Renal Basic Facts Check Flashcards
What expresses AT1R
efferent arteriole
JG cells
UV/P=
Clearance
Solute filtered/unit time
filtered load
What monitors GFR as tubular flow?
macula densa
TGF mechanism
What 3 things are used for hormonal compensation for hypotension?
aldosterone
AVP
Angiotensin II
What receptor is used for compensation for HTN?
AT2-R
What are pharmacologic targets for HTN?
AT1-R
Renin
Aldosterone
ENaC
What are the renal mineralocorticoid targets?
ENaC
ROMK
NHE3
What’s responsible for proximal tubule Na+ transport?
“Reabsorption”
SGLT
NHE3
Angiotensin II
What’s responsible for distal nephron Na+ transport?
"Reabsorption" ENaC NKCC NHE3 Aldosterone NCC
What is responsible for renal glucose handling?
“Reabsorption”
GLUT
SGLT
What is a Ca2+ sparing drug?
HCTZ
What is a K+ wasting drug?
HCTZ
Furosemide
What targets NKCC?
Furosemide
Name a mineralocorticoid antagoinist.
sprinolactone
What is responsible for renal excretion of H+?
NHE3
Aldosterone
NH4+
What condition is characterized by:
metabolic acidosis: aldosterone resistance?
Type 4 RTA
What condition is characterized by:
high plasma aldosterone with hyperkalemia?
pseudohypoaldosteronism
What condition is characterized by:
metabolic acidosis: glucosuria w/ euglycemia?
Type 2 RTA
What condition is characterized by:
euvolemic, hypovolemia, hypervolemic?
hyponatrimia
What condition is characterized by:
metabolic acidosis: defect in NH3 and carbonic anhydrase?
Type 2 RTA
What is the (potential) pathogenesis of salt-sensitive hypertension?
ouabain
What conditions can be neurogenic or nephrogenic?
DI and SIADH
What condition is characterized by:
elevated serum PTH with hypocalcemia?
secondary hyperparathyroidism
What is synthesized in response to PTH?
calcitriol
If unchecked, what would cause hyperphosphatemia?
calcitriol or secondary hyperparathyroidism
If unchecked, what would cause hypoglycemia?
insulin
What is secreted in response to hyperglycemia?
insulin
What is a marker to monitor DM2?
hyperglycemia; Hb1Ac
What is used for glycemic control?
insulin
What are signs of DM2?
glomerular hyperfiltration microalbuminuria glomerulosclerosis hyperglycemia insulin resistance
What condition is characterized by:
hyponatremia w/ elevated urine specific gravity?
SIADH
What condition is characterized by:
polydipsia with polyuria?
DI and DM1
What condition is characterized by:
V2R loss of function?
SIADH
DI
What mediates distal H2O reabsorption?
AVP
What condition is characterized by:
dyslipidemia, hypoalbuminemia and proteinuria?
nephrotic syndrome
What condition is characterized by:
doubling of plasma creatinine?
acute kidney failure
Does aldosterone increase reabsorption/excretion of:
Na+?
K+?
NH4+?
Na+: reabsorption
K+: excretion
NH4+: excretion
What is the effect of K+ regarding volemic state? (the aldosterone paradox)
- In hypovolemia with eukalemia, AII and aldosteone work together to facilitate Na+ secretion w/o overt hypokalemia
- in hyperkalemia (w/o hypovolemia), there is a blunted response in terms of Na+ reabsorption and a profound response in K+, so you can get K+ secretion without hypervolemia (due to a change in gene expression to upregulate ROMK (K+ excretion) coupling with aldosterone)
What condition classically presents with glucose urea with euglycemia?
Type 2 (proximal ) RTA
What are classic symptoms of Type 4 RTA?
(aldosterone deficiency/resistance)
metabolic acidosis, hyperkalemic, normal AG, BP MAY be a little off, Urinary AG > 0 (decreased NH4+ excretion means less Cl- (low NH4Cl), therefore less urinary anion: POSITIVE AG
What are characteristics of primary hyperaldosteronism?
increased pH (bc high H+ secretion due to aldosterone’s effect on NHE3 in PT and TAL) –> HYPOKALEMIC METABOLIC ALKALOSIS
What are the characteristics associated with hypoaldosteronism?
lowered aldosterone so less H+ secretion –> lowered pH –> HYPERKALEMIC METABOLIC ACIDOSIS
What is insulin’s bioactivity at low concentrations?
