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Flashcards in PBL #2 Deck (21):
1

How do you interpret arterial blood gases?

  • pH
    • normal = 7.35 - 7.45
    • <7.35 →  Acidemia
    • >7.45 → Alkalemia
  • PCO2
    • normal = 34-45 mmHg (think 40)
    • <40 → respiratory alkalosis
    • >40 → respiratory acidosis
  • PO2
    • normal: >90 mmHg
    • <90 → hypoxia
  • HCO3-
    • normal = 22-32 mEq/L (think 24)
    • <24 → metabolic acidosis
    • >24 → metabolic alkalosis

2

How do you calculate the anion gap and relate it to the mechanisms of fluid and electrolyte disorders?

  • Anion Gap = Na+ – (Cl- + HCO3-)
    • normal = 8-12
    • Metabolic Acidosis with Anion Gap:
      • M: methanol
      • U: Uremia
      • D: DKA
      • P: Paraldehyde, Propylene Glycol
      • I: Iron pills, Isoniazid
      • L: Lactic acidosis
      • E: Ethylene glycol
      • S: Salicylates
    • Metabolic Acidosis with normal Anion Gap:
      • H: Hyperalimentation, post-Hypervenitlation
      • A: Addison disease
      • R: Renal Tubular Acidosis (RTA)
      • D: Diarrhea
      • A: Acetazolamide
      • S: Spironolactone
      • S: Saline infusion
    • Low anion gap think → Multiple Myeloma

3

What are the major body fluid compartments?

  • Human total body water= 60% H2O Males, 50% H2O Females
    • 2/3 of total H2O → Intracellular
    • 1/3 of total H2O → Extracellular
      • 3/4 of Extracellular H2O → Interstitial
      • 1/4 of Extracellular H2O → Intravascular (Plasma volume)
  • If 70 kg male: 
    • Total body water = 42 L
      • Total intracellular water = 28 L
      • Total extracellular water = 14 L
        • Total interstitial water = 11 L
        • Total intravascular water = 3 L

4

What is the role of osmotic and hydrostatic pressure in determining the volume of the major bodily fluid compartments?

  • Osmotic Pressure
    • will want to draw fluid into the capillary
  • Hydrostatic Pressure
    • will want to push fluid away/out of capillary
  • These two forces will balance each other out throughout the body with Albumin driving osmotic pressure primarily and your BP driving your hydrostatic pressure.
    • Only spot where these don’t balance out is in the renal corpuscle...driving filtration!

5

What is osmotic diuresis? When does it occur?

  • Occurs when the normal tight coupling between sodium and water reabsorption in the proximal tubule is disrupted.
    • Osmotic diuresis → 
      • increased urine flow due to abnormally high amount of any solute that is not reabsorbed (e.g. mannitol)
      • solute is filtered at such a high rate that much is left in the tubule (e.g. very high plasma glucose), leaving large amounts of solute in the lumen (INCREASE OSMOLARITY → More stuff)

 

6

What is the the physiology behind orthostatic hypotension?

  • Stand up → blood goes to legs, shifts out of central venous compartment to peripheral venous compartment → decreased stroke volume → decreased BP
    • Reflex to decreased BP → decreased baroreceptor firing → increased sympathetic nervous system → increased RAAS in kidneys & increased heart rate

7

What is the mechanism of Tm (transport maximum) transport of glucose?

  • Normally 100% of filtered glucose is reabsorbed in the proximal tubule 
    • BUT → Na+/Glucose transporters (SGLT's) have a saturation point = Transport maximum (Tm)
      • once this is reached, any additional glucose will NOT be reabsorbed → pee out in urine
        • Tm = 15 mM glucose → about 200 mg/dL
          • GLUCOSURIA!

8

Describe potassium homeostasis.

  • 98% is stored intracellularly
  • Low extracellular (plasma)
  • K+ Regulation:
    • Insulin → increases activity of Na+/K+ ATPase
      • drives K+ into cells
    • Catecholemines → activate ß2 receptors → stimulate Na+/K+ ATPase
      • drives Kinto cells
    • pH → increase [H+] → Hpumped into cells, Kpumped out to buffer metabolic acidosis after HCO3- is depleted
    • Exercise → muscle cells release K+
  • Renal excretion:
    • Passive movement of K+ into lumen driven by concentration gradient
    • Physiologic regulator: Aldosterone
      • ​stimulates Na+/K+ ATPase
      • increases presence of ROMK channel
        • Inhibited by Angiotensin II & Mg2+
    • BK channel present in High Kstates
  • Renal reabsorption:
    • Alpha-Intercalated cell in Collecting Duct
      • K+/H+ ATPase (H+ exchanged for K+)

9

What are the mechanisms and rationale for potassium movement across cell membranes in DKA?

