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CVPR > Renal Week 2 > Flashcards

Renal Week 2 Flashcards

1
Q

Hyponatremia

A
  • low plasma concentration of sodium due to a deficit of sodium or a relative excess of water (Na less than 135)
  • osmoregulation accomplished via changes in water balance (excretion or retention) and intake (thirst)
  • Tonicity of ECF reflects tonicity of cells (because water freely moves between compartments)
  • In patients with normal renal function, excessive water intake alone does not cause hyponatremia unless it exceeds 1 L per hour
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2
Q

Two questions when determining the type of hyponatremia?

A

What is serum osmolality?

If hypotonic –> what is volume status?

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3
Q

Hypertonic Hyponatremia

A

(>300mOsm/kg)

shift of water from cells into ECF in response to non-sodium solute (elevated serum osmolality)

Often due to hyperglycemia or mannitol/glycerol administration

“Water shift” hyponatremia

Treat underlying uncontrolled diabetes → osmolality goes back to normal

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4
Q

Isotonic Hyponatremia

A

(280-399 mOsm/kg)

Often due to lab artifact caused by hyperlipidemia or hyperproteinemia that reduce plasma water

-direct measurement of serum Na by ion-sensitive electrode will yield normal value

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5
Q

Hypotonic Hyponatremia

A

(less than 280 mOsm/kg) “True hyponatremia”

–> Check volume status

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6
Q

Hypovolemic Hypotonic Hyponatremia

-Causes?
-ADH response?
Treatment?

A

volume contraction, low total body sodium

1) Renal loss (UNa>20)
Salt losing nephritis, mineralocorticoid deficiency, osmotic diuresis, diuretics

2) Extrarenal loss (UNa less than 20)
Hemorrhage, GI loss, excessive sweating

ADH released appropriately → water retention

Treatment: normal saline

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7
Q

Euvolemic Hypotonic Hyponatremia

Causes?

A

normal total body sodium, normal ECF volume

  • Usually due to inappropriate ADH secretion
  • ADH secretion increased despite absence of physiologic stimuli (Posm or decreased EABV)

EX) SIADH (syndrome of inappropriate ADH secretion), primary polydipsia, hypothyroidism, adrenal insufficiency

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8
Q

Euvolemic Hypotonic Hyponatremia

Treatment

A

hypertonic saline (if seizure)

If asymptomatic → water restriction, correction of underlying disorder, stop offending drugs

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9
Q

Hypervolemic Hypotonic Hyponatremia

A

increased ECF volume, increased total body sodium

Sign = Edema, rales

Urinary concentration of sodium can be less than or greater than 20 –> indicative of different causes

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10
Q

Hypervolemic Hypotonic Hyponatremia

UNa less than 20 →

ADH response?

A

UNa less than 20 –> CHF, cirrhosis, nephrotic syndrome

Reduction in volume sensed despite an absolute increase in total body salt and water
Cirrhosis → vasodilation, CHF → low CO

ADH released because reduced effective blood volume is sensed

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11
Q

Hypervolemic Hypotonic Hyponatremia

UNa>20 →

ADH response?

A

UNa>20 → ARF, SKD

Diluting mechanism in distal tubule does not work or RBF and GFR are too low

Can also be caused by thiazide diuretics that prevent dilution of urine (block Na/Cl cotransporter)

ADH independent

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12
Q

Treatment of Hypervolemic Hypotonic Hyponatremia

A 
Water and salt restriction (giving salt makes it worse!)
Loop diuretics (stop thiazides)
Inotropes for CHF
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13
Q

Hypernatremia

A

Disorders of concentrating ability

Na>145

Always associated with increased serum osmolality

Must ask what total body Na is (ECF volume)

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14
Q

Hypernatremia occurs due to…

A

1) ADH is decreased or ineffective
E.g Diabetes insipidus

2) Addition of hypertonic fluids (hypervolemic hypernatremia) - usually iatrogenic
3) Renal or extrarenal water losses exceed sodium loss (hypovolemic hypernatremia)

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15
Q

Hypernatremia with:

Decreased Total Body Na

A

total body water loss&raquo_space; total body salt loss

UNa>20 → renal loss
UNa

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16
Q

Hypernatremia with:

Normal total body Na

A

Due to ADH deficiency or resistance

No response to ADH –> Nephrogenic Diabetes insipidus

No ADH –> Central diabetes insipidus

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17
Q

Nephrogenic Diabetes insipidus

A

ADH resistance (renal duct does not respond to ADH)

Can be congenital (rare), or acquired from CKD, hypercalcemia, hypokalemia, drugs

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18
Q

Central Diabetes insipidus

A

ADH deficiency

Mostly idiopathic, but can be caused by head trauma, surgery, neplasms

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19
Q

Treatment of nephrogenic vs. central diabetes insipidus

A

Nephrogenic DI:
-NOT ADH responsive –> treat with large fluid intake and thiazide diuretic

Central DI:
-ADH responsive, treat with DDAVP

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20
Q

Hypernatremia with increased total body Na

A

RARE

-usually due to receiving hypertonic fluid

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21
Q

Symptoms of Hypernatremia

A

Neuromuscular irritability, seizures, coma, death

Very severe and deadly - high mortality rate, serious marker of underlying disease

Extreme thirst

Failure to thrive in infants

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22
Q

Treatment of hypernatremia

A

restore tonicity to normal and correct sodium imbalances
SLOWLY restore water deficits to prevent cerebral edema
Must calculate water needed

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23
Q

Equation for water needed

A

Water needed (L) = 0.6 x body weight (kg) x [(actual Na/140) - 1]

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24
Q

ADH secretion stimulated by: (2)

A

osmoreceptors (hypothalamus) + baroreceptors (aortic arch, carotid sinus → emergency volume sensors)

Severe volume depletion can cause hyponatremia

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25
Q

Normal renal concentrating mechanisms allow excretion of urine 4x as concentrated as plasma. Requires: (4)

A

1) Ability to generate hypertonic interstitium
2) Secretion of ADH
3) Normal Collecting Duct Responsiveness to Vasopressin
4) ADH: release stimulated by serum osmolality AND intravascular blood volume

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26
Q

Basic facts about sodium (4)

A

1) Sodium is most abundant solute in ECF
2) Sodium is more important determinant of ECF volume
3) Disorders of sodium balance = disorders of ECF volume
4) Maintenance of ECF volume determines MAP and LV filling volume

