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FDN Week 5 (Block 2) > Dr. Winter Labs > Flashcards

Dr. Winter Labs Flashcards

1
Q

What is the is the differential diagnosis of afebrile, tachycardia, groggy, abnormal focal neurological findings and seizure.

A

Several options:

  1. Metabolic abnormalities
  2. CNS pathologies
  3. Toxicology
  4. Infection
  5. Onset epilepsy
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2
Q

When checking for metabolic causes what lab studies should be run?

A

Check for Na+, Glucose, Calcium - all of which can be the source of seizures.

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3
Q

What are diabetics more afraid of hyper or hypoglycemia?

A

Hypo - it in the short term is far more dangerous.

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4
Q

What are adrenergic symptoms?

A

The are a set of symptoms that are the result of hypoglycemia and are the result of adrenal gland release of adrenalin.

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5
Q

What are the clinical presentation of hypoglycemia?

A

Adrenergic and Neuroglycopenia

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6
Q

What are examples of adregenic symptoms?

A

Tachycardia, palpitations, pounding heart, sweating, anxiety, nervousmess.

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7
Q

What is neuroglycopenia?

A

The consequences of hypoglycemia on the CNS.

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8
Q

What are examples of neuroglycopenic symptoms?

A

faintness, headache, confusion, hunger, blurred vision, parasthesias (tingling, pins and needles)

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9
Q

How do we establish diagnosis of hypoglycemia?

A

glucose = <45mg/dL

Symptoms

Response to glucose administration

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10
Q

What is the difference between - whole blood, plasma and serum.

A

Plasma = 55% mostly water and contains proteins, minerals, clotting factors and minerals and hormones.

Serum = Plasma without the clotting factors or fibrinogen

Whole Blood = Unmodified blood other than the addition of an anticoagulant

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11
Q

What is the clinical indication for hypoglycemia?

A

Draw blood to perform study

Administer IV glucose

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12
Q

What is the cause of hypoglycemia?

A

The best thing to check for is hyperinsulinism. This would drive down of blood sugar.

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13
Q

What are the two types of hypoglycemia?

A

hyperinsulinemic hypoglycemia

&

non-hyperinsulinemic hypoglycemia

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14
Q

How do we determine if it is hyperinsulinemic hypoglycemia?

A
  1. elevates insulin levels for fasting reference interval
  2. The I/G ratio is off >0.3

**In general you probably shouldn’t be able to measure insulin levels if hypoglycemia is present.

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15
Q

Why might someone have high levels of insulin and be hypoglycemic?

A

Excess endogenous insulin = beta cells stimulation

Excess exogenous insulin = Injection of insulin

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16
Q

How do we determine if the insulin is endogenous or exogenous?

A

Look for the c-peptide. When insulin is manufactured in the body one of the products of endogenous insulin production.

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17
Q

If the reason for hypoglycemia is excess insulin and it is not injected but released from the pancreas how do we determine if it is drugs or pancreatic?

A

Check for drug history, urine test for drugs.

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18
Q

If it turns out that we are hypoglycemic due to hyperinsulinism and it isn’t drugs what do we check for?

A

Insulinoma

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19
Q

What are the characteristics of insulinoma?

A
  • beta cell tumors of islet
  • 90% benign
  • Uncommon
  • Usually single tumors
  • Symptoms can be around from weeks to years.
20
Q

How are insulinomas treated?

A

Resection and chemo (if malignant)

21
Q

If you are hypoglycemic and it is not because of hyperinsulinism what are the dx?

A

You are not making glucose in the liver. Interference with gluconeogenesis by other liver pathologies.

22
Q

During apnea what happens to pCO2?

A

It increases (no excreting CO2)

23
Q

What is minute ventilation?

A

MV = TV x RR

tidal volume x respiratory rate

24
Q

What happens when MV drops?

A

pCO2 increases so we see a drop in pH (acidity)

25
Q

If we are retaining CO2 and our pCO2 is up can we rule out also having metabolic acidosis?