  • Acidosis buffer mechanism:
    • After blood bicarbonate is depleted, compensation for low blood pH occurs by pushing H+ into cells → need to balance this incoming charge → K+ is antiported out into the serum → Hyperkalemia
    • occurs at the cost of her body cells losing their K+ → her cells are hypokalemic and K+ will need to be repleted during treatment

10

How does the respiratory system compensate for metabolic acid-base disorders?

  • Body wants to get rid of CO2 (acid)
    • to do this you breath more → Kussmaul breathing (rapid, deep, and labored breathing)
  • CO2 + H2O ⇔ H2CO3 ⇔ HCO3- + H+
    • Le Chatelier’s Principle
      • Breathe off some CO2, pull equation to the left → gets rid of H+, decreasing the acidity caused by ketoacids

11

The following are what type of insulin?

insulin lispro, insulin aspart, insulin glulisine

Rapid Acting (ultra rapid)

fast onset, very short duration

12

The following are what type of insulin?

Insulin glargine, Insulin detemir

Long Acting

(slow onset)

13

What type of insulin is NPH insulin?

Intermediate-acting

(not used very often)

14

What type of insulin is Regular Insulin?

Short acting

(slower onset than the rapid acting, but longer duration)

15

What are the signs and symptoms typical of diabetic ketoacidosis?

  • Kussmaul respirations (rapid/deep breathing)
  • N/V
  • abdominal pain
  • psychosis/delirium
  • dehydration
  • fruity breath (exhaled acetone)
  • Chief concerns: polyuria, polydipsia, polyphagia, fatigue, dyspnea, abdominal pain, N/V, HA, confusion, lethargy

16

What are the preventive care and disease-related risk management strategies appropriate for patients with diabetes?

  • cigarette smoking → cessation
  • blood pressure → <130/80
  • LDL  → <100 mg/dL
  • HDL → raise HDL (no set goal)
  • prothrombotic state → low dose aspirin therapy
    • (esp. patients with CHD and other risk factors)
  • glucose → HbA1C < 7%
  • overweight/obesity → decrease BMI
  • exercise prescription based on patient’s status
  • nutrition

17

What is the prevalence of Type I diabetes in the United States?

  • Prevalence of newly diagnosed Type I diabetes per 1,000 persons
    • 1.93 overall (95% CI 1.88-1.97)
    • 2.55 in whites (95% CI 2.48-2.62)
    • 1.62 in blacks (95% CI 1.5-1.75)
    • 1.29 in Hispanics (95% CI 1.21-1.37)
    • 0.35 in American Indians (95% CI 0.26-0.47)

18

What are the risk factors for Type I Diabetes?

  • high birth weight 
  • childhood obesity 
  • increasing maternal age at birth may be associated with increased risk of childhood type 1 diabetes

19

What is the role of genetics in Type I Diabetes?

  • Type 1 has a hereditary component but inheritance pattern is unknown.
    • Mutations in HLA-DR3 and HLA-DR4 are associated with increased risk of developing type 1 diabetes
      • (HLA complex helps the immune system distinguish the body’s own protein from proteins made by foreign invaders)
    • Onset of type 1 diabetes by age 60 years reported in 65% of monozygotic twins of persons with type 1 diabetes. This is based on cohort studies.

20

What is the mechanism of action of insulin, emphasizing receptors and signal transduction pathways?

  • Insulin binds to → Insulin receptors
    • Metabolic:
      • activation of phosphatidylinositol-3-kinase→  activation of serine/threonine kinase Akt
      • Akt activation → glucose transporter (GLUT) 4–containing vesicles into cell membrane → increases glycogen and lipid synthesis → stimulates protein synthesis through the activation of mTOR.
    • Mitogenic signaling pathway:
      • activation of Ras → cascade of activating phosphorylations in MAP kinase pathway → cell growth and proliferation.

21

What is the difference between primary gain and secondary gain?

  • Primary gain:
    • positive reasons to use treatments (take insulin→ not sick/acidotic)
      • e.g. Tx of medical condition
  • Secondary gain: 
    • reasons that a patient would want to NOT take treatment (no insulin → attention from boyfriend and others)
      • e.g. attention from boyfriend