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27
Q

Afferent limb of ECF volume sensors

A

1) Low pressure baroreceptors
2) High pressure baroreceptors
3) Intrarenal sensors (JGA)
4) Hepatic and CNS sensors

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28
Q

Low pressure baroreceptors

A

cardiac atria receptors + LV receptors + pulmonary vascular bed receptors

On VENOUS side of circulation

Protect body against ECF volume expansion and contraction

Volume expansion → increased venous return → low pressure baroreceptors change discharge rate → decrease SNS → alter natriuresis, diuresis, HR and peripheral vascular resistance

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29
Q

High pressure baroreceptors

A

carotid sinus body and aortic body

  • On ARTERIAL side of circulation
  • Assess pressure of arterial circulation
  • Work to maintain MAP

Goal: normalize ECF volume in response to volume expansion or contraction

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30
Q

Intrarenal sensors (JGA)

A

Decrease in arterial pressure stretches membrane receptor → increase intracellular Ca2+ → increase renin secretion → increase sodium reabsorption

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31
Q

Physiological processes that serve to maintain GFR

A

1) Renal autoregulation
2) Tubuloglomerular feedback
3) Glomerulotubular balance

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32
Q

Renal autoregulation

A

ability of kidney to keep renal blood flow and GFR constant by contraction of vascular smooth muscle

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33
Q

Tubuloglomerular feedback

A

increased distal delivery of NaCl to macula densa → increases afferent arteriolar tone → return RBF and GFR towards normal

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34
Q

Glomerulotubular balance

A

property of kidney whereby changes in GFR automatically induce a proportional change in rate of proximal tubular sodium reabsorption

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35
Q

Humoral effectors that increase sodium reabsorption (antinatriuresis) (4)

A

Angiotensin II
Aldosterone
Catecholamines
Vasopressin

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36
Q

Humoral effectors that decrease sodium reabsorption (natriuresis) (4)

A

Natriuretic peptides
Prostaglandins
Bradykinin
Dopamine

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37
Q

Renal sympathetic nerves

A

SNS innervation of afferent and efferent arterioles of glomerulus

Activation → anti-natriuretic effect

Nerve stimulation enhances renin release from JGA

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38
Q

Causes of Extracellular volume contraction

A

Renal Causes

Non-renal causes: GI tract, dermal, third space fluid loss

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39
Q

Physiologic responses to extracellular volume contraction

A

preserve sodium and water

-cardiovascular and renal responses

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40
Q

Cardiovascular response to ECF volume contraction

A

Increased HR, increased cardiac inotropy, systemic vascular resistance, increased angiotensin II, increased ADH, increased endothelin

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41
Q

Renal response to ECF volume contraction

A
  • Decreased GFR → smaller filtered load of Na+
  • Activation of renal sympathetic nerves
  • Decreased hydrostatic pressure, and increased oncotic pressure in peritubular capillaries
  • Stimulation of renin-angiotensin-aldosterone system
  • Increased secretion of arginine vasopressin (AVP)
  • Inhibited secretion of ANP from atrial myocytes
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42
Q

Clinical Manifestations of ECF volume contraction

A 
Thirst, postural dizziness
Weakness, palpitations
Decreased urinary output, confusion
Weight changes
Orthostatic BP, tachycardia, hypotension
Decreased elasticity or turgor of skin
Dry mucous membranes
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43
Q

When ECF volume is contracted what are your serum values?

BUN, acid/base balance, albumin, Hct?

A

Increased BUN - plasma creatinine ratio

Metabolic alkalosis during upper GI loss of fluid or metabolic acidosis during lower GI loss of fluid

Increased hematocrit/serum albumin because of hemoconcentration

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44
Q

When ECF volume is contracted what are your urine values?

UNa
FE Na
Specific gravity
Osmolality

A

Urine sodium > 20mEq/L = Renal losses Urinary sodium less than 20mEq/L = Extra-renal losses

FE Na less than 1%

Specific gravity > 1.010

Urine osmolality > 300mOsm/Kg

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45
Q

Treatment of ECF volume contraction

A

expand ECF volume

**Replacement fluid should resemble lost fluid

Blood, albumin, and dextran solutions contain large molecules that preferentially expand intravascular volume

Isotonic normal saline preferentially expands ECF volume

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46
Q

3 Causes of ECF volume expansion?

A

1) Disturbed starling forces: CHF, nephrotic syndrome, cirrhosis
2) Primary hormone excess: primary hyperaldosteronism, Cushing’s syndrome, syndrome of inappropriate secretion of ADH
3) Primary renal sodium retention: acute glomerulonephritis

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47
Q

Formation and persistence of edema with ECF volume expansion due to…(3)

A

1) Alteration in Starling forces
2) Arterial underfilling resulting in decreased effective arterial circulating volume
3) Excessive renal sodium and water retention

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48
Q

Clinical manifestations of ECF volume expansion

A

Weakness, exercise intolerance, DOE

Weight gain

Orthopnea, LE edema, distended neck veins

Increased urination at night

Basilar pulmonary rales
CXR with fluid overload and cardiomegaly

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49
Q

Treatment of ECF volume expansion (3)

A

Carbonic Anhydrase → acts at proximal tubule - weak diuretic to reduce Na+ reabsorption

K+ Sparing → distal segment Na/Cl cotransporter blocker

Loop diuretic → block Na/K/Cl cotransporter

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50
Q

K+ actions at proximal convoluted tuble

A

K+ reabsorption (reabsorb 80% of filtered load)

K+ reabsorption is paracellular (through tight junctions), passive reabsorption (driven by basolateral transport of Na+)

NOT regulatable, not a major player from clinical perspective unless GFR is significantly reduced

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51
Q

K+ actions at descending limb of loop of Henle

A

K+ secretion

ADDS K+ into tubule → back up to 100% of filtered load at base of loop

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52
Q

K+ actions at ascending limb of loop of Henle

3 channels that make this happen?

