
1. transport to portal vein directly (serum albumin)
2. chylomicron assembly (CE and TG)
how is lipid soluble in blood ?
Serum albumin: which has FA binding sites
form A lipoprotein particle: with hydrophobic core and hydrophilic shell
- inherited disorder in electrolyte transfer across mmb
> lung infection/congestion
> cannot secrets digestive ez
> malabsoption of lipids, proteins. and lipud soluble vitamins
> visual impairment
> dieat rich n short and medium FA
oral pacreatic ez and vitamin supplement
MOA: block lipases and cholesterol esterase
> fat droplets excreted
a succrose polyester
not a substrate for pancreatic lipase but mough fell as TG,
used as fat substitution in some tooth
>>> anal leakage
The 4 types of lipoprotein particle
which form(s) have both TG and CE?
ranking good, bad
> hylomicron and VLDL have both TG and CE
> LDL and HDL have CE only
> from chylomicron to HDL: increasing density (decreasing % lipid), increasing % protein
>> HDL good
Why LDl bad, HDL good?
LDL: longer half life, more damage and accumulation in the arteries
HDL: involve in removal of cholesterol from tissue.
What are the sources of chylomicron, VLDL, LDL, HDL?
Chylomicron: intestinal cells
VLDL: liver cell
LDL: VLDL derived
HDL: liver cells chylomicron- derived
What is required for assembling and secretion chylomicron?
(AI: function is not well unsterstood )
role of HDL in assembling chylomicron
donate apoE and apoCII required gor chylomicron function
release of chylomicron cargo for storage
ApoCII activate LPL (lipoproten Lipase found in cells lining cappilaries)
>dipose tissue reak chylomicron to FA + remnant , FA stored in api
roles of apolipoprotein: ApoB48, Apo CII, Apo E
Apo B48: assembly and structure
ApoCII trnasfer of lipid from chylomicron to tissue
Apo E: removal old chylomicron by liver
What stimulate lipoprotein lipase? (2)
Insulin and ApoCII
Insulin deficientcy : ineffecient storage
Hyperlipidemias from elevated chylomicron: type I a, And Ib?
Ib: Apoprotein CII
Fate of chylomicron remnant
Apo CII block uptake by liver, ApoCII and Apo E transferred to HDL when TG content decreases.
Then ApoE bind to LRP and LDL in liver (LDL receptor-like protein - more dominant than LDL R in liver)
>endocytosis in liver> break down to FA +C+ amino acid in lysosome
Assembly of VLDL
new secreted VLDl from liver has B100 and AI
HDL comes in donate A and ApoCII
Delivery of FA via LPL
2 fates of VLDL:
1. uptake by liver again via endocytosis, E +LRP like chylomicron
2. Hepatic lipase: FA + LDL+Apo E, free FA take up by liver cell
LDLhow many apoprotein, how to get access to the cargo?
only Apo protein B100
B100 adotp new conformation to bind LDL R
two pathway for LDL removal from plasma
1. 75%: LDL receptor to cell. to produce free cholesterol, FA and aa. Free cholesteroll inhibits this
2. 25% scavenger R of MO: scavenger: low affinity for LDL, high affinity for oxidized and glycosylated LDl (correlated with high glucose level). Rceptor is not regulated bu intracellular cholesteroll
uncontrolled accunmulation of cholesterol in cell
contribute to atherogenesis
Reverse cholesterol transport
HDL & peripheral cell
- Apo AI mediates binding cell surface
- Free cholesterol from cell diffuse to HDL
- Apo AI stimulated LCAT
- LCAT esterifies transferred free cholesterol
Lecithin-cholesterol acyl transferase,
-makes cholesterol >> CE
transfer of CE from HDL to liver (2 ways )
1. Transfer CE to chylomicron and VLDL remnant, couple to removal of TG , uptake by liver
2. Transfer of CE to liver via SR-B1 receptor allows CE transfer to lover cells without endocytosis
Fates of Excess cholesterol ester in liver,(2), which one has feed back inhibition
1. bile acids (feedback, too many bile will inhibits)
2. new VLDL
1. starting compound
2. step products
2. which one is rate-limiting step
1. Acetyl coA
2. HMG CoA> Mevalonate> Squalene > lanosterol> cholesterol
3. HMG CoA reductase
What are 3 FB of free cholesterol
inhibits HMG CoA reductase
stim ACAT turn to droplet for storage
inhibit synth of new LDL receptor
convert free cholesterol to CE to store in small intracellular droplet
how cholesterol regulate gene transcription?
via what receptor
LDL R and HMG CoA reductase genes
> high Free cholesterol> low gene expression (via SRE binding)
High cholesterol: SREBP, SCAP, Insig in ER
Low: INSIG release SCAP, SREBP, these 2 travel to golgi, travvel to nucleus, activate SRE
2 strategies to reduce LDL
- increase removal of LDL from bloodstream by LDL receptor-mediated endocytosis
- decrease synth of LDL
pharmacological agents that reduce cholesterol levels
1. Bile-acid biding resins
how does cholestyramine work?
what natural product works the same?
