Urinary Flashcards
Function of nephron?
Acid Water balance Electrolyte balance Toxin removal Bp control Erythropoietin D vitamin
Renal corpuscle blood pathway?
Afferent arteriole-glomeruli (filtered)-leaves efferent arteriole - peritubular capillaries - vasa recta - renal vein
Fenestrations?
Endothelial lining w/ neg charged “openings”
What can get through fenestrations?
Anything smaller than an RBC
Glomerular basal lamina layers?
- Lamina rara interna
- Lamina densa
- Lamina rara externa
GLomerular basal lamina purpose?
-3 layers for efficient and highly selective sieve-like filter
Where in glomerular basla lamina do you find glycosaminoglycans?
-The lamina rara interna and lamina rara externa
What glucosaminglycans are found in glomerular basal lining?
Heparin
Lamina densa composition?
-Filamentous type 4 collagen (kinked sheet pattern)
What is the glycoprotein laminin?
Cross links that bind type 4 collagen in the glomerular basal lamina
Podocytes?
Specialized epithelial cells covering the basement membrane of the glomerulus in the kidney.
What lines and stabilizes the slit diaphragms (podocytes)
-Podocin, nephrin (proteins), and glycocalyx (neg charged glycoprotein)
Minimal change disease?
- Nephropathy (defect in podocin)
- Loss of podocyte foot processes -> proteinuria -> and water imbalance -> edema
JAG?
Juxtaglomerular apparatus - regulates function of each nephron
Mesangial cells?
Modified smooth muscle cells in glomerulus
Messangial cells functions?
-Regulate blood flow->affterent caps
Produce extracellular proteins
Phagocytically remove filatration (filter and clean)
What synthesizes, stores, and secretes the enzyme renin?
JAG cells
Antiglomerular basement antibody disease?
Good pastures syndrome
Goodpastures syndrome vs alport’s syndrome?
Goodpastures-autoimmune
Alport’s- Genetic mutation
Good pastures syndrome?
- Autoimmune attacks type 4 collagen of basal lamina of glomeruli and alveoli -> inflammation of glomeruli
- Rapidly progressive glomerular nephritis
Alports syndrome?
- Genetic mutation of type 4 collagen-deposition of IgG
- Leads to inflammatory destruction of the glomeruli (glomerulonephritis)
PCKD?
Polycystic kidney disease
-Inherited disorder-noncancerous cysts develop w/in kidneys, round sacks containing water-like fluid
Non-proliferative glomerular disorders?
- minimal change glomerulonephritis
- focal segmental glomerulosclerosis
- Hereditary glomerulonephritis (alports syndrome)
- IgA nephropathy (bergers disease)
Proliferative glomerular disorders?
- HEnoch-schonlein purpura
- Membranoproliferative glomerulonephritis
- Goodpastures syndrome and wegners granulomatosis
- Postinfectious glomerulonephritis
Diabetic neuropathy?
- Progressive thinking of glomerular structure w/ destruction of glomeruli
- Increasing protein in urine
Regions of the nephron?
PCT
Loop of Henle
DCT
Collecting duct
Nephron anatomy?
- Glomerulus:filters blood
- PCT:reabsorbs ions, water, nutrients, removes toxins, adjusts pH
- Descending loop:aquaporins; water->ISF
- Ascending loop:reabsorbs Na+ and Cl- into ISF
- Distal tubule: secretes+absorbs ions to maintaining pH and electrolytes
- Collecting duct: reabsorbs solutes and water.
Where is water absorbed?
PCT, LOH, Collecting duct (Aquaporin 2)
Glucose reabsorption?
Urine side-> SGLT1/2 -> GLut 1/2 -> blood side
High serum glucose affect on urine?
-Down regulates GLUTE and indirectly inhibits SGLT-> keeps glucose in urine
Resorption of AA, proteins, and peptides?
-99% reabsorption via molecule-specific channels in PCT
Sodium reabsorption?
PCT
thick ascneding loop
DCT
Collecting duct
Where is most/least sodium reabsorbed?
65% NA/K/ATPase channgel in PCT
5% aldosterone-regulated Na/k channels in colelcting duct
K reabsorption?
65% passive diffusion PCT
20% LOH
Cl- reabsorption?
- Passive channels in PCT
- Sodium potassium chloride co-transporter in LOH
- Sodium potassium chloride co-transporter in DCT
What allows the exchange of chloride ions for bicarb ions in the nephrons?
The Cl/HCO3 exchanger
What is CIC-5?
-Chloride channel in renal tubules critical for normal tubular function
HCO3 reabsorption?
80-90% in the PCT
How much urea filtered in the glomeruli is found in urine?
40%
Where does the largest portion of uerea reabsorption occur?
50% occurs via passive transport channels in PCT
What drives reabsorption of Ca2+ and PO43 in the DCT?
Vitamin D and PTH = Ca2+
Vitamin D=PO43
Best way to measure GFR?
- Most accurately measured by insulin
- Most practical=blood creatine (from muscle breakdown of creatine phosphate)
GFR normal vs CKD5 failure?
Normal= 90ml/min with proteinn in urine
Failure= 15ml/min (1/6th of normal)
Where does the RAAS start?
JAG apparatus
DEfine RAAS?
- Renin-angiotensin-aldosterone system
- Regulatory pathway involving kidney, liver, lung, adrenals, pituitary gland, and selected arterioles (kidney)
What is the macula densa and how does it work?
Regulates blood volume using Na+ and gaseous NO
What causes renin to be secreted?