A

K+ reabsorption (reduces K from 100% to 10-15% of filtered load)

Transcellular

  • Na/K/2Cl cotransporter at apical membrane → K+ into cell (secondary active transport) → some K+ leaks out of cell into tubule through K+ channel (apical membrane)
  • K/Cl channel on basolateral side (allows reabsorption of K and Cl)
  • Na/K ATPase on basolateral side → Na out/K in
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53
Q

K+ action at Cortical Collecting Tubule/Principal cells

A

K+ secretion –> K+ load back up to 100%

**KEY for regulating K+ excretion when GFR is relatively normal

-Most of K+ is obligatorily reabsorbed (only 10-15% remaining post distal convoluted tubule)

→ regulated K+ secretion in principal cells of fine tuning segments important in determining K+ excretion and ECF K+ balance

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54
Q

Regulators of K+ secretion in Cortical Collecting Tubule / Principal Cells

A

1) Mineralocorticoid receptors
2) Na+ delivery
3) WNK proteins

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55
Q

Effect of mineralocorticoid receptors in CCT

A

-regulates amount of activity of Na/K ATPase, Na and K channel

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56
Q

Why does Na+ delivery to CCT effect K+ secretion?

A

Can’t secrete potassium if there is no Na+ delivery to this distal nephron site - Na/K pump relies on high intracellular Na from Na entry via apical Na channel - without this, Na/K pump won’t be as good at bringing K into cell (K can then be secreted)
→ Hyperkalemia

due to…Hypovolemia, CHF, cirrhosis, etc.

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57
Q

Mechanisms of Na+ reabsorption and K+ secretion at CCT (principal cells)

A

Na+ reabsorption via apical Na+ channel (ENAC) → extruded via Na/K ATPase

Basolateral entry of K+ into cell + Apical secretion into tubular lumen

1) K+ secretion - Enters tubule via K+ apical channel
2) Na/K pump on basolateral side, pumps K+ into cell → K+ flows down electrochemical gradient into lumen and excreted in urine

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58
Q

Intercalated cells and K+ action

what transporter is responsible for this?

A

K+ reabsorption - between collecting duct and urine 50% of K+ reabsorbed

50% of K+ reabsorbed→K+ added into tubule at descending limb

K/H transporter (K in, H+ out)

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59
Q

Complete path of K+ reabsorption/secretion

glomerulus
proximal tubule
descending loop
ascending loop
cortical collecting tubule/principal cells
Intercalated cells
A

K+ is filtered freely (glomerulus)
Reabsorbed (Proximal tubule),
Then secreted (descending loop of Henle)
Then reabsorbed (ascending loop of henle/distal convoluted tubule)
Then secreted (Cortical collecting tubule / principal cells)
Then finally reabsorbed post collecting tubule (intercalated cells)

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60
Q

What is the effect of GFR on K+ secretion/reabsorption

A

GFR is a minor player

-no real impact until GFR is VERY low

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61
Q

Mass action effect in regulation of K+ secretion

A

first-line regulator of K+ secretion

Increase K+ in ECF → basolateral ATPase Na/K pump runs faster (K+ is a cofactor for the pump, and rate limiting step needed for ATP splitting) → increase in intracellular [K+]

Best for large changes in K+ concentration

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62
Q

When you increase K+ what happens to aldosterone levels?

A

Increased K+ → stimulate adrenal zona glomerulosa cells to synthesize aldosterone → increase secretion of K+

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63
Q

How does aldosterone increase the secretion of K+? (3)

A

ACTS AT CCT (principal cells)

1) Increase # of Na/K/ATPase pumps on basolateral surface → increase rate of K+ entry and [K+] intracellularly
2) Increase # of apical Na+ channels → increase apical K+ secretion, and movement of Na+ in
3) Increase # of K+ channels → easier for K+ to flow into lumen

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64
Q

What happens to K+ levels when you have:

1) no aldosterone or renin
2) ACEI
3) Spironolactone/eplerenon
4) Ameloride

A

1) No aldosterone or renin → can’t secrete K+ at cortical collecting tubule → hyperkalemic
2) ACEI → decrease K+ secretion → hyperkalemia
3) Spironolactone, eplerenone → Block aldosterone binding to mineralocorticoid receptor → hyperkalemia
4) Ameloride → blocks epithelial Na+ channel → hyperkalemia

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65
Q

Effect of loop diuretics on K+ levels

A
  • selectively inhibit ascending limb Na/K/Cl cotransporter
  • Causes massive increase in K+ secretion

Inhibition of Na/K/Cl cotransporter → make interstitium less hypertonic at descending limb and fine tuning segments → more water remains in tubule → increased tubular flow –> more K+ secretion

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66
Q

Effects of tubular flow on K+ secretion

A

Slow Tubular Flow → reduce K+ secretion

Fast Tubular Flow → increase K+ secretion

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67
Q

Why does slow tubular flow decrease K+ secretion

A

Buildup of K+ in tubular fluid before it is “washed away” by flow of tubular fluid downstream

As K+ lumen concentration rises, electrochemical gradient decreases → reduced secretion

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68
Q

Why does fast tubular flow increase K+ secretion?

A

K+ washed away really fast from apical side of membrane, so there is greater electrochemical gradient

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69
Q

How does alkalosis (increased pH) effect K+ balance

A

Increases K+ secretion → HYPOKALEMIA

Shift K+ into cells → reduce ECF [K+] and increase [K+] intracellular
→ increase driving force for apical K+ secretion into lumen → increase K+ secretion and increase K+ excretion → HYPOKALEMIA

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70
Q

How does acidosis (decreased pH) effect K+ balance

A

Shift K+ out of cells → inhibit apical K+ channels by lowered pH → decrease in K+ secretion

-can “depend”, unpredictable sometimes

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71
Q

Major determinants of urinary K+ excretion (4)

A

1) Normal distal tubule function (adequate Na+ delivery also)
2) Aldosterone activity (stimulate distal nephron K+ secretion - *most important)
3) Urine flow rate (increased flow rate, increase K+ excretion)
4) Delivery of non-reabsorbed anions to distal nephron

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72
Q

Factors that influence potassium shifts between intracellular and extracellular fluid spaces (6)

A

1) pH
2) Insulin
3) Adrenergic activity
4) Physical conditioning and exercise (leak K+ into ECF)
5) Cell membrane Na/K ATPase (Na out, K+ in)
6) Hyperosmolality (shift K+ out of cells)

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73
Q

plasma K+ _____ with acidemia (usually), and _____ with alkalemia

A

rises

falls

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74
Q

Effect of insulin on K+

A

first line defense against hyperkalemia, major regulatory of internal K+ balance

Increase plasma K+ → stimulate insulin release (K+ moves into cells even without glucose)

