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FOO > INSULIN RESISTANCE AND TYPE 2 DIABETES > Flashcards

INSULIN RESISTANCE AND TYPE 2 DIABETES Flashcards

1
Q

WHICH CELLS OF THE PANCREAS HAVE AN EXOCRINE FUNCTION AND SECRETE DIGESTIVE ENZYMES?

A

ACINAR CELLS

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2
Q

WHERE AND HOW ARE PANCREATIC DIGESTIVE ENZYMES TRANSPORTED?

A

INTO THE DUODENUM, BY THE PANCREATIC DUCT

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3
Q

WHAT PERCENTAGE OF PANCREATIC CELLS ARE INSULIN RELEASING BETA CELLS?

A

60%

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4
Q

WHAT PERCENTAGE OF PANCREATIC CELLS ARE GLUCAGON RELEASING APLHA CELLS?

A

30%

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5
Q

WHERE ARE INSULIN, GLUCAGON AND SOMATOSTATIN RELEASED TO AND HOW?

A

PANCREATIC ISLETS ARE DRAINED BY THE CAPILLARIES, SO THEY ARE SECRETED DIRECTLY INTO THE BLOOD STREAM

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6
Q

WHAT IS THE MAIN GLUT IN THE PANCREAS?

A

GLUT 2

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7
Q

INSULIN WON’T BE SECRETED IF THE GLUCOSE LEVELS ARE BELOW?

A

3.5 mmol/L

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8
Q

K+ CONCENTRATION IS USUALLY HIGHER INSIDE OR OUTSIDE THE CELL?

A

INSIDE

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9
Q

STEPS IN GLUCOSE STIMULATED INSULIN SECRETION BY THE PANCREAS:

A
  • PANCREAS USES GLUCOSE TO PRODUCE ATP VIA GLYCOLYSIS
  • ATP WILL CLOSE THE POTASSIUM CHANNELS AT THE CELL MEMBRANE WHICH LEADS TO HYPERPOLARIZATION
  • THIS STIMULATES CALCIUM CHANNELS AND THE CALCIUM INDUCES THE RELEASE OF INSULIN-CONTAINING VESICLES (EXOCYTOSIS)
  • INSULIN IS THEN SECRETED INTO THE BLOOD STREAM
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10
Q

HOW DO FATTY ACIDS REGULATE INSULIN SECRETION AND WHAT CAN BE RESULTS OF EXCESSIVE FATTY ACID CONSUMPTION RELATED TO INSULIN FUNCTIONING?

A
  • AFTER A MEAL, APART FROM GLUCOSE, WE ALSO HAVE A CERTAIN AMOUNT OF FATTY ACIDS IN OUR SYSTEM
  • WHEN VERY HIGH AMOUNTS OF FATTY ACIDS ARE EATEN, THE CLOSING OF K+ AND OPENING OF Ca2+ CHANNELS INDUCED BY THOSE FATTY ACIDS WILL INCREASE THE SECRETION OF INSULIN EVEN FURTHER
  • THIS LEADS TO HYPERINSULINEMIA, WHICH WILL LEAD THE BODY TO STATRT DEVELOPING INSULIN RESISTANCE TO AVOID GLUCOSE DISAPPEARING TOO FAST
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11
Q

2 MAIN SUBSTRATES REGULATING INSULIN SECRETION?

A

GLUCOSE AND FATTY ACIDS

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12
Q

HOW DOES GLUCAGON INFLUENCE INSULIN AND WHY?

A

GLUCAGON STIMULATES INSULIN TO SOME EXTENT; IT IS LIKE A SAFETY BELT TO MAKE SURE THE BODY DOESN’T USE ALL ITS RESERVES TOO QUICKLY; IF INSULIN IS SECRETED WITH GLUCAGON IT WILL BALANCE ITS EFFECTS

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13
Q

WHAT IS THE MAIN ROLE OF SOMATOSTATIN?

A

MAKING SURE NEITHER INSULIN OR GLUCAGON ARE SECRETED IN EXCESSIVE AMOUNTS

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14
Q

WHAT DOES INSULIN DO TO GLUCAGON SECRETION?

A

SUPPRESSES IT

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15
Q

WHAT ARE INCRETINS + ONE EXAMPLE?

