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Year 1/2 > Digestion & Metabolism 2: Diabetes Mellitus > Flashcards

Digestion & Metabolism 2: Diabetes Mellitus Flashcards

1
Q

the RIGHT LOBE of the pancreas is located in the…

the LEFT LOBE of the pancreas is located in the…

A

RIGHT = MESODUODENUM

LEFT = GREATER OMENTUM

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2
Q

when the PANCREAS is INFLAMED (pancreatitis), it can cause signs from WHAT 2 regions?

A
  1. UPPER GI SIGNS
  2. COLITIS (can still reach LI via TRANSVERSE COLON)
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3
Q

2 components of PANCREAS?

which is MAJORITY/WHAT DOES IT DO?

A
  1. MAJORITY is EXOCRINE
  2. ISLETS of LANGERHANS
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4
Q

2 main FUNCTIONS of pancreas?

in the SECOND one, list WHAT CELLS perform this function & 4 THINGS it makes!

A
  1. EXOCRINE pancreas = secretes DIGESTIVE ENZYMES & BICARBONATE
  2. ENDOCRINE PANCREAS via ISLETS OF LANGERHANS = secretes HORMONES, such as…
  3. INSULIN
  4. GLUCAGON
  5. SOMATOSTATIN
  6. PANCREATIC POLYPEPTIDE
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5
Q

ISLETS of LANGERHANS…

contains WHAT 4 kinds of cells? what does each kind make?

A
  1. ALPHA CELLS = GLUCAGON
  2. BETA CELLS = INSULIN
  3. DELTA CELLS = SOMATOSTATIN
  4. F CELLS = PANCREATIC POLYPEPTIDE
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6
Q

insulin is synthesized as a ____-___- HORMONE

has WHAT 3 components that make it up?

AFTER insulin is synthesized ___ ___ is CLEAVED OFF, leaving only WHAT 2 components for its ACTIVE form?

A

insulin synthesized as a PRE-PRO-HORMONE

made up of A, B & C CHAIN

after synthesis, C CHAIN CLEAVED OFF, so only A & B CHAIN LEFT in active form

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7
Q

the C PEPTIDE is secreted in ___ amounts to INSULIN, why?

why is this a HELPFUL parameter?

when insulin is ADMINISTERED….

A

EQUAL, because INSULIN ENDOGENOUSLY produced WITH C CHAIN, but CLEAVED OFF upon activation

HELPFUL parameter because it can be HARD to measure transient levels of insulin in the body, but presence of C CHAIN would indicate ENDOGENOUS INSULIN presence!

when insulin is ADMINISTERED, only A & B CHAIN are on it (since it’s active), so STILL NO C CHAIN WOULD BE DETECTED

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8
Q

INSULIN function…

anabolic/catabolic

= functional definition

A

ANABOLIC

= takes CARBOHYDRATES, AMINO ACIDS & FATTY ACIDS after we eat MEALS and STORES THEM AS GLYCOGEN, FAT & PROTEIN

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9
Q

INSULIN effect on GLUCOSE? (3)

A
  1. pushes glucose from BLOOD –> MUSCLE & ADIPOSE CELLS
  2. increases GLYCOGEN SYNTHESIS IN LIVER
  3. STIMULATES GLUCONEOGENESIS
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10
Q

GLUCONEOGENESIS…

= definition?

what HORMONE promotes this?

A

= the FORMATION of GLUCOSE from AMINO ACIDS

promoted by INSULIN

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11
Q

KETOGENESIS…

ketones are an ____ form of energy from ___

= definition?

A

ketones are an EXPENSIVE (energy wise) form of ENERGY from FAT

= BREAKING DOWN FATS TO MAKE KETONES FOR ENERGY

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12
Q

INSULIN effect on PROTEIN? (3)

A
  1. pushes AMINO ACIDS INTO MUSCLE
  2. INCREASES PROTEIN SYNTHESIS in MUSCLE & LIVER
  3. DECREASES PROTEIN CATABOLISM in MUSCLE
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13
Q

INSULIN effect on FAT? (4)

A
  1. INCREASES LIPID SYNTHESIS in ADIPOSE TISSUE
  2. DECREASES KETOGENESIS
  3. ACTIVATES LIPOPROTEIN LIPASE
  4. INHIBITS HORMONE-SENSITIVE LIPASE
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14
Q

LIPOPROTEIN LIPASE

located in ___

= function?

anabolic/catabolic?