Reduce intracellular cholesterol by inhibiting reapsoption in small intestine >> excretion in large amount
fiber (oatmeal) bind to bile acids prevent reabsoption
more bile acids excretion > less free cholesterol > More LDL R? reduce LDL level in blood
What does Statins do?
would statin work for homozygoud defect in LDl receptor
inhibit HMG CoA reductase> inhibit cholesterol synth
> decrease cholesterol synth > less free cholesterol> More LDL R to uptake > reduce LDL in blood
No, will not work
How does Ezetimibe work?
inhibit absorption of dietary cholesterol into intestinal cells (to assemble chylomicron)
less cholesterol from chylomicron remnant > less free cholesterol? more LDL R
inhibits VLDL synth > less VLDL, less LDL, mechanism unclear
effect of insulin in FA metabolism
Insulin: glucose> stored as triglyceride > VLDL > FA
effect of glucagone in FA metabolism
triglyceride > FA + glycerol > FA
Oxidation of FA:
FA >beta oxidation> Acetyl coA> TCA> oxidative phosphorylation
Beta oxidation: location in the body, locaation in cells
in heart, muscle, kidney and liver
happened in mitochrondrion
How FA cross the inner mitochondrial mmb
step of the shuttle
Carnitin Shuttle :
FA> FA acyl coA synthetase
carnitine + FA coA > acyl carnitine
carnitine release for the next shuttle
Acyl CoA >>Acyl coA dehydrogenase (FAD to FADH2) > double bond > add H2O> oxidation (NAD to NADH) > ez Thiolase (SH-CoA) >
Acetyl Co A + new FA is 2 C shorter than before
What happens when FA has odd number of carbon? pathway after that ?
the last 3C FA rleased as propionyl -CoA
Propionnyl CoA caarboxylase (biotin )
Methylmalonyl CoA racemase
Methyylmalonyl CoA Mutase (metabolite of Vitamin B12)
>> Succinyl CoA : fees into TCA cycle
2. primary product
3. building block
1. cytoplasm, liver
palmitic acid (16C)
Acetyl CoA and malonyl CoA
how does Acetyl co A from inside mitochondria trnafer to cytoplasm for FA synthesis?
Acetyl coA > Citrate synthase> Citrate > outside > citrate lyase> acetyl coA
Multi ez complex in FA synthesis
what are the 2 groups attached on it
cystein and phosphopantethine (Vit B5)
>> it is a acyl carrier protein
5 Steps in FA synthesis
1. priming (attachment of Acetyl coA and malonyl co A in FAS)
2. condensation: connect the 2, release Co2
3. reduction if beta ketone group
4. dehydration of the reduced intermediate
5. reduction of double bonds
transfer the new product to
FA product release when reach 16 C
palmitoyl thioesterase> palmitic acid
regulation of FA synthesis by substrate and product:
what is the rate limiting step in FA synth?
AcetylcoA > MalonylCoA (AcetylCoA carboxylase)
Citrate activates this ez
palmitoyl coA inactivate
how insulin ans glucagon regulate FA synth?
Glucagon> cAMP> PKA> acetyl CoA carboxylase active > inactive
insulin > protein phosphatase> inactive> active
Hormone sensitive lipase: role, process
what +/- it?
convert TG into DG/MG/Glycerol + FA(s)
- serum albumin prefer short FA to transport
- insulin: inhibit it > reduce mobility
- glucagon, NE, ACTH> activate it > increase
regulation of FA synthesis and oxidation in liver
1. direct regulatory controls
2. prevent crosstalk between the 2 pathway
Most statin are metabolized by CYP except
(rosuvastatin 10% metabolized by CYP)
Teratogenic (Pregnant Cat. X) of Statin
cannnot prescribe HMG CoA reductase inhibitor to prego
MOA of resin ( treating hyperlipidemics)
bile acid binding, prevent the reabsoprtion of bile acids
Ex: cholestyramine, colestipol
- works best with patient with LDL R
increase VLDL ( >> no use with pt with hyper TG )
MOA of Ezetimibe
prevent take up of cholesterol into small intestinal cell
MOA of Niacin , side effect
reduction of VLDL secretion
hot flush , GI distress, hepatotoxicity, hyperuricemia
enhance oxidation of FA:rduce VLDl secretion from liver, increase VLDL uptake in muscle
side effect: myopathy, hepatotoxicity, gallstones
Ex: Gemfibrozil (renal elim)
Omega 3 acid ethyl esters
MOA , side effects
only for patient with side TG> 500 mg/dL
reduce synthesis of TG and enhance TG removal
side effect: burping, upset stomach, allergy , bleeding
Macula densa: location, roles
in juxtaglomerular apparatus:
thicckened portion of the distal convoluted tubule: sense the composition of the tubular fluid
in juxtaglomerular apparatus: specialized smooth muscle cells in the wll of the afferent arteiol, secretes the ez renin
Renal blood flow
= 20-25% X Q ml/min
Renal plasma flow
= 55% Renal blood flow (RBF)
Glomerular filtratio rate
= 20% renal plasma flow
Net filration pressure (NFP)
NFP = Force favoring - force opposing filtration
= PGlomerular cap - P Bowman's - Pi Glomerular Cap
Force of filtration does not change along the glomerular length (T/F)
Afferent > efferent
Permeability of filtration coefficient Kf
GFR in terms of Kf
Kf = hydraulic permeability * SA
GFR = NFP * Kf
How hypoalbuminemia affect GFR?