A

HORMONES SECRETED BY THE INTESTINE WHICH ACTIVATE INSULIN SECRETION (REDUCE BLOOD GLUCOSE) AND DECREASE FOOD INTAKE.

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16
Q

STRESS HORMONE (LIKE ADRENALINE AND CORTISOL) WILL ACTIVATE WHICH PANCREATIC ENZYME?

A

GLUCAGON; INDICATE THAT BODY NEEDS MORE GLUCOSE

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17
Q

HOW MANY PHASES IN INSULIN SECRETION ARE THERE AND WHAT ARE THEY?

A

2;

  • ACUTE RESPONSE TO GLUCOSE WHERE THE INSULIN SPIKES
  • SUSTAINED SECRETION INDEPENDENT OF GLUCOSE
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18
Q

HOW MUCH DO THE PHASES OF INSULIN SECRETION LAST AND WHAT ARE THE MAIN GOALS OF EACH PHASE?

A

1) 10 MINS, GOAL IS TO DRAMATICALLY REDUCE BLOOD GLUCOSE LEVELS AFTER A MEAL
2) 3-4 HRS, SLOW RELEASE, GLUCOSE LEVELS SHOULD BE NORMAL BY THE END OF IT

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19
Q

WHEN DOES THE 2ND PHASE OF INSULIN SECRETION REACH PLATEAU?

A

AT AROUND 3 HRS

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20
Q

DURING WHICH PHASE OF INSULIN SECRETION DOES INSULIN TURN OFF ALL OTHER PATHWAYS THAT WERE PRODUCING GLUCOSE?

A

2ND PHASE

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21
Q

WHICH PHASE OF INSULIN SECRETION IS LOST IN INSULIN RESISTANCE AND DIABETES?

A

1ST

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22
Q

NORMAL GLUCOSE LEVELS IN A FASTED STATE (E.G. AFTER AN OVERNIGHT SLEEP)?

A

3.9-5.5 mmol/L

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23
Q

WHAT ARE THE NORMAL BLOOD GLUCOSE LEVELS 2 HRS AFTER A MEAL?

A

<7.8 mmol/L

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24
Q

HbA1C LEVELS SHOULD NOT EXCEED WHAT PERCENTAGE IN HEALTHY INDIVIDUALS?

A

6%

25
Q

WHAT IS Hb TURNOVER TIME AND HOW IS THAT HELPFUL IN TERMS OF INTERPRETING SOMEONE’S GLUCOSE LEVELS?

A

3 MONTHS

A WAY TO KNOW IF GLUCOSE LEVELS HAVE BEEN HIGH FOR A LONG TIME

26
Q

INSULIN’S 3 MAJOR TARGET TISSUES?

A

LIVER, MUSCLE AND ADIPOSE TISSUE

27
Q

TISSUES CONTAINING GLUT 4 ARE ACTIVATED DURING WHICH PHASE OF INSULIN SECRETION?

A

1ST

28
Q

WHAT PERCENTAGE OF DIABETES CASES ARE ATTRIBUTABLE TO T2D?

A

90%

28
Q

WHAT PERCENTAGE OF DIABETES CASES ARE ATTRIBUTABLE TO T2D?

A

90%

29
Q

WHICH TYPE OF DIABETES IS ALSO REFERRED TO AS ‘JUVENILE DIABETES’?

A

T1D

30
Q

DIFFERENCES BETWEEN TYPE I AND TYPE II DIABETES?

A

TYPE I: ONSET USUALLY IN YOUNGER YEARS, SHORT HISTORY, ACUTE ONSET, DESTRUCTION OF BETA CELLS BY THE IMMUNE SYSTEM, PATIENTS USUALLY NOT OVERWEIGHT, INSULIN DEFICIENCY, REQUIRES DAILY INSULIN INJECTIONS FROM DIAGNOSIS, OFTEN RANDOM, ASSOCIATED WITH WEIGHT LOSS, CONSTANT HUNGER AND SOME OTHER T2D SYMPTOMS

TYPE II: APPEARS LATER IN LIFE, INSIDIOUS ONSET, INSULIN RESISTANCE NOT LACK OF SECRETION, PATIENTS OFTEN OVERWEIGHT, LIFESTYLE CHANGES CAN HAVE A REVERSING EFFECT, IF UNTREATED THE PANCREAS CAN GET EXHAUSTED AND DECREASE INSULIN SECRETION SO THE SYMPTOMS START TO RESEMBLE T1D MORE, DRY MOUTH, EXCESSIVE THIRST, FATIGUE, BLURRED VISION

31
Q

WHAT IS THE GREATEST RISK FACTORS FOR T2D?