Insulin deficiency can cause rise in plasma K+ chronically (hyperkalemia)

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75
Q

Effect of adrenergic activity on K+ levels

A

B2 agonists (catecholamines) → stimulate entry of K+ into cells, major regulator of internal K+ balance

B-Blockers may potentiate hyperkalemia
A-agonists impair K+ entry into cells –> hyperkalemia

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76
Q

Potassium Adaptation

A

Relatively slow process that allows adaptation to gradually increasing amounts of K+ in diet

  • Rapid increase in K+ could be fatal
  • Involves aldosterone, insulin, and induction of Na/K ATPase in the renal tubular cells

Can be impaired in acute renal failure or in chronic renal failure when GFR is extremely depressed

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77
Q

Treatment of hypokalemia

A

Harder to treat than hyperkalemia

  • restore plasma and total body K+ to normal
  • Preferable to give K+ as oral supplements
  • Diuretics that reduce renal K+ excretion (spironolactone, triamterene, amiloride)
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78
Q

Consequences that hypokalemia

cardio and neuro?

A

worse than hyperkalemia

1) Neuro = weakness, paralysis
2) Cardio = atrial/ventricular arrhythmias (worse with digitalis), U waves on ECG

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79
Q

Acute causes of hypokalemia

A

CELL SHIFT

1) Catecholamine Excess - B2AR
- Medications - B2AR agonists
- Physiology - Stress
- Chest pain, asthma, alcohol or drug withdrawal

2) Insulin excess (Rare)

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80
Q

Causes of hypokalemia without K+ deficit (4)

A

1) alkalosis
2) familial hypokalemic periodic paralysis
3) B-adrenergic drugs
4) too much insulin

81
Q

Causes of hypokalemia with K+ deficit

A

1) Poor dietary intake
2) Cellular incorporation
3) *GI loss
4) Urinary loss
5) Excessive mineralocorticoid effect (too much aldosterone)
6) Renal tubular acidosis

82
Q

Causes of chronic hypokalemia

A

renal or extrarenal

differentiate with Urine K

  • Low (less than 20 Meq/L) → extrarenal
  • High (>20 Meq/L) → renal
83
Q

Hyperkalemia defined as serum K+ > ______

A

Serum K+ > 7.0, above 10 is often fatal

84
Q

Consequences of Hyperkalemia

A

Cardiac effects:

  • Push cell potential toward threshold →
    1) Tall T wave
    2) Wide QRS complex, flat P waves
    3) Sine wave QRST pattern with vfib or cardiac arrest

Neuromuscular effects: weakness, paralysis

85
Q

Pseudohyperkalemia

A

Caused by:
hemolysis of drawn blood, increased WBC or platelet count, tourniquet applied too tightly

Hyperkalemia in the test tube but not in the patient

Assess with ECG

86
Q

Causes of acute hyperkalemia (7)

A

CELL SHIFT

1) Digitalis intoxication
2) Acidosis
3) B-adrenergic block
4) A2 adrenergic agonists
5) Hyperosmolality
6) Inadequate insulin response (diabetes)
7) Ischemic/dead body part (rhabdomyolysis, intestinal or peripheral vascular arterial insufficiency)

87
Q

Chronic hyperkalemia - differentiate between the different types how?

A

Differentiate based on GFR

GFR less than 20 –> chronic or acute renal failure

GFR > 20 –> CHECK ALDOSTERONE LEVEL

88
Q

If GFR is > 20 how do you differentiate etiology based on aldosterone levels

A

Low aldosterone → check renin

  • renin Low → DM
  • renin High → adrenal insufficiency

High aldosterone → check urine Na

  • Low UNa → decreased Na delivery
  • High UNa → drugs, PHA
89
Q

Treatment of hyperkalemia (3)

A

K > 6.0 → medical emergency

1) Reverse depolarization with calcium infusion

2) Shift K+ into cells
- Glucose/insulin, B2 Agonists (albuterol, catecholamine), NaHCO3- infusion (move K into cells)
- K exchange resin (effective chronically)

3) Remove K+ from body:
Diuretics, hemodialysis

90
Q

Prevalence of HTN in the US and lifetime risk of developing HTN

A

80 million people in US and 1 billion people worldwide with HTN

90% lifetime risk of developing HTN if you are normotensive at age 55
-Systolic BP more important that DBP as a CVD risk factor

Only 35% of persons with HTN have their BP under control (below 140/90)

91
Q

Essential hypertension

A

single reversible cause of elevated BP CANNOT be identified - (90-95%) of HTN cases

92
Q

Causes of essential HTN

A

Environmental factors: high dietary NA, LOW GFR, excess caloric intake (obesity), alcohol, stress, sedentary lifestyle, smoking, low K+ or Ca2+ intake

Genetic factors (higher incidence in African Americans)

93
Q

Why does HTN occur due to an increase in SVR?

two hypotheses for explaining this

A

1) Guyton hypothesis

2) VSMC hypothesis

94
Q

Guyton Hypothesis (5 steps)

A

1) Primary defect in renal sodium excretion
2) Increase in plasma volume
3) Increase in CO → overperfusion of vital/nonvital organs
4) Autoregulatory increase in systemic vascular resistance (to maintain normal organ perfusion)
5) Increase in BP (afterload mediated normalization of CO)

95
Q

“Unwillingness to Excrete Na” Theory

A

humans with essential HTN possess a genetically determined impairment of kidney’s ability to excrete excess Na

96
Q

Vascular Smooth Muscle Cellular Hypothesis (5 steps)

A

1) Inhibit Na/K ATPase
2) Increase in vascular cell Na
3) Decrease in cell Na in/Ca out exchange
4) Increase in cell Ca → increase VSMC contraction
5) → Increase in systemic vascular resistance and increase in BP

97
Q

Salt and HTN

A

Modern diet is much higher in Na than we evolved to have

Excessive Na intake alone not sufficient to cause HTN

All Na absorbed in GI tract → kidney must excrete excess Na to prevent ECF volume expansion and maintain Na balance

Natriuresis = renal Na excretion

98
Q

Mechanisms of impaired natriuresis

A

1) Loss of nephron mass or impaired GFR
2) Activation of SNS and neurohormonal axis (increases renin, AgII –> Na and water reabsorption)
3) Abnormal blood vessel response to vasoconstrictors (increase afferent constriction –> decrease GFR)

99
Q

Secondary HTN

A

HTN caused by an identifiable mechanism (5-10%)

100
Q

Causes of secondary HTN

A

1) Renal causes:
- Parynchymal disease
- Renal artery stenosis

2) Other causes:
- Cushing’s, coarctation of aorta, sleep apnea, drug induced, thyroid or parathyroid disease
- Primary hyperaldosteronism
- Pheochromocytoma

101
Q

Stimuli for renin release (3)

A

1) Activation of B-sympathetic nerves
2) Stimulation of renal baroreceptors by decreased arteriolar pressure (due to renal artery stenosis)
3) Activation of macula densa chemoreceptor by reduced delivery of NaCl to distal tubule

102
Q

How does renal artery stenosis cause HTN?