Cellular K+ uptake (caution: treating someone with low K+ with insulin can lead to hypokalemia)
What is the reason and effects for DM1?
lack Beta cells so can’t make insulin or recognize glucose, therefore: hyperglycemic with insulin resistance (due to signaling or receptor probs)
-3 Ps (polydipsia, polyuria, polyphagia
How can metabolic acidosis lead to hyperaldosteronism?
when cells swap EC H+ for intracellular K+, they can get to a state of hyperkalemia, which induces release of aldosterone
Describe Type 2 DM
syndrome of metabolic obesity (adroid pattern)
- hyperinsulinemia (make a whole bunch of insulin)
- insulin resistance
Tx:
- metformin (biguanides: block GI Glu absorption, block gluconeogenesis, stimulate glucose intake)
- sulfonylureas: stimulate insulin production
- DPP-4: inhibit glucagon secretion and stim insulin prod
- SGLT2 inhibitor blocks glucose reabsorption
How do the kidneys interact with insulin?
They break it down
In case of renal failure –> hyperinsulinemia –>hypoglycemia
Tx for pts in diabetic kidney failure w/ electrolyte imbalence
DON’T GIVE ARB (mineralocorticoid receptor agonist or ACEI)
instead target aldosterone receptor (sprinolactone)
What is the effect of calcitriol on PTH? on Kidney? on Small intestine?
PTH: negative feedback
Kidney: stimulates Ca2+ reabsorption
Small intestine: Ca2+ absorption
What is the effect of PTH in kidneys?
stimulates Ca2+ reabsorption, PO4 elimination (blocks PO4 reabsorption), stimulates synthesis of calcitriol (bioactive Vit D)
What is the effect of calcitriol in small intestine?
stimulate Ca2+ reabsorption form diet
What is the effect of PTH on bone?
Reabsorption:
breaking apart Ca2+ and PO4 from salts to put back into circulation
NB: excess PO4 would promote the ppt of Ca2+. This effect is counteracted by renal effects of PTH
Where does Vit D synthesis occur?
proximal tubule epithelium
What is the effect of CYP27B1? What affects it?
CYP271B metabolizes 25-OH vit D (inactive) into 25-(OH)2D: Calcitriol (active
PTH stimulates it’s activity
Ca2+, hyperphosphatemia, and calcitriol downmodulate its activity
What are the mineral effects on urine after a surge of PTH?
hyperphosphateurea and hypocalcmiurea
What is the effect of amilorides?
block Na+ reabsorption in the CT
What are the effects of chronic kidney disease on calcium?
- inability to produce sufficient calcitriol (lose Ca2+ reabsorption in kidney and absorption in GI) –>
- hypocalcemia stimulates the release of PTH (SECONDARY HYPERPARATHROIDISM) –> stimulates PO4 and Ca2+ reabsorption in bone (can cause hyperphosphatemia, which has (-)fb on PTH production)
NB: Ca2+ increase does not stay in plasma because kidneys get the FL but can’t reabsorb it –> elevated Ca2+ excretion and metastatic calcifications
What are the signs and symptoms of hypoparathyroidism?
Loss of resistance to PTH
Labs: hypocalcemia, hyperphosphatemia, hypocaliurea
Symptoms: impaired neuromuscular function
Tx: give PTH, Vit D, and Ca2+
What is the countercurrent multiplier and exchange?
maintenance of medullary interstitial osmotic gradient
What is the significance of a decreased PRA:PAC ratio?
Primary hyperaldosteronism
What is the significance of a increased PRA:PAC ratio?
Secondary hyperaldosteronism
What are the functions of insulin? (what does it simulate? prevent?)
Promotes: STORAGE OF GLU IN SKEL MUSCLE, storage of fat, and storage of glucose in liver
Prevents: (general) lipoloysis and (liver:) glucogenolysis, gluconeogenesis
What is the effect of carbonic anhydrase IV?
(located within the apical membrane of the tubule epithelium)
CAIV maintains a favorable gradient for proton secretion
- catalyzes the dissociation of HCO3- into CO2 and OH-
CAII
catalyzes the formation of HCO3- from OH- and CO2-
What are the common states of K+ and Cl- in a pt with metabolic alkalosis?
hypokalemia; hypochloremia; HYPERGLYCEMIA (esp with hyperosmolality; if hyperglycemic with glucosuria, they will have polyurea)
