Renal Basic Facts Check Flashcards

1
Q

What expresses AT1R

A

efferent arteriole

JG cells

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2
Q

UV/P=

A

Clearance

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3
Q

Solute filtered/unit time

A

filtered load

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4
Q

What monitors GFR as tubular flow?

A

macula densa

TGF mechanism

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5
Q

What 3 things are used for hormonal compensation for hypotension?

A

aldosterone
AVP
Angiotensin II

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6
Q

What receptor is used for compensation for HTN?

A

AT2-R

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7
Q

What are pharmacologic targets for HTN?

A

AT1-R
Renin
Aldosterone
ENaC

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8
Q

What are the renal mineralocorticoid targets?

A

ENaC
ROMK
NHE3

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9
Q

What’s responsible for proximal tubule Na+ transport?

A

“Reabsorption”
SGLT
NHE3
Angiotensin II

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10
Q

What’s responsible for distal nephron Na+ transport?

A
"Reabsorption"
ENaC
NKCC
NHE3
Aldosterone
NCC
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11
Q

What is responsible for renal glucose handling?

A

“Reabsorption”
GLUT
SGLT

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12
Q

What is a Ca2+ sparing drug?

A

HCTZ

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13
Q

What is a K+ wasting drug?

A

HCTZ

Furosemide

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14
Q

What targets NKCC?

A

Furosemide

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15
Q

Name a mineralocorticoid antagoinist.

A

sprinolactone

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16
Q

What is responsible for renal excretion of H+?

A

NHE3
Aldosterone
NH4+

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17
Q

What condition is characterized by:

metabolic acidosis: aldosterone resistance?

A

Type 4 RTA

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18
Q

What condition is characterized by:

high plasma aldosterone with hyperkalemia?

A

pseudohypoaldosteronism

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19
Q

What condition is characterized by:

metabolic acidosis: glucosuria w/ euglycemia?

A

Type 2 RTA

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20
Q

What condition is characterized by:

euvolemic, hypovolemia, hypervolemic?

A

hyponatrimia

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21
Q

What condition is characterized by:

metabolic acidosis: defect in NH3 and carbonic anhydrase?

A

Type 2 RTA

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22
Q

What is the (potential) pathogenesis of salt-sensitive hypertension?

A

ouabain

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23
Q

What conditions can be neurogenic or nephrogenic?

A

DI and SIADH

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24
Q

What condition is characterized by:

elevated serum PTH with hypocalcemia?

A

secondary hyperparathyroidism

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25
What is synthesized in response to PTH?
calcitriol
26
If unchecked, what would cause hyperphosphatemia?
calcitriol or secondary hyperparathyroidism
27
If unchecked, what would cause hypoglycemia?
insulin
28
What is secreted in response to hyperglycemia?
insulin
29
What is a marker to monitor DM2?
hyperglycemia; Hb1Ac
30
What is used for glycemic control?
insulin
31
What are signs of DM2?
``` glomerular hyperfiltration microalbuminuria glomerulosclerosis hyperglycemia insulin resistance ```
32
What condition is characterized by: | hyponatremia w/ elevated urine specific gravity?
SIADH
33
What condition is characterized by: | polydipsia with polyuria?
DI and DM1
34
What condition is characterized by: | V2R loss of function?
SIADH | DI
35
What mediates distal H2O reabsorption?
AVP
36
What condition is characterized by: | dyslipidemia, hypoalbuminemia and proteinuria?
nephrotic syndrome
37
What condition is characterized by: | doubling of plasma creatinine?
acute kidney failure
38
Does aldosterone increase reabsorption/excretion of: Na+? K+? NH4+?
Na+: reabsorption K+: excretion NH4+: excretion
39
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)
40
What condition classically presents with glucose urea with euglycemia?
Type 2 (proximal ) RTA
41
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
42
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
43
What are the characteristics associated with hypoaldosteronism?
lowered aldosterone so less H+ secretion --> lowered pH --> HYPERKALEMIC METABOLIC ACIDOSIS
44
What is insulin's bioactivity at low concentrations?
Cellular K+ uptake (caution: treating someone with low K+ with insulin can lead to hypokalemia)
45
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
46
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
47
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
48
How do the kidneys interact with insulin?
They break it down In case of renal failure --> hyperinsulinemia -->hypoglycemia
49
Tx for pts in diabetic kidney failure w/ electrolyte imbalence
DON'T GIVE ARB (mineralocorticoid receptor agonist or ACEI) | instead target aldosterone receptor (sprinolactone)
50
What is the effect of calcitriol on PTH? on Kidney? on Small intestine?
PTH: negative feedback Kidney: stimulates Ca2+ reabsorption Small intestine: Ca2+ absorption
51
What is the effect of PTH in kidneys?
stimulates Ca2+ reabsorption, PO4 elimination (blocks PO4 reabsorption), stimulates synthesis of calcitriol (bioactive Vit D)
52
What is the effect of calcitriol in small intestine?
stimulate Ca2+ reabsorption form diet
53
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
54
Where does Vit D synthesis occur?
proximal tubule epithelium
55
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
56
What are the mineral effects on urine after a surge of PTH?
hyperphosphateurea and hypocalcmiurea
57
What is the effect of amilorides?
block Na+ reabsorption in the CT
58
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
59
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+
60
What is the countercurrent multiplier and exchange?
maintenance of medullary interstitial osmotic gradient
61
What is the significance of a decreased PRA:PAC ratio?
Primary hyperaldosteronism
62
What is the significance of a increased PRA:PAC ratio?
Secondary hyperaldosteronism
63
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
64
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-
65
CAII
catalyzes the formation of HCO3- from OH- and CO2-
66
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)