A

1) decreased EABV sensed by kidney → abnormal activation of renin release by kidney
2) Renin: → AgI → AgII → bind AT1 and AT2 receptors
3) Raise arteriolar pressure by: direct arteriolar constriction and Na/water retention

103
Q

How to diagnose renal artery stenosis (4 steps/tests)

A

1) Elevated renin levels in blood
2) Doppler study of renal vasculature to visualize stenosis
3) CTA (contrasted study to visualize stenosis)
4) Angiogram - looking for pressure drop across the lesion (no pressure drop= not functional, pressure drop = functional)

104
Q

Treatment of renal artery stenosis

A

Due to atherosclerosis > 70% in renal artery → HTN

High BP with time causes damage to contralateral kidney which will maintain HTN even if original renal artery stenosis removed → TIMELY REPAIR IS CRITICAL

Percutaneous balloon dilation of renal arteries + anti-hypertensive medication

105
Q

Primary hyperaldosteronism

A

excess aldosterone secretion due to pathological defect in adrenal cortex → high aldosterone, low renin → expansion of ECF volume, suppression of plasma renin

106
Q

Two causes of primary hyperaldosteronism

A

1) Aldosterone producing adenoma

2) Idiopathic adrenal hyperplasia

107
Q

Aldosterone producing adenoma presentation and treatment

A

(UNILATERAL)

  • TX with unilateral adrenalectomy
  • NaCl administration will decrease aldosterone
  • Fludrocortisone → salt retention, decrease aldosterone
108
Q

Idiopathic adrenal hyperplasia presentation and treatment

A

(BILATERAL)

NaCl administration no change in aldosterone

Fludrocortisone → may or may not do anything, competes with aldosterone for receptor

TX with spironolactone (gynecomastia side effects)

109
Q

Pheochromocytoma

A

benign tumor of adrenal medulla → excess catecholamines → increase vascular resistance

110
Q

Target Organ Damage with HTN (5 main organ systems)

A 
Heart: LVH, angina or prior MI, prior coronary revascularization, HF
Brain: stroke, TIA
Chronic Kidney Disease
Peripheral arterial disease
Retinopathy
111
Q

Non-Pharmacologic Treatment of Essential HTN

A

STOP SMOKING, weight reduction, DASH eating plan, dietary sodium reduction, physical activity, moderation of alcohol consumption

112
Q

How do you treat a patient with prehypertension

A

(120-139) → no pharm, only lifestyle modification

Still associated with increased risk of CV events

113
Q

How do you treat a patient with Stage 1 HTN

A

140-159/90-99

Lifestyle + one or two drugs

Thiazide diuretic + may consider…
ACEI/ARB
Beta-Blocker
Calcium Channel Blocker

114
Q

How do you treat a patient with Stage 2 HTN

A

> 160/>100

Lifestyle + Two drug combination:

Thiazide diuretic + ACEI/ARB or BB or CCB

115
Q

Goals of HTN treatment

A

Treat BP to less than 140/90 or BP less than 130/80 with diabetes or chronic kidney disease

116
Q

2 medications that work on the proximal tubule

A

1) Mannitol

2) Acetazolamide

117
Q

Mannitol

mechanism of action

A

non metabolized, non-reabsorbed osmotic diuretic

Mechanism of action: elevates osmolarity of glomerular filtrate → hinder tubular water reabsorption, excess water excreted by kidneys

118
Q

Mannitol

uses (2)
adverse effects (1)
A

Use: management of intracranial pressure, glaucoma

Adverse effects: acute increase in ECF volume (because increases ECF osmolarity)

119
Q

Acetazolamide

mechanism of action

A

Carbonic Anhydrase Inhibitor

Inhibits regeneration of bicarb in proximal tubule → Na and bicarbonate loss
Induces metabolic acidosis (due to loss of HCO3-)

120
Q

Acetazolamide

uses (3)

A

glaucoma, prevention/treatment of high altitude sickness, metabolic alkalosis

121
Q

Loop diuretics

Names of drugs (3)

Mechanism of action

A

furosemide, torsemide, ethacrynic acid (non-sulfa)

Mechanism of action: inhibit Na/K/2Cl cotransporter in thick ascending loop of Henle → decrease tonicity of medullary interstitium → inhibit water reabsorption in collecting duct

122
Q

Loop diuretics

Uses (4)

A

volume overload –>
heart failure
BP reduction
pulmonary edema

Hypercalcemia

123
Q

Loop diuretics

Adverse effects

lowers what 4 ions?
increases what?
causes what acid/base problem?

A

Hypokalemia
Hypocalcemia
Hypomagnesemia
Hyponatremia

Uric acid retention → Precipitate gout attack

Metabolic alkalosis

124
Q

Thiazides

names (4)
Mechanism of action

A

hydrochlorothiazide, chlorthalidone, metolazone, indapamide

Mechanism of action: inhibit Na/Cl cotransport in distal convoluted tubule (less efficacious than loops because smaller portion of filtrate Na+ reabsorption remains)

  • Less efficacious than loop diuretics
  • Need more efficacious loop diuretic at GFR
125
Q

Thiazides

uses (2)

A

1) Antihypertensive effect secondary to decreased plasma volume and decreased CO
2) Secondary mild vasodilation

126
Q

Thiazides

Adverse effects

  • increases 3 things
  • decreases 3 things
  • and a problem with acid/base balance
A