decrease Glomerular cap oncotic pressure
What is autoregulation of kidney ?
how does it work
the ability to regulate on its own blood flow without involvement of extrinsic factor
1. Myogenic FB: - increase perfusion pressure> increase stretch smooth muscle > open stretch-activated, non-selective cation channels > depolarizing, influx of Ca> contraction > increase R
2. Tubuloglomerular feedback : a transient increase in pressure in the glomerular cappilaries increase GFR> more NaCl to macula densa> vasocontriction in adjacent afferent aterioles
actions of angiotensin II
stim aldosterone secretion
Stim Na reabsorption
Stim ADH secretion
synth by kidney,
protective role: provide a buffer against excessive vasoconstriction
GFR formula using innulin
GFR = U.V/P = (conc inulin. flow rate )conc plasma
Renal: the entry of Na across the apical mmb is (down/up hill)
the Na across the lasolateral is (down/up hill)
renal: for a weak acid, renal clearance is low at an (acidic/alkalike) pH?
high at an (acidic/alkaline) pH ?
acidic: low pH = low clearance of weak acid
alkaline: high pH = high clearance of weak acid
what affects the pH of Urine?
exercise (lactic acid)
dsease condition (ketoacidosis in type I diabetes)
hydration state: prolong vomiting deplete water volume, stim acid secretion
combine with peniciline?
competitive inhibitor of secretory mechanism
slow down the clearance of peniciline
block creatinien secretion
Inulin clearnace is independent of inulin plasma conc ( T/F)
why mannitol cause osmotic diuresis ?
mannitol is freely filtered but not reabsorbed in proximal tubule
> increase osmotic pressure
> water retention > Na diffuse into the lumen
> excess Water and Na
Polyuria and poly dipsia in Type I diabetes
Tm for glucose and ketone increase
> osmotic diuresis
how is a hyperosmotic medulla generated?
Peritubular capillaries vs Vasa Recta ?
Peritubular Cap: reabsobed material quickly removed
Vasarecta: not immediatedly removes, enabling maintenace of gradient
Adverse: hypokalemia, sulfa- allergy- ototoxicity, NSAID decrease efficacy of loop agents: NSAID inhibit protaglandin (vasodiator)
indication: hypertension, mild edema, chronic hypercalciuria, stone formers
Spirolactone , eplerenon
aldosterone antagonist: inhibit Na reabsorption iin cortical collecting duct > prevent K excretion
K sparing diuretics
Adverse: HyperK, antiandrogen effect: gynecoastia, impotence
physiologic antagonist of aldosterone: block Na channel in cortical colecting tubules
K sparing diuretics
cell shrink ?
Cell swells: decrease in solute concentration in interstitial fluid > OsmoR gains water > need to stop diuretic> ADH promoted
cell shrink: increase in conc of interstitial fluid , water comes out, need to promote diuretics > prevent ADH relelased
baroR compared to osmoR in controlling ADh
less sensitive but incudes a greater ADh release
what happens to Diabetes insipidus?
ADH is either not produces or is incapbable acting
> Massive urine flow, low osmolarity
> secretion from where?
from zona glomerulosa
- Small increase in plasma K
- Decrease in plasma Na
- Angiotensin II (most important)
Atrial Ntruretic Peptide (ANP)
secreted from cells in atria
Blood increase atria stretch > ANP secretion
> increase NA excretion in 3 ways
1. increasing GFR
2. inhibit Na reabsorption in the medullary collecting duct
3. inhibiting renin , aldosterone and ADH
ANP also a vasodilator
High Extracellular K stim which hormones? (3)
insulin: K goes to muscle and liver
Epinephrine : K goes to muscel
aldosterone: stim K secretion in CCD
stimulate Na-k ATPase pumps K into the cell to low ECF K