DIABETES Flashcards

0
Q

WHAT DOES INSULIN AND GLUCAGON DO?

A

WORKS DURING FAST AND FEAST. RESPONSIBLE FOR CARB, FAT, AND PROTEIN METABOLISM.

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1
Q

WHAT ARE THE 2 TYPES OF CELLS THAT MAKE UP THE PANCREAS AND WHAT DO THEY DO?

A

ACINAR CELLS AND ISLETS OF LANGERHANS.

ACINAR CELLS-MAJORITY 98-99% PANCREAS WEIGHT. EXOCRINE PORTION. SECRETES DIGESTIVE ENZYMES/BICARB INTO PANCREATIC DUCT.

ISLETS OF L- 1-2%. PRODUCE INSULIN WHICH IS SECRETED INTO BLOOD (ENDOCRINE). HAS CHOLINERGIC AND ADRENERGIC FIBERS. CONSISTS OF 3 TYPES OF CELLS:
ALPHA CELLS-SECRETE GLUCAGON
BETA CELLS-MOST ABUNDANT; PRODUCE INSULIN.
DELTA CELLS-SECRETE SOMATOSTATIN.

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2
Q

WHAT DOES SOMATOSTATIN DO?

A

DISTRIBUTED IN CNS AND RESPONSIBLE FOR INHIBITION OF ANTERIOR PITUITARY GROWTH HORMONE RELEASE.

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3
Q

WHAT IS THE PRIMARY ENERGY SOURCE OF THE BODY?

A

GLUCOSE! BRAIN USES ONLY GLUCOSE BECAUSE ITS AN OBLIGATE GLUCOSE ORGAN. (BUT IT DOES NOT NEED INSULIN)

OTHER MUSCLES AND TISSUES ARE FACULTATIVE GLUCOSE ORGANS USING GLUCOSE IF AVAILABLE BUT CAN USE AMINO ACIDS/FAT IN ITS ABSENCE.

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4
Q

NORM GLUCOSE LEVELS?

A

FASTING= < 100
PRE DIABETIC = 100-125
DIABETIC= > 125 X 2 OCCASIONS

SLEEPING= 80-90
AFTER FOOD= 120-140

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5
Q

WHAT IS NORM HB A1C?

A

< 6.05
GOAL IN DIABETIC PT IS KEEP < 7-7.5

CONCENTRATION OF GLYCOSATED HGB REFLECTS MEAN GLUCOSE OVER 60 DAYS.

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6
Q

WHAT DOES INSULIN DO?

A

PROMOTES STORAGE OF CARBS FAT PROTEIN. INSULIN DRIVES SUBSTANCES INTO CELLS.
CARBS: DECR INSULIN TRIGGERS RELEASE OF STORED GLUCOSE BACK INTO BLOOD.
PROTEIN: INSULIN MAKES AMINO ACIDS MOVE INSIDE CELLS. PROTEINS ARE CREATED AND THEIR BREAKDOWN INHIBITED.
FAT: INSULIN FAVORS FAT STORAGE.CARBS—FATTY ACIDS + GLYCEROL—-=TRIGLYCERIDE.

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7
Q

DOES INSULIN FAVOR LIPOGENESIS?

A

YES! IT STRONGLY INHIBITS LIPOLYSIS.

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8
Q

WHAT IS THE MOST IMPORTANT STIMULATOR OF INSULIN?

A

PLASMA GLUCOSE. INSULIN PEAKS 30-60 MIN AFTER A MEAL.

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9
Q

HOW DOES THE ANS EFFECT INSULIN SECRETION?

A

VAGAL (PNS)—INCR INSULIN
BETA SNS STIM——INCR. INSULIN
ALPHA SNS STIM—–PREVENT INSULIN RELEASE.
“GENERAL” SNS STIM—PREVENT INSULIN RELEASE BECAUSE ALPHA PREDOMINATES THE SNS.

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10
Q

WHAT IS GLUCAGON? WHAT DOES IT DO?

A

ENHANCE HEPATIC GLUCOSE RELEASE TO INCR. PLASMA GLUCOSE.

WHEREAS CORTISOL STIMULATES INSULIN RELEASE.

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11
Q

WHAT IS DIABETES?

A

WHEN THE PANCREAS DOESNT PRODUCE ENOUGH INSULIN OR
THE BODY’S TISSUES BECOME RESISTANT TO INSULIN.

THERE ARE 4 TYPES OF DIABETES.

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12
Q

WHAT WILL A TYPE 1 DIABETIC LOOK LIKE?

A

GLUCOSE IN URINE….KIDNEYS CAN NO LONGER ABSORB EXCESS.
LOTS OF URINE….GLUCOSE ACTS AS OSMOTIC DIURETIC….THEY TEND TO BE DEHYDRATED.
POLYDIPSIA…COMPENSATE FOR HYPOVOLEMIA
WT LOSS.

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13
Q

WHAT ARE S/S OF TYPE 2 DIABETIC?

A

S/S TYPE 1 AND INFECTIONS, PARASTHESIA, BLURRED VISION.

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14
Q

WHAT ARE THE 2 TYPES OF INSULIN THAT CAN BE GIVEN IV?

A

REGULAR AND INSULIN LISPRO

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15
Q

IS INSULIN GLARGINE COMPATABLE WITH OTHER INSULINS?