___ by INSULIN

A

located in CAPILLARIES

= TAKES FATTY ACIDS FROM BLOOD & STORES THEM AWAY

ANABOLIC

STIMULATED by INSULIN

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15
Q

HORMONE-SENSITIVE LIPASE…

= function?

anabolic/catabolic?

___ by INSULIN

A

= takes STORED FAT & LYSES THEM to MAKE KETONES/ENERGY

CATABOLIC

INHIBITED by INSULIN

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16
Q

besides affecting FAT, PROTEIN & CARBS, insulin can… (2)

A
  1. INCREASES CELL GROWTH
  2. increases UPTAKE of K, Mg, + P into CELLS
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17
Q

COUNTER-REGULATORY HORMONES…

alternative NAME to COUNTER-REGULATORY?

what are the 4 names?

what DOES it counter? (2, hormone & process)

A

alternative name? = DIABETOGENIC (INCREASES blood glucose)

4 names?
1. GLUCAGON
2. GCCs
3. CATECHOLAMINES
4. GROWTH HORMONE

it counters INSULIN-INDUCED HYPOGLYCEMIA

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18
Q

4 FUNCTIONS of GLUCAGON?

anabolic/catabolic?

A

4 functions?
1. INCREASES GLYCOGENOLYSIS
2. INCREASES LIPOLYSIS
3. INCREASES KETONE BODY FORMATION
4. INCREASES GLUCONEOGENESIS

CATABOLIC

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19
Q

which out of the FOUR DIABETOGENIC hormones are the MOST EFFECTIVE & why?

A

GLUCAGON because it COUNTERACTS INSULIN on ALL 3 fronts: CARBS, FATS & PROTEIN

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20
Q

____ ____ from ____ ____ are needed to form KETONES

A

FATTY ACIDS, FAT BREAKDOWN

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21
Q

in the FED state = INSULIN/GLUCAGON dominates

in the FASTED state = INSULIN/GLUCAGON dominates

A

FED state = INSULIN dominates

FASTED state = GLUCAGON dominates

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22
Q

SODIUM-GLUCOSE COTRANSPORTER TYPE 1 & 2 (SGLT 1 & 2)

SGLT1 is located…

SGLT2 is located…

which one is MORE clinically significant?

A

SGLT 1 located in INTESTINE

SGLT 2 located in the PROXIMAL RENAL TUBULES

SGLT2 MORE CLINICALLY SIGNIFICANT

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23
Q

if SGLT1 IS DYSFUNCTIONAL, patients usually present with ___ because they CANNOT absorb ____

A

D+, GLUCOSE

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24
Q

SGLT2…

located in WHAT organ?

= function?

if it is DYSFUNCTIONAL, expect WHAT clinical sign?

A

located in KIDNEYS

= responsible for REABSORPTION of GLUCOSE that might’ve SPILLED INTO URINE

if DYSFUNCTIONAL, then GLUCOSURIA

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25
Q

SGLT2 INHIBITORS cause….

for treatment of…

A

cause GLUCOSE to be SPILLED OUT INTO URINE

for treatment of DIABETES MELLITUS

26
Q

if a GLUCOSE TRANSPORTER is located in NEURONAL TISSUE or PLACENTA, they have ____ affinity for glucose

if a GLUCOSE TRANSPORTER is located in BETA CELL (in pancreas), they have a ____ affinity for glucose. why?

A

NEURONAL TISSUE or PLACENTA = HIGH affinity for glucose!