A

No. We need to look at electrolyte measurements and the anion gap to know if we are dealing with a combination of respiratory and metabolic.

26
Q

In the case of apnea that causes respiratory acidosis what happens if breathing doesn’t start?

A

Anaerobic respiration –> lactic acid –> metabolic acidosis in conjunction with respiratory.

27
Q

When someone has respiratory alkalosis what happens to pCO2?

A

We would expect to see a small decrease / no change.

28
Q

When someone has combined respiratory and metabolic alkalosis what do we expect to happen with pCO2 and HCO3?

A
29
Q

When calculating BSA (body surface area) what do we use?

A

We use a normogram: Draw a line between height and weight to calculate M^2 in 1500xM^2 /day

30
Q

How do we calculate fluid needs in a person using the Kg method?

A

1-10 kg 100 mL/kg/d

11-20 50 mL/kg/d

>20 20 mL/kg/d

Example: 220lb person

220/2.2 = 100kg

10x100mL + 10x50mL + 80x20mL = 3100mL per day

31
Q

What is more likely with DMT1, HHS or DKA?

A

DKA is the most common in uncontrolled DMT1 patients.

32
Q

What is more likely in DMT2, HHS or DKA?

A

HHS (hyperosmolality and hyperglycemia)

33
Q

What are the characteristics of DKA?

A

In DKA BHB (beta-hydroxybuterate) and HCO3 is normal

34
Q

What are the characteristics of HHS and who is most likely to have it?

A

DMT2 patients and they have hyperglycemia and hyperosmolarity.

35
Q

What is the equation for calculating osmolarity?

A

(Na+x2 + )(Glucose/18)+(BUN/2.5)

Reference interval = 275-295

36
Q

Why might a CVD patient experienve edema in the legs?

A

lowered BP leads to higher hydrostatic pressure in the lower extremities. This leads to lower oncotic pressure and fluid buildup in the interstitium. Lymph can also account for inadequate fluid removal.

37
Q

What is MCD disease and how does it cause edema?

A

MCD is a kidney disease in children.

  1. Decrease in albumin concentration in blood
  2. Lower oncotic pressure due to decreased osmolarity in blood
  3. Fluid remains in interstitium
  4. Edema
38
Q

Whay does liver disease cause edema in the legs?

A

end stage cirrohsis of the liver means the liver is producing less albumin. This decrease in albumin reduces the oncotic pressure in the kidney and we have fluid left in the interstitum.

39
Q

What nonpharmacological treatments are there for treating DMT2?

A

Diet

excercise

low carb

weight loss

40
Q

What five classes of drugs can be used to treat DMT2?

A

Sulfonylureas

Meglinitides

Exenatides

Sitagliptin

Linagliptin

41
Q

How do sulfonyureas and meglinitides work?

A

They bind to the SUR1 receptor which in turn closes the K+ channel, beta cell depolarizes, Ca+ released and insulin released. Normally ATP binds when glucose is high in the cell but if glucose is low insulin is low and so the sulfonylureas and meglinitides act as analogues.

These drugs increase the release of insulin from the cell.

42
Q

What does exenatide do?

A

Exenatide is an incretin stimulator. Incretins GIP and GLP are the natural incretins. Incretins increase the sensativity of cells to insulin. Exenatide is an exogenous incretin activator.

43
Q

What do DPP-4 inhibitors do?

A

DPP-4 is an enzyme that breaks down incretins. If we inhibit DPP-4 we increase the amount of time that incretins are in the system and that the tissue is sensitive to insulin.

44
Q

What other mechanism are there to treat DMT2?

A

Reduce gastric emptying

Reduce digestion of starches

Reduce the output of glucose from the liver (<hgo>
</hgo>

45
Q

How does metformin work?

A

It reduces the amount of HGO.

Can cause nausea

FDN Week 5 (Block 2) (10 decks)

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