Metabolic alkalosis

Hypokalemia
Hypomagnesaemia
Hyponatremia

Hyperuricemia → gout
Hyperglycemia
Hypercalcemia

127
Q

K+ sparing diuretics

names (2)
mechanism of action

A

Spironolactone, Eplerenone

Mechanism of action: aldosterone antagonist
Competitively inhibit mineralocorticoid receptor in collecting tubule → reduce Na reabsorption and K+ secretion

Eplerenone more specific (less gynecomastia)

128
Q

Uses of K+ sparing diuretics (4)

A

Hypokalemia
Heart failure
Hyperaldosteronism
Resistant Hypertension

129
Q

Adverse effects of K+ sparing diuretics (3)

A

Hyperkalemia
Gynecomastia
Amenorrhea

130
Q

Hydralazine and minoxidil do what?

mechanism of action

A

vasodilators (arterial)

increase intracellular cGMP → relaxation of arterial smooth muscle → decrease systemic pressure and contractility

Preferential dilation of arteries → increased renin secretion → reflex sympathetic discharge and sodium reabsorption

131
Q

Hydralazine and minoxidil

adverse effects (5)
uses (2)
A

Adverse Effects:
Edema, tachycardia, neuropathy
Lupus rash (hydralazine)
Hair growth (minoxidil)

Uses:
HTN, heart failure

132
Q

ACE inhibitors

names?
Mechanism of action

A

Lisinopril, enalapril, “-pril”

Mechanism of action: inhibit ACE enzyme, prevent conversion of AgI → AgII

  • Prevent AgII vasoconstriction and stimulation of aldosterone release
  • No effect on non-ACE controlled pathways
  • Reduce aldosterone levels, reduce breakdown of bradykinin
133
Q

ACE inhibitors

use

A

1st line therapy for HTN, CKD, HF, DM nephropathy

134
Q

ACE inhibitors

adverse effects (5)

A

Cough (Secondary to increase in bradykinin and substance P)

Hyperkalemia

Rise in serum creatinine (transient, due to dilation of efferent arteriole)

Contraindicated with bilateral renal artery stenosis

Angioedema (allergic rxn)

135
Q

ARBs

Mechanism of action

A

Mechanism of action: block AngII at AT1 receptor → prevent AgII mediated vasoconstriction and aldosterone release

  • Reduce aldosterone levels
  • No effect on Bradykinin
136
Q

ARBs use

A

1st line therapy for HTN, CKD, HF, DM nephropathy

137
Q

ARBs adverse effects (3)

A

Adverse Effects:

  • Hyperkalemia
  • Rise in serum creatinine (transient, dilation of efferent arteriole)
  • Angioedema
138
Q

Terazosin, doxazosin, prazosin do what?

A

alpha-1 receptor antagonists

139
Q

Alpha-1 Receptor Antagonists: (terazosin, doxazosin, prazosin)

mechanism of action

A

Peripheral postsynaptic blockade → decrease in arterial tone

Relaxes smooth muscle of bladder neck

140
Q

Alpha-1 Receptor Antagonists: (terazosin, doxazosin, prazosin)

use (1)

A

primarily for BPH

141
Q

Alpha-1 Receptor Antagonists: (terazosin, doxazosin, prazosin)

Adverse effects (5)

A

Postural hypotension, dizziness, somnolence, impotence, nasal congestion/rhinitis

142
Q

Clonidine and methyldopa do what?

A

central alpha-2 receptor agonists

143
Q

Alpha-2 Receptor Agonists: Clonidine, Methyldopa

Mechanism of action

A

Mechanism of action: centrally acting agent, stimulate alpha-2 receptors in CNS and periphery→ decreases sympathetic tone, decreases PVR and CO, inhibit peripheral NE release

-Methyldopa safe in pregnancy

144
Q

Alpha-2 Receptor Agonists: Clonidine, Methyldopa

Adverse effects (5)

A

dry mouth, depression, lipid abnormalities, sedation, orthostatic hypotension

145
Q

Alpha-2 Receptor Agonists: Clonidine, Methyldopa

Uses (4)

A

HTN, ADHD, smoking cessation, ETOH withdrawal

146
Q

Sodium Nitroprusside

Mechanism of action
onset, duration

A

Mechanism of action: nitric oxide donor which activates endovascular guanyl cyclase causing myosin dephosphorylation and vascular smooth muscle relaxation

→ arterial and venous dilation

Onset in seconds
Lasts only 1-2 minutes

147
Q

DHP calcium channel blockers

names?
effect?

A

amlodipine, felodipine, -dipine

Block L-type calcium channels (selective for vascular LTCC) –> potent vasodilators with no effect on cardiac contractility or conduction

148
Q

Adverse effects of DHP (4)

A

Reflex tachycardia
Headache
Peripheral edema (due to vasodilation)
Gingival hyperplasia

149
Q

Uses of DHPs (2)

A

1) HTN - Good 2nd line agents for BP reduction especially in African Americans, elderly
2) Migraine prophylaxis

150
Q

Non-DHPs

names?
effect?

A

verapamil, diltiazem

Block LTCC, more cardioselective, less potent vasodilators

Verapamil efficacy > diltiazem

Cardiac effects: decrease cardiac contractility, decrease SA node automaticity, decrease AV node conduction

151
Q

Adverse effects of non-DHPs (5)

A

Constipation
Bradycardia
Nausea
Conduction defects

-inhibits CYP450 –> drug interactions

152
Q

Uses of non-DHPs (4)

A

primarily reserved for negative inotropic activity

Angina
Rate control for AFIB
Migraine prophylaxis
HTN

153
Q

atenolol, metoprolol, bisoprolol, and nebivolol are beta blockers with what selectivity?

A

cardio selective - B1 receptors

-no alpha blockade

154
Q

propanolol and timolol are beta blockers with what selectivity?

