H20/NA Blance; Na/K+ Balance Flashcards

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1
Q

How does ANP affect ECF Volume and Osmolarity?

A

ANP stimulates decrease in ECF volume and osmolarity by increasing H2O/Na+ excretion

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2
Q

How do control of RAAS and ANP differ from ADH?

A

RAAS and ANP depend on changes in body volume while ADH release largely depends on plasma osmolarity

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3
Q

Differentiate Positive vs Negative Na Balance.

A

Positive Na Balance: ExcretionIntake

  • DEC ECF volume
  • DEC BP
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4
Q

What are characteristic of all Natriuretic peptides?

A
  • similar Renal, vascular, and RAAS suppression effects
  • Derive from prohormone
  • Cause INC cGMP
  • Short half life (3-20 min) by Vasopeptidases
  • Internalizes via receptor-edited endocytosis
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5
Q

What secretes renin?

A

Granular cells of the JG apparatus

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6
Q

What is the major stimulator of renin secretion? What are three factors which increase release?

A

Decreased pressure in Afferent arterioles

  1. Low perfusion pressure n afferent arteriole
  2. Low tubular flow in macula densa
  3. Highs sympathetic activity
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7
Q

What are the functions of Angiotensin II?

A
  • Release of Aldosterone
  • Release of AHD
  • Increase tension in systemic blood vessels

***Very Potent vasoconstrictor

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8
Q

What type of chemical is the Latin American Pit Viper venom?

A

Ace Inhibitor (Captopril)

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9
Q

What role does Ace play in the trachea, lungs and diaphragm. How would ACE inhibitors affect this?

A

ACE breaks down bradykinin

Increased Bradykinin —> Vasodilation and inflammation of airways

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10
Q

What are significant side effects of ACE Inhibitors?

A
  • Coughing
  • Angiodemeda
  • Dysgeusia
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11
Q

What are the stimuli for Aldosterone?

A

Major:

  • High plasma angiotensin II
  • High plasma K+

Minor:

  • Acidosis
  • Hyponatremia
  • ACTH
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12
Q

What are the physiological actions of Aldosterone?

A
  1. Na+ Reabsorption
  2. K+ Secretion
  3. H+ Secretion
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13
Q

What type of hormone is aldosterone? What type of receptor does is bind?

A

Steroid mineralcorticoid hormone

Cytoplasmic receptor

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14
Q

What is Conn’s Syndrome?

A
  • Primary hyperaldosteronism
  • Renin-Independent aldosterone overproduciton
  • INC ECF volume
  • Hypervolemia, hypertension, hypernatremia, Hypokalemia, and metabolic alkalosis
  • May exhibit “Aldosterone escape” —> Polyuria and Reduced nHypertension
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15
Q

What are the different types of Hypernatremia?

A

Conns Syndrome: INC body Na+

Diabetes insipidus: Low Body water; Normal Na+

Heat stroke: Low Na and Lower H20

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16
Q

Describe Secondary hyperaldosteronism

A
  • Renin-dependent
  • ex. Renal artery stenosis
  • Renovascular hypertension
17
Q

What is Bartter’s Syndrome?

A
  • Mutation in Na/K/2CL transporter
  • Hypokalemia, Hypercalceuria, Polyura

*similar to symptoms of abuse of loop diuretics

18
Q

What is the use of loop diuretics for?

A
  • Decrease positive lumen charge

- DEC paracellular trans sport of Ca and Mg

19
Q

Describe Addisons Disease

A
  • Primary adrenal cortical hyposecretion
  • Low aldosterone and cortisol
  • Weight loss, dehydration
  • Hypotension, hypovolemia, postural hypotension
  • Abnormal cutaneous pigementation
  • GI disturbance
  • Hyper pigementation
20
Q

What is Liddell syndrome?

A
  • Pseudohypoaldosteronism
  • Amiloride Sensitive NA channels are defective (Hyperactive) —> Hypokalemia
  • Autosomal dominant
  • Severe hypertension with Hypokalemia
21
Q

What is normal K+ levels?

A

3.5 - 5.5 mEq/l

22
Q

What promotes K+ secretion in the distal tubule and collecting duct?

A
  • High dietary K+
  • Aldosterone
  • High filtrate flow rate
23
Q

Which cells are dependent on the state of K+ balance, and which secrete or absorb K+?

A

Secretion: Principal cells in cortical collecting duct and outer medulla

Reabsorption: H/K ATPase in alpha-intercalated cells of inner medullary collecting ducts

24
Q

What is the function of Thiazides diuretics?

A

Inhibit Na/Cl symporter in early distal tubule

25
Q

What is the function of Amiloride and spironolactone?

A
  • Close Na channels on apical membrane

- Inhibit Na/K ATPase in principal cells

26
Q

How do Insulin and B2-Agonists affect K+ Balance. Clinical implications?

A

Insulin + B2Ags —> K+ into Cells

Diabetes mellitus —> Excess insulin —> Hypokalemia

27
Q

Describe Crush Syndrome

A
  • BReakdown of cell on massive scale results from elevation of some substances and ions in blood

(Hyperkalemia)

28
Q

How does abnormal potassium affect the T wave on electrocardiograph?

A

Hyperkalemia —> INC height of T Wave

Hypokalemia —> Inverts T Wave

29
Q

How can Hyperkalemia be treated?

A
  • Administration of NaHCO3