A

OBESITY

32
Q

MAIN SIMILARITY BETWEEN T1D AND T2D?

A

IN BOTH CASES CELLS DON’T UPTAKE GLUCOSE FROM THE BLOOD STREAM SO THE PLASMA GLUCOSE LEVELS ARE HIGH

33
Q

1ST STEP OF IMPAIRED GLUCOSE METABOLISM IS?

A

INSULIN RESISTANCE

34
Q

WHAT HAPPENS TO GLUCOSE METABOLISM AND INSULIN SECRETION AFTER INSULIN RESISTANCE DEVELOPS?

A
  • INSULIN SECRETION INITIALLY INCREASES TO COMPENSATE FOR THE RESISTANCE
  • AFTER AWHILE THE RATE BECOMES TOO HIGH FOR THE PANCREAS AND THE HIGH AMOUNT OF FAT IS TOXIC FOR BETA CELLS
  • THE INSULIN SECRETION STARTS DECLINING BUT THE LEVELS ARE STILL ABOVE NORMAL
  • GLUCOSE LEVELS START GETTING HIGHER AFTER THIS
  • STATE OF IMPAIRED GLUCOSE TOLERANCE AND CLEARANCE
35
Q

IF INSULIN RESISTANCE IS SUSPECTED, WHICH TEST ARE PEOPLE ASKED TO DO?

A

ORAL GLUCOSE TOLERANCE TEST (OGTT)

36
Q

TISSUES WITH WHICH GLUT MAINLY BECOME INSULIN RESISTANT?

A

GLUT 4 (MUSCLE AND ADIPOSE TISSUE)

37
Q

DIABETES IS REALLY DECLARED WHEN GLUCOSE LEVELS ARE SO HIGH THAT WHICH ORGAN PARTICIPATES IN CLEARING THE GLUCOSE AND HOW IS THIS DETECTED?

A

KIDNEYS, THERE IS GLUCOSE IN THE URINE

38
Q

WHAT DOES ‘GLUCOSURIA’ MEAN?

A

PRESENCE OF GLUCOSE IN THE URINE

39
Q

WHAT IS LIPID SPILL OVER AND WHICH CONDITION CAN CAUSE IT?

A

LIPID ACCUMULATION IN TISSUES APART FROM ADIPOSE TISSUE
CAN HAPPEN IN TYPE II DIABETES BECAUSE LIPOLYSIS ISN’T SUPPRESSED AND MUSCLES NEED TO USE FATTY ACIDS AS FUEL INSTEAD OF GLUCOSE BECAUSE THEY CAN’T UTILIZE GLUCOSE, AND ALL THIS LEADS TO MASSIVE AMOUNT OF FATTY ACIDS IN THE BLOOD

40
Q

EXAMPLES OF METABOLIC PATHWAYS IMPAIRED BY DIABETES AND INSULIN RESISTANCE?

A

INSULIN PROPERTIES LOST SO:

  • GLYCOGEN SYNTHESIS ISN’T ACTIVATED SO THE EXCESS GLUCOSE CAN’T BE STORED
  • INCREASED PROTEOLYSIS (WASTING)
  • MUSCLE USES FATTY ACIDS FOR ENERGY; FATTY ACIDS OXIDATION INCREASED
  • LIVER PRODUCES GLUCOSE AT ALL TIMES
  • FASTING GLUCOSE LEVELS ARE ALSO INCREASED
41
Q

ECTOPIC TISSUE MEANING:

A

GROWTH OF NORMAL TISSUE IN THE INCORRECT ANATOMICAL POSITION

42
Q

IN INSULIN RESISTANT INDIVIDUALS, THE INCREASED RELEASE OF FATTY ACIDS WILL RESULT IN INCREASED ACETYL CoA PRODUCTION. WHAT WILL THE CONSEQUENCES OF THIS BE ON THE GLYCOLYSIS PATHWAY?