A

non-selective B1 (cardiac) and B2 (bronchial/vascular)

155
Q

Labetolol and carvedilol are beta blockers with what selectivity

A

beta and alpha blocker

Provides extra antihypertensive effect - no cardioselectivity, has a-blockade

156
Q

Adverse effects of B-blockers (5)

A

Decrease libido, bradycardia, bronchospasm, glucose/lipid changes, fatigue

157
Q

Normal pH range

A

7.35-7.45

158
Q

60 kg person → add __ mEq of H+ to ECF every day

A

60

159
Q

Total bicarb in ECF = ___ mmol → only a ___ day supply of ECF bicarb available (60-70 mmol destroyed every day)

A

360 mmol

5-6

160
Q

Carbon dioxide

A

“volatile” gaseous acid

1.Eliminated by lungs effectively under normal conditions

161
Q

Organic acids

A

(e. g. Lactic and citric acid)

1. Metabolized to neutral products (glucose, water, CO2)q

162
Q

Metabolism and acids

A

generates “nonvolatile acid” from proteins and nucleic acids

  1. Proteins (sulfur containing amino acids) → Sulfuric acid (H2SO4)
  2. Nucleic acids → Phosphaturic acid (H3PO4)
  3. Must be eliminated by the kidneys
163
Q

Buffering of nonvolatile acid

A

buffers bind H+ but H+ is NOT ELIMINATED - goal is to prevent H+ from binding to vital proteins in heart/brain

164
Q

Bone as a buffer

A

Bone (acidosis → suppress osteoblasts, stimulates osteoclasts → release Na, K, CO3 2- and HPO3- from bone)

165
Q

Bicarb buffering system

A

buffers and eliminates H+ from the body

  1. H+ + HCO3- → H2CO3 → CO2 + H2O (removed by lungs)
    - Low CO2 required to drive rxn to right (high CO2 stimulates hyperventilation → blow down CO2)
  2. Convert nonvolatile acid to a gaseous volatile form that can be eliminated rather than simply buffered
  3. Elimination of each H+ requires the “suicide” destruction of a bicarbonate anion → bicarbonate lost in elimination of acid must be continually replaced
166
Q

CO2 can build up at the tissue level if: (2)

A

1) Rise in metabolic rate without proportional increase in blood flow

2) Decrease in blood flow without a change/decrease in metabolic rate
→ impairs function of BBS → less H+ removed → H+ binds proteins and disrupts function

167
Q

Role of kidney in maintenance of bicarb levels (3)

A
  1. eliminate acid ions
  2. Reabsorption of filtered bicarb
  3. Synthesis of bicarb
168
Q

Kidney role in elimination of acid anions

A

Acid anions that produce hydrogen ions (HSO4-, H2PO4, etc.) must be eliminated → filtered at glomerulus and excreted in urine

169
Q

Reabsorption of filtered bicarb in kidney

A

Bicarb anion freely filtered (small solute) → needs to be avidly reabsorbed

85-90% of filtered load of bicarb reabsorbed in proximal tubule

170
Q

Two pumps involved in reabsorption of bicarb and how they function

A
  1. Sodium-Hydrogen Exchanger (NHE): in apical membrane
    - H+ secreted from inside cell → lumen of tubule
    - Once in lumen, combines with bicarb → H2CO3 → CO2 and H2O
    - CO2 then diffuses into cell
    - CO2 + H2O in cell → (via carbonic anhydrase) H2CO3 → H+ + HCO3-
    - H+ excreted into tubule via NHE
    - HCO3- into blood via NBC
  2. Sodium-Bicarb Cotransporter (NBC): on basolateral angle transports Na and HCO3- into blood
171
Q

End result of bicarb reabsorption

A

**No net gain/loss of ECF H+ or HCO3-

i. DOES NOT change ECF acid/base balance
ii. Filtered bicarb is simply reabsorbed to ECF while H+ is secreted into urine
iii. BUT impaired proximal bicarb reabsorption will result in a proximal renal tubular acidosis (RTA) due to net loss in bicarb

172
Q

Bicarb synthesis

A
  1. Kidneys synthesize bicarb to replace exactly what is lost in acid elimination process (every H+ excreted/secreted, HCO3- generated)
  2. Done by epithelial alpha intercalated cells of collecting duct
    a. Generates NET increase in H+ → acidifies urine
173
Q

After new bicarb is synthesized, which results in H+ increase in tubule, what happens?

A

MUST buffer urine because H+ pumped into urine in collecting duct

174
Q

How is the H+ buffered in bicarb synthesis? (2)

A
  1. Titratable acid

2. Ammonia trapping

175
Q

Titrateable acid and H+ trapping

A

complexing hydrogen ion to a filtered acid anion (HPO4 2-) or other buffers (creatinine, urate)

i. Only 30-40 mmol H+ titrated this way (half)
ii. Constant

176
Q

Ammonia trapping

A
  1. NH3 diffuses easily through apical membrane → binds H+ in tubule → NH4+ that is “trapped”

i. Ammoniagenesis: in proximal tubule cells
- Glutamine metabolized to NH3 and bicarbonate
- NH3 binds H+
- Bicarb added to peritubular capillary

  1. Process augmented by high intracellular [H+] in proximal cells (chronic acidosis or hypokalemia)
  2. Can be increased up to 200 mmol of H+ buffering per day
177
Q

Daily bicarb reabsorption > ____ mmol, daily bicarb synthesis = ____ mmol →

A

> 4000 mmol
60-70

no bicarbonate synthesis can take place until bicarbonate reabsorption is complete upstream
- As long as there is HCO3- in tubular lumen, bicarb will be reabsorbed but will not be synthesized

178
Q

Net acid excretion (NAE):

A

balances nonvolatile acid production

i. NAE = NH4+ excretion + titratable acid excretion - HCO3- excretion
1. Normal conditions:
a. 40-50% of NAE is titratable acid (constant), 50-60% of NAE is NH4+ excretion (can increase), and bicarb excretion is zero

179
Q

Renal response to metabolic acidosis

A

a. Increases number of apical H+ transporters and basolateral HCO3- transporters → increase H+ secretion capacity available for HCO3- synthesis

b.Increase buffering with HCO3- →
1) Increased CO2 production → elimination of CO2 by lungs
2) Increased destruction of HCO3-
→ decrease filtered load of HCO3- → decreases H+ secretion required for HCO3- reabsorption → increase H+ secretion capacity available for HCO3- synthesis

c.→ Increased HCO3- synthesis, replenishment of lost HCO3-

180
Q

NAE: metabolic acidosis

A

a. NH4+ excretion increases
b. Titratable acid excretion unchanged
c. Bicarb excretion remains zero

181
Q

Renal response to respiratory acidosis

A

Refer to Mady Lion’s notes: search renal response to respiratory acidosis (complicated chart)

182
Q

Renal response to chronic metabolic acidosis

A
  1. Bicarb excretion increases (up to 80 mmol/day)
    a. Decreased reabsorption
  2. NH4+ and titratable acid excretion decreases
183
Q

