Dr. Winter - DMT1 Flashcards

1
Q

What are deep and increased respiratory rate called?

A

Kousmall breathing

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2
Q

How do define mild, moderate and severe weight loss?

A

5% = mild

10% = moderate

15% = severe

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3
Q

What are the desirable glucose values?

A

Fasting < 100 (65-100)

Random < 200

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4
Q

When a patient has been vomiting what should we think of their glucose numbers?

A

We should be looking for fasting numbers (65-99) they are essentially fasting due to vomit.

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5
Q

What causes hyperglycemia?

A

insulin action = [insulin] x insulin sensitivity of responding tissue.

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6
Q

Insulin works on insulin receptors of what tissues?

A

Adipose, Muscle, Liver

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7
Q

What cells of the body produce insulin?

A

Beta cells of the liver release insulin via endocrine secretion.

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8
Q

What other ways can hyperglycemia occur?

A

The elevation of counterregulatory hormones responsible for the increase of blood glucose can also cause hyperglycemia. These are glucagon and epinephrine.

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9
Q

How does the cell respond to “perceived” low glucose levels?

A

When insulin repsonse is poor either DMT1 and DMT2 the cell thinks it is starving and tells the body to release glucagon and make glucose. This increases the level of glucose in the blood.

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10
Q

What is the process of making glucose from glycogen?

A

Glycogenolysis

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11
Q

What is the process of making glucose from precursors?

A

Gluconeogenesis

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12
Q

In what circumstances does signaling for glucose happen?

A

Increased glucagon and decreased insulin

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13
Q

What are the percentages of T1 and T2 DM?

A

90% is T2

10% is T1

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14
Q

What are some of the acute symptoms of DM?

A

Polyuria, polydipsia, dehydration, infection, nocturia, weight loss.

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15
Q

What are some of the chronic conditions of DM?

A

Macrovascular disease

Microvascular disease

Neuropathy

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16
Q

How many hormones lower blood sugar and mitigate hyperglycemia?

A

1 - insulin

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17
Q

How many hormones signal for glucose release?

A

(4)

Epinephrine

Glucagon

Cortisol

Growth Hormone

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18
Q

Why do we need to tightly regulate blood glucose?

A

Hypo:

Impaired CNS, decreased mentation,Seizure, coma, death

Hyper:

Peripheral Vascular Disease

Carotid Artery Disease

Coronary Artery Disease

Blindness

Renal Failure

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19
Q

Why is there increased urination in DM?

A

Glucose levels in the filtrate exceed the capacity of the Na+ / Glucose transporter proteins in the kidney and glucose is not entirely reabsorbed into the extracellular fluid. Glucose is a solute that draws water with it - this increases urine output.

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20
Q

What is the progression of dehydration in DM?

A

Hyperglycemia –> glucose in filtrate exceed kidney –>glycosuria –> Osmotic diuresis –>fluid loss

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21
Q

What happens if you have polyurea, nocturia and don’t compensate?

A

Dehydration –> Coma –> Death

22
Q

Why is there weight loss in DMT1?

A

Protein and fat catabolism causes weightloss. Increased appetite (polyphagia) is a compensatory response.

23
Q

What percentage of TBW (total body water) is a well hydrated body?

A

60%

24
Q

66% of TBW is?

A

Intracellular fluid

25
Q

33% of TBW is?

A

Extracellular fluid (interstitium and plasma)

26
Q

Extracellular fluid is divided into?

A

Plasma - 20% of ECF

Interstitum - 80% ECF

27
Q

What factors control the flow of fluid between extra and intra cellular space?

A

hydrostatic pressure - flow of fluid from capillary to interstitium

Oncotic pressure - fluid flow back into cappilary due to protein concentration

28
Q

Loss of fluid but not whole blood?

A

dehydration, this will lead to hypovolemia (reduced circulating blood flow)

29
Q

Why does Hgb concentration drop after blood loss?

A

Immediatly afterward the Hgb is the same. Kidney produces fluid quickly and Hgb concentration drops.

30
Q

How does Hgb concentration change from dehydration?

A

We see an increase in the hemaglobin concentration.

31
Q

What are the consequences of dehydration?

A

Dehydration –> hypovolemia –> Reduced cardiac pre-load —> reduced cardiac output –> reduced BP –> reduced perfusion of tisue –> tissue hypoxia –> acidosis

32
Q

What is LVEDV?

A

Left ventricle end-diastolic volume

33
Q

What happens if you “over increase” LVEDV?

A

You can experience LV disfunction and less “return on investment” this is known as the starling form.

34
Q

Why is sodium measurement so important?

A

It is the primary extracellular cation and the primary extracellular cation. It can be used to measure total body sodium.

35
Q

What is osmolarity?

A

of particles for Kg of fluid. This is the driver for osmosis.

36
Q

What happens to a cell in a hyperosmolar ECF?

A

H2O moves out of the cell and cell shrinkage.

37
Q

What happens to a cell in a hypoosmolar ECF?

A

H2O moves into the cell and the cell swells

38
Q

How do you calculate osmolarity?

A

(Nax2) + BUN/2.8 + Glucose/18

39
Q

What is normal osmolarity?

A

275-295 mosm/L

40
Q

What is the significance of measureing Cl- in the plasma?

A

It is the major ECF anion like Na is the cation. Cl usually follows Na. The measurement of Cl is important for anion gap.

41
Q

What is the major intracellular cation?

A

potassium and measuring it for determining hypo or hyper kalemia which are sources of fatal cardiac arrythmia.

42
Q

Na+ / K ATPase pumps?

A

3 Na+ out of the cell

2 K+ into the cell

43
Q

Why might someone exhibit hyponatremia?

A

DMT1 increases EC glucose due to lack of glucose uptake. This leads to movement of H20 from cell to interstitum = diluted NA+ concentration

This also leads to polyurea and loss of Na+ in urine.

44
Q

Why might someone who is DMT1 exhibit hyperkalemia?

A

reduced glucose uptake results in reduced Na+ / K+ ATPase activity and less K+ being pumped into the cell.

45
Q

Why does increased EC K+ not reflect total body K+?

A

Because polyurea excretes potassium in the urine and reduced K+ pumping into the cell reduces the accuracy of total body K+

46
Q

What two factors impact Na+ & K+ concentrations?

A

Fluid volumes and electrolyte content.

47
Q

What regulates fluid balance in the body?

A

Fluid input - IV fluids, intestinal absorption

vs.

Fluid output - kidney, urine, sweat, exhalation

48
Q

How will sodium levels change with diarrhea locss of 1L (40mg/L) and no intake of H2O

A

Because we are losing less sodium than the concentration of the serum the concentration of Na+ rises.

49
Q

What are the clinical assessment of fluid status?

A

BP

Heart Rate

Orthostatic BP

Physical: turgor, sunken eyes.scaffoid abdomen

50
Q

What are the lab assessments for the fluid balance?

A

Urine output

Urine conc.

Glomular flow rate (kidney)

51
Q

What are the consequences of DKA and why?

A

hyponatremia: oncotic flow of H2O into interstitum due to increased glucose concentration. Dilution of Na+
dehydration: Diuresis and vomiting
hyperkalemia: decreased ATPase pump activity due to less glucose uptake and this results in less K+ pumping into cell.