A
  • IT WILL FIRSTLY INHIBIT PYRUVATE HYDROGENASE FROM CONVERTING PYRUVATE INTO MORE ACETYL CoA
  • PYRUVATE WILL ACCUMULATE
  • THIS WILL SUPPRESS THE 1ST STEP OF GLYCOLYSIS (CATALISED BY HEXOKINASE)
  • GLUCOSE WILL THEREFORE NOT BE BROKEN DOWN AND THE LEVELS WILL BE EVEN HIGHER
43
Q

WHY DO BETA CELLS START DYING IN OBESE INSULIN RESISTANT INDIVIDUALS?

A

BECAUSE THE CONTINUOUS RELEASE OF FATTY ACIDS LEADS TO CONTINUOUS ACTIVATION OF THE BETA CELLS AND THE PANCREAS CAN’T KEEP UP,
FATTY ACIDS ARE TOXIC TO BETA CELLS!!!!!

44
Q

FATTY ACIDS INDUCE INFLAMMATION. HOW WILL THIS AFFECT INSULIN FUNCTIONING?

A

INFLAMMATION WILL LEAD TO PRODUCTION OF MOLECULES (OFTEN CYTOKINES) THAT THEMSELVES DISRUPT THE INSULIN SIGNALLING

45
Q

GESTATIONAL DIABETES AFFECTS WHAT PERCENTAGE OF PREGNANCIES?

A

10%

46
Q

GESTATIONAL DIABETES PREVALENCE IS ESP. HIGH IN WOMEN OF WHICH DESCENT?

A

BLACK SOUTH AFRICAN WOMEN

47
Q

AT WHICH STAGE OF PREGNANCY DOES GESTATIONAL DIABETES USUALLY APPEAR?

A

END OF THE 2ND TRIMESTER

48
Q

WHICH WOMEN WILL BE GIVEN OGTT TEST WHEN PREGNANT REGARDLESS OF IF THEY HAVE THE SYMPTOMS?

A

OLDER WOMEN, OBESE WOMEN, WOMEN WITH HISTORY OF T2D…

49
Q

CHANGES IN INSULIN SECRETION AND GLUCOSE METABOLISM IN ALL PREGNANT WOMEN?

A

ALL WOMEN DEVELOP INSULIN RESISTANCE WITH HYPERINSULINEAMIA BUT WITH NORMAL GLUCOSE LEVELS SO THE GLUCOSE OF THE MOTHER CAN BE SPARED AND USED FOR THE FETAL DEVELOPMENT

50
Q

WHAT HAPPENS TO INSULIN PRODUCTION IN GESTATIONAL DIABETES?

A

BETA CELLS DON’T PRODUCE ENOUGH INSULIN TO COMPENSATE FOR THE NORMAL INSULIN RESISTANCE WHICH LEADS TO HYPERINSULINEMIA WITH HYPERGLYCAEMIA

51
Q

GESTATIONAL DIABETES IS A DISORDER OF WHICH ORGAN AND HOW?

A

PLACENTA; LINKED DIRECTLY TO THE GOOD FUNCTIONING OF THE PLACENTA, RESOLVES AFTER DELIVERY

52
Q

EFFECTS OF GESTATIONAL DIABETES ON INFANTS?

A

MACROSOMIA, INCREASED RISK OF OBESITY, DIABETES AND OTHER DISORDERS LATER IN LIFE

53
Q

1ST LINE MANAGEMENT OF T2D?

A

FOLLOWING DIET AND EXERCISE PLAN

54
Q

DRUGS FOR INSULIN RESISTANCE MANAGEMENT?

A
  • INSULIN SENSITIZERS
  • INCREASED INSULIN SECRETION (GLP1 ANALOGUES)
  • REDUCED HEPATIC GLUCOSE PRODUCTION (METFORMIN)
55
Q

WHAT DOES METFORMIN DO?

A

REDUCES HEPATIC GLUCOSE PRODUCTION

56
Q

DPPiV INHIBITORS HAVE TO BE GIVEN WITH WHAT MEDICATION TO AVOID INACTIVATION OF IT?

A

GLP1 ANALOGUES

57
Q

WHAT ARE THIAZOLIDINEDIONES (TZD)?

A

DRUGS WHICH ACT LIKE INSULIN SENSITIZERS; INCREASE INSULIN SENSITIVITY AND DECREASE LYPOLYSIS, BUT LEAD TO INCREASE IN ADIPOSE TISSUE AND INCREASED STROKE RISK SO THEY WERE REMOVED FROM THE MARKET

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