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Endocrine > Pathophysiology: DKA and HHS Fisher > Flashcards

Pathophysiology: DKA and HHS Fisher Flashcards

1
Q

What is the diagnostic difference between DKA and HHS? (emphasized)

A

HHS:
>600gluc.
>7.3 pH
>15 bicarb

DKA:
>250gluc.
<10 bicarb

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2
Q

What is DKA seen in?

A

Type I DM

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3
Q

What is HHS seen in?

A

Type II DM

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4
Q

What is DKA?

A

High sugar
High Acid
High Ketones

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5
Q

What are metabolic acid states?

A

Lactic acidosis
Hyperchloremic acidosis
Drug-induced acidosis
Uremia

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6
Q

What are other ketotic states?

A

Alcoholic KA
Starvation KA
Ketotic Hypoglycemia

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7
Q

What are other hyperglycemic states?

A

DM
HHS
Impaired glucose tolerance
Stress

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8
Q

What hormones or factors go up with insulin stimulation? (*very important)

A 
Basically everything but glucose and C peptide:
Glucagon
Epi
Growth Hormone
Cortisol
NE
ACTH
Prolactin
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9
Q

What is the MAIN cause of DKA and HHS in DM?

A

Infection!

Usually pneumonia!

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10
Q

What is the second most cause of DKA and HHS?

A

New onset DM

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11
Q

What causes use of ketones in normal body? (remember that…)

A

Stress: any type
Epi–> Fat cells make free fatty acids
Glucagon–>Alanine/AA from muscle
–> liver gluconeogenosis/glycogenolysis

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12
Q

What are the main effects of acute insulin deficiency on glucose?

A 
more glycogen breakdoen
less glucose use, glucose buildup in blood
polyuria
polyphagia
loss of fluid and electrolytes
circulatory collapse (shock)
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13
Q

What are the main effects of acute insulin deficiency on protein?

A

increased protein breakdown
increase plasma AA
BUN increase
liver gluconeogenesis–>circulatory collapse

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14
Q

What is the main effect of acute insulin deficiency on pH?

A 
Epi-->lipocyte-->FFA
FFA become VLDL-->Hyperlipidemia 
FFA liver oxidation-->ketone formation
ketone acids suck up alkali reserves
Acidosis
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15
Q

What is the endpoint of ABSOLUTE insulin deficiency?

A

DKA:
High glucose
Hyperlipidemia
Ketoacidosis

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16
Q

What is the endpoint of RELATIVE insulin deficiency

A

HHS: NO KETONES!!!! no hyperlipidemia

Hyperglycemia–>dehydration–>hyperosmolarity

17
Q

What is the summary of DKA?

A

Metabolic acidosis
and
Volume depletion

18
Q

What enzyme releases FFA from fat?

A

Lipase

19
Q

What enzyme in blood stimulates FFA release in fat?

A

Protein kinase (activates lipase)

20
Q

What does FFA become?

A

Fatty acid CoA
and
Triacylglycerol (hyperlipidemia!)

21
Q

What does Fatty acid CoA become?

A

Malonyl CoA
CAT1 (catecholamine1)
Fatty acid carnitine (which enters the mitochondria)

22
Q

What does Fatty acid carnitine become?

A

Ketones (FFA–>FACoA–>FAC–>K)

23
Q

What molecule causes hyperlipidemia in DKA?

A

Triacylglycerol

24
Q

Fatty acyl CoA inhibits what enzyme in mitochondria?

A

Citrate synthetase, shunting Fatty acid carnitine into mitochondria for ketogenesis

25
Q

What 4 enzymes complete the gluconeogenesis in the mitochondria?

A

PC: Pyruvate carboxylase
PEP CK
F1.6 Carboxylase

26
Q

What enxyme allows glucose into the cell?

A

G-6-phosphatase

27
Q

What is blocked in the mitochondria during DKA, and how?

A

the TCA cycle (it does ketogenesis instead)

Fatty acyl CoA blocking Citrate synthase makes Fatty acid carnitine the only thing that can come in

28
Q

What are the enzymes of gluconeogenesis?

A

PC
PEP CK
F1,6BP
G6Phosphatase

29
Q

What enzymes are blocked by FFA in the biochemistry of insulin deficiency? (emphacized twice)

A

Fatty acid blocks:
HK: hexokinase
PFK: phosphofructokinase
PK: pyruvate kinase

30
Q

What happens to body compartments size during DKA?

A

All are shrunk!

31
Q

How do you fix the dehydration of all body compartments in DKA? (his research!)

A

1 L of normal isotonic saline
then
1 L of HYPOtonic saline

Endocrine (15 decks)

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