-Changes in arteriole BP activate special nerve cells in JAG (macula densa) -> JAG cells releases renin
Where dfoes renin fit into the RAAS?
REnin is an enzyme that acts on angiotensinogen -> angiotensinogen I
What are Renin inhibitors?
-Block the conversion of angiotensinogen -> angeotensin I, treating high BP
How do macula densa cells work?
- High Na levels (osmolarity is high) overwhelms the macula densa
- High Na and osmotic gradient ->macula densa swelling
- Swelling activates stretch activated channels allowing atp to escape
- ATP is converted into adeonsine
- Adenosine receptors allow for constriction of afferent and dilation of efferent arterioles
- Slows down GFR, converting less urine -> decrease in Na concentration decreasing macula densa swelling
NOS?
Nitric oxide synthase activated by low blood flow through glomules
Macula densa summary?
High Na->densa swelling->release ATP/adenosine->vasoconstriction
Low Na->densa NOS activation -> vasodilation
Angiotensinogen pathway?
-Angiottensinogen+renin->angiotensinn 1+ACE-Angiotensin II + aminopeptidase - angiotensin III+angiotensinases - degradation of product
Raise BP
WHere do ACE inhibitors work?
-STOPS ACE FROM converting angiotensin I - Angiotensin II
Angiotensins II effect on heart?
Vasoconstriction
Raise BP
Angiotensin II effect on brain?
Increased ACTH by pituitary
Raise BP
Avoiding ACE sifde effects?
use angiotensin receptor blocker class of meds
ARB
Mineralcorticoids action?
- maintain blood volume/BP by increasing Na+ reabsorption in DCT
- INcreased Na+ -> excretion of K+ and protons H+ leading to reabsoption of water
What is the primary mineralcorticoid?
Aldosterone
Action of aldosterone?
Binds to mineralcorticoid receptors in DCT->upregulation of Na+/K+ pumps (ATP dependent basolateral pumps)
Concentrates Na+ in interstitium -> more Na+ in blood and more K+ in urine
What are ENaCs?
Epitheal sodium channels - upregulated by aldosterone w/ increasing apical membrane (Facing the lumen) permeability for Na+
Conn syndrome?
-Overproduction of aldosterone
Higher BP and metabolic alkalosis
Addisons disease?
Acidons disease
Underproduction of aldosterone
Low BP and metabolic acidosis
Potassium sparing diuretics and aldoesteron regulation?
Competitive inhibitor for aldosterone receptors in collecting duct -> blocks effects (membrane permeability and # of Na-K pumps) -> decreasing Na and H2O reabsorption but keeping more K
Vasopressin aka ADH?
Affects H2O content by urine by affecting aquaporin-2 channels
Defects of AQ2 channels?
Aquaporin2 channel defects cause water loss (pts w/ nephrogenic diabetes insipidous) or water retention (pregnancy/congestive heart failure)
Diabetes insipidus 2 types?
Nephrogenic diabetes insipidus-mutations of AQ2 channel
Neurogenic central diabetes insipidus-no vasopressin (hypthal or pituitary gland failure) - tumors, trauma
Types of natriuetic peptides?
ANP- atrial natiuretic peptide
BNP- Brain natriuretic peptide
Naturietic peptides function?
Opposite of aldosterone- released when H blood volume/BP
Proposed medical use for ANP/BNP ?
Treating CHF
Normal pH range?
7..35-7.45
Respiratory vs metabolic acid base balance mechanisms?
Respiratory-pulmonary expiration of CO2
Metabolic- kidney elimination of HCO3, H+
Carbonic anhydrase?
Enzyme that affects intercalated cells (both H+ and HCO3 secreting)
Increased blood acidosis causes?
REabsorption of HCO3 from PCT, LOH, and Collecting duct back into blood
Secretion of H from collecting duct
Increased blood alkalosis causes?
Decreted H secretion
Less resorption (more secretion) of HCO3
Metabolic acidosis info
PH <7.35
HCO, pCO are low
Causes-diabetic ketoacidosis; lactic acidosis
Compensation - Hyperventilate excrete CO2
Metabolic alkalosis info?
Ph >7.45
HCO, pCO HIGH
Causes-vomiting
Compensation-hypoventilation-retention of CO2
Respiratory acidosis info?
Ph <7.35
HCO, PCO high
Causes- COPD, resp muscle paralysis
Compensation- retention of HCO, increased H secretion
Respiratory alkalosis info?
Ph >7.45
HCO, pCO LOW
Causes anxiety; acute pain
COmpensation - excretion of HCO, decrease H secretion
Hyperammonemia?
NH3 toxicity
Free NH3 = toxic to nervous system
What can Noxic ammonia do to our body?
Mental retardation, seizures, uncontrolled muscle movements, breathing irregularities, poor control of body temp
Erythropoietin?
Glycoprotein cytokine and hormone that regulates production of RBCs
Where is EPO made?
Kidneys
Peritubular capillaries
In endothelial cells
What enzyme is needed for one of the final steps of vitamin D synthesis?
1-a-hyroxylase in the PCT (25-hydroxyvitamin d2 1-alpha-hydroxylase
Kidney stone types+causes?
Calcium oxalate-H oxalate in urine+Ca2+= stone
Uric acid- increase uric acid in urine makes uric acid stones
Struvite ammonium magnesium phosphate -urea splitting bacteria raises acidity and makes stones
Calcium phosphate-hyperPTH makes more ca and phos which makes stones
Cystine-defect transport channel in PCT -> H cystine (acid) -> cystine stones