A

NO!

ITS LONG ACTING WITH NO PEAK.

16
Q

WHAT IS THE GOAL WITH INSULIN THERAPY?

A

TO KEEP GLUCOSE AS CLOSE TO NORMAL AS POSSIBLE.

17
Q

HOW IS GLUCOSE METABOLIZED AND WHY IS IT IMPORTANT?

A

ANAEROBIC. CAN LEAD TO LACTIC ACIDOSIS.

18
Q

HOW DOES METFORMIN WORK AND WHAT IS ITS RISK?

A

SENSITIZES TISSUE TO INSULIN AND DECREASES LIVER GLUCOSE OUTPUT.
D/C 2 DAYS PRIOR TO SURGERY TO AVOID LACTIC ACIDOSIS….ALTHOUGH ITS RARE.

19
Q

WHAT WILL AN MI IN DIABETIC PATIENT BE LIKE?

A

S/S: COUGH, N/V, SOB, TIRED, EKG CHANGES.

IMPROVED SURVIVAL POST MI WITH BETA BLOCKER.

20
Q

IS DIABETIC CARDIOMYOPATHY DUE TO CAD?

A

NO! ITS INDEPENDENT OF CAD, HTN, AND VALVULAR HEART DISEASE.

THEY HAVE IMPAIRED DIASTOLE. SYSTOLIC FXN INTACT. THEY HAVE CONCENTRIC HYPERTROPHY.

GOAL: PREVENT AND TREAT HTN.

21
Q

TYPE 1 VS 2 DIABETICS AT RISK FOR MICRO/MACRO VASCULAR DISEASE?

A

T1: MICROVASCULAR ….RETINA, KIDNEY.
T2: MACROVASCULAR…..CORONARY, PERIPHERAL VASCULATURE (ULCERS)

22
Q

WHY ARE DIABETICS DIFFICULT TO INTUBATE?

A

STIFF JOINT SYNDROME….TISSUE PROTEINS GLYCOSYLATED. HAVE THEM DO PRAYER SIGN (SENSITIVE PREDICTOR)
OBESITY.
CONSIDER RSI D/T GASTROPARESIS AND PRETREAT WITH PEPCID/REGLAN. …MORE PRONE TO ASPIRATION.

23
Q

WHAT DRUG DO YOU NEED TO BE CAREFUL GIVING IF DIABETIC PT ON ACE INHIBITOR?

A

EPHEDRINE.

24
Q

WHAT CV ISSUES MAY YOU SEE UNDER ANESTHESIA WITH DM PT?

A

LABILE BP. HYPOTHERMIA. MORE POTENT VASOPRESSORS OFTEN NEEDED. PT MAY NOT COMPENSATE ANESTHESIA WITH INCR. HR AND VASOCONSTRICTION. ….THINK EPI.

25
Q

WHAT IS HYPOGLYCEMIA AND HOW DO YOU TREAT?

A

BS 40-50. RESULTS IN SNS STIMULATION. INCREASE BS TO > 100
EACH ML D50 RAISES BS BY 2

26
Q

WHAT IS DKA AND HOW TO TREAT?

A

EMERGENCY TRIGGERED BY HIGH BS. TYPE 1 PRONE TO THIS. S/S: BS> 250. DEHYDRATED. METABOLIC ACIDOSIS (< 7.3) RAPID DEEP BREATHING (KUSSMAULS) LOW ELECTROLYTES (POTASSIUM) HYPEROSMOLARITY.

TX: HAVE GOOD IV’S. RESTORE FLUID BALANCE. GIVE BICARB. INSULIN GTT.
EACH UNIT OF INSULIN LOWERS BS BY 50.

27
Q

WHAT IS HHNK?

A

HYPEROSMOLAR STATE TRIGGERED BY HIGH BS. COMMON IN T2 DM. S/S: SAME AS DKA EXCEPT IT IS NOT ASSOCIATED WITH ACIDOSIS OR KETOGENESIS. TX: SAME AS DKA EXCEPT NO NEED FOR BICARB.

28
Q

WHAT ARE THE ANESTHESIA GOALS FOR DM PT?

A

MIMIC NORMAL METABOLISM. AVOID EXTREMES.

29
Q

WHAT ARE PTS AT RISK OF IF THEYRE ON SULFONUREAS?

A

HYPOGLYCEMIA.

30
Q

WHICH PTS ARE AT RISK FOR ALLERGIC RXN TO PROTAMINE SULFATE?

A

PTS ON NPH OR PROTAMINE ZINC.

31
Q

WHAT INNATE SUBSTANCES CAUSE STRESS HYPERGLYCEMIA?

A

CATECHOLAMINES, GLUCOCORTICOIDS, AND GROWTH HORMONE…..ALL THESE INCREASED UNDER ANESTHESIA.

32
Q

WHAT DOES HYPOGLYCEMIA LOOK LIKE UNDER ANESTHESIA?

A

MIMIC “LIGHT” ANESTHESIA WITH INCR. HR AND HTN.

33
Q

WHERE DO YOU SET AN INSULIN INFUSION RATE?

A

BS/150

OR IF PT ON STEROIDS OR INFECTION… BS/100 (SO INSULIN DELIVERY INCREASES)

1 UNIT OF REGULAR INSULIN DECREASES BS BY 50.