Respiratory alkalosis

A

Decreased ECF CO2 → decreased H+ → decreases number of apical H+ transporters and basolateral HCO3- transporters

184
Q

Hypokalemia and plasma pH

A

in response, K+ shifts out of cells into ECF, and exchanges with H+ which shifts into cells

  1. More intracellular H+ available in renal tubules for secretion
  2. Increased ammoniagenesis → more H+ trapping and excretion
  3. Intercalated cells will preferentially reabsorb K+ and secrete H+
    a. Via H+/K+ ATPase on apical membrane
  4. More H+ secretion/excretion = more HCO3- synthesis
  5. PREDISPOSES TO METABOLIC ALKALOSIS
    a. Alkalosis → hypokalemia and hypokalemia → alkalosis
185
Q

Hyperkalemia and plasma pH

A

in response K+ shifts into cells from ECF, and exchanges with H+ out of cells

  1. Less intracellular H+ available in renal tubules for secretion
  2. Decreased ammoniagenesis → less H+ trapping and secretion
  3. Less H+ secretion/Excretion = Less HCO3- synthesis
  4. PREDISPOSES TO METABOLIC ACIDOSIS
    a. But hyperkalemia stimulates aldosterone → increases H+ secretion and HCO3- synthesis
    i. Counteractive
186
Q

Metabolic acidosis compensation assesment

A

expected CO2 = 1.5x[HCO3-] + 8 +/- 2

  1. Compensation adequate → “SIMPLE”
  2. Compensation inadequate → “MIXED”
  3. COMPENSATION IS ALWAYS THE SAME DIRECTION AS PRIMARY CHANGE
187
Q

Respiratory alkalosis (including compensation assessment)

A

always due to hyperventilation

  1. Anxiety, fever, pain, lung disease, liver disease, sepsis, brain disease, pregnancy
  2. Acute or chronic (before or after renal compensation)
    a. Acute = Change in HCO3- = decrease 2:10 PCO2
    b. Chronic = change in HCO3- = decrease 4:10 PCO2
188
Q

Respiratory acidosis (including compensation rules)

A

breathing too little

  1. Neuro problem, muscle fatigue, aspiration, pneumonia, COPD, ILD, hypokalemia, hypothyroidism
  2. Acute or chronic (before or after renal compensation)
    a. Acute = Change in HCO3- = decrease 1:10 PCO2
    b. Chronic = change in HCO3- = decrease 4:10 PCO2
189
Q

Metabolic alkalosis

A

increased pH, increased HCO3-

190
Q

Causes of metabolic alkalosis (5)

A

1) Addition of bicarbonate (antacids)

2) Contraction alkalosis (loss of chloride rich fluids)
- Vomiting, ng suctioning, diuretics
- Lose water, which essentially increases [HCO3-]

3) Loss of hydrogen (GI, renal)
- Renal losses due to diuretics or mineralocorticoid excess
- H+ excretion causes HCO3- resorption

4) Post hypercapnia
- Development of metabolic alkalosis in a patient with chronic respiratory acidosis who is being mechanically ventilated → rapid lowering of CO2 with high bicarb

5) Hypokalemia

191
Q

Maintenance of metabolic alkalosis

A

always the kidney’s fault - unable to excrete excess bicarb

a.Chloride depletion → resorption of bicarb

b. Increased mineralocorticoid activity
- Mineralocorticoids stimulate H+-ATPase pump of intercalated cell in distal tubule → more H+ secretion and bicarb reabsorption → maintains alkalosis

c.Hypovolemia - commonly accompanies metabolic alkalosis
→ aldosterone release

192
Q

Chloride responsiveness vs unresponsiveness in metabolic alkalosis

A

UCl less than 20mEq –> chloride responsive
-Due to loss of intravascular volume (diuretics, vomiting, CF, congenital chloride losing diarrhea)

UCl > 20 mEq → chloride resistant
-Due to excess mineralocorticoids (hyperaldosteronism, Cushing’s, Licorice ingestion)

193
Q

Metabolic acidosis

A

reduction in bicarb and pH

1.Kidney must handle daily acid load of 60mEq H+, which consumes 60 mEq of HCO3-

194
Q

What happens in the proximal and distal tubule in metabolic acidosis

A

Proximal tubule → reabsorb HCO3-

i.Carbonic anhydrase inhibitors (acetazolamide, topiramate) → excretion of bicarb

Distal tubule (Collecting duct)

i. Principal Cell:
1. ENaC brings Na into cell
2. RomK allows K+ to flow out into tubule
3. Na pumped into blood via Na/K ATPase on basolateral membrane
ii. Intercalated Cell:

  1. Secretes H+ (H+ ATP pump)
  2. Makes HCO3-
  3. Acidifies urine
  4. Excretes daily acid load
195
Q

Non anion gap metabolic acidosis

A

loss of bicarb causing metabolic acidosis

a. Loss of bicarb typically from GI or kidney
- Renal loss of bicarb = + urine anion gap
- GI loss of bicarb = negative urine anion gap

b.Can result in renal tubular acidosis

196
Q

Renal tubular acidosis

A

Proximal → problem with reabsorption of bicarb at proximal tubule

    • urine anion gap

Distal → unable to excrete H+ → can’t produce HCO3-
- + urine anion gap

Hyperkalemic → increased K+ inhibits NH3 production
- + urine anion gap

197
Q

Anion gap metabolic acidosis

A

caused by addition of acid (not CO2) that uses up HCO3-

a. Anion gap “increased” when it is > 18
b. MUDPILES

i. Methanol
ii. Urate (renal failure)
iii. DKA (ketones)
iv. Propylene glycol
v. Isoniazid
vi. Lactate (hypoxia)vii.Ethylene glycol, Ethanol
viii. Salicylate (ASA)

198
Q

Utility of serum and urine anion gap

A

can be used to determine if renal acid excretion (new bicarbonate generation) is appropriate

199
Q

Urine anion gap

A

If metabolic acidosis present, NH4+ production should increase

  1. Urine anion gap = Na+ + K+ - Cl-
    a. NH4+ production increased → urine Cl- should also increase to maintain electroneutrality
  2. Negative urine anion gap suggests NH4+ production is occurring in kidney → non-anion gap metabolic acidosis due to GI loss
  3. Positive urine anion gap → renal NH4+ production impaired, RTA present

CVPR (12 decks)

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