BETA CELL in PANCREAS = LOW affinity for glucose

when glucose enters BETA cell in pancreas, STIMULATES INSULIN SECRETION, but we ONLY WANT THIS WHEN GLUCOSE IS ABOVE A CERTAIN THERSHOLD; if BETA cells were to have a HIGH affinity for glucose, then could cause HYPOGLYCEMIA

27
Q

DIABETES means =

MELLITUS means =

A

DIABETES = POLYURIA

MELLITUS = SWEET

28
Q

TYPE 1 DIABETES MELLITUS

____-DEPENDENT because…

usually occurs in ____ patients

often _____-mediated

NOT associated with…

dogs vs. cats?

A

INSULIN-DEPENDENT because PATIENTS REQUIRE EXOGENOUS INSULIN tx

usually occurs in YOUNG patients

often IMMUNE-MEDIATED

NOT associated with OBESITY

MOST COMMON CAUSE IN DOGS & maybe CATS

29
Q

TYPE II DIABETES MELLITUS

____-DEPENDENT because

usually occurs in ____ patients

often ____-associated

dogs vs. cats?

A

NON-INSULIN DEPENDENT because tx MIGHT NOT REQUIRE INSULIN, such as SGLT2 inhibitors

usually occurs in OLDER patients

often OBESITY-associated

NOT SUPER COMMON IN DOGS/CATS

30
Q

TYPE 1 DIABETES associated with DESTRUCTION of…

REQUIRES….

etiologies? (4)

A

DESTRUCTION of BETA CELLS, which causes NO INSULIN TO BE PRODUCED

REQUIRES INSULIN TREATMENT

etiologies?
1. GENETIC
2. IMMUNE-MEDIATED
3. INFECTIOUS
4. TOXIC

31
Q

which GENES’ altered function could be responsible for TYPE 1 DIABETES MELLITUS?

what do they code for? what do these molecules do?

in TYPE 1 DIABETES, these molecules…

what SPECIES does this occur in? what SPECIES does this process (likely) NOT occur in?

A

MHC genes

code for HLA CLASS 2 PROTEINS, which BIND TO ANTIGENS & PRESENT TO T CELLS to be CLEARED

in TYPE 1 DIABETES, HLA CLASS 2 PROTEINS ERRONEOUSLY PRESENT PROTEINS in BETA CELLS to T CELLS & invoke IMMUNE RESPONSE & DESTRUCTION OF BETA CELLS

HOWEVER THIS OCCURS IN HUMANS, (likely) NOT DOGS!

32
Q

2 breeds at INCREASED RISK for TYPE 1 DIABETES MELLITUS?

what REGION & SEASON do dogs tend to develop TYPE 1 DIABETES?

A

2 breeds?
1. SAMOYEDS
2. AUSTRALIAN TERRIERS

common in NORTHERN US & WINTER in TYPE 1

33
Q

TYPE 2 DIABETES MELLITUS…

commonality in DOGS/CATS?

CHARACTERIZED BY what 2 problems? which one is WORSE?

what +/- might be present/necessary? (2)

3 causes?

A

RARE in dogs, UNCOMMON in cats

CHARACTERIZED BY…
1. INSULIN RESISTANCE –> WORSE
2. IMPAIRED INSULIN SECRETION

+/- BETA CELL DESTRUCTION
+/- INSULIN TREATMENT/CONCENTRATION

causes?
1. GENETIC predisposition
2. OBESITY
3. AMYLOID DEPOSITION

34
Q

what is the MOST COMMON reason for INSULIN RESISTANCE?

what TYPE of DZ do we expect to see this?

A

OBESITY

expect to see this in TYPE 2 DIABETES MELLITUS

35
Q

why might insulin be HIGH in TYPE 2 DIABETES in an OBESE DOG?

A

if there’s INSULIN RESISTANCE due to OBESITY, then pancreas MIGHT BE MAKING MORE AND MORE INSULIN to try and compensate FOR IT NOT WORKING

36
Q

OVERWEIGHT cats are ____X MORE likely to develop ____ ____ DIABETES MELLITUS

cats that go OUTDOORS are ____ likely to develop DIABETES than INDOOR cats

A

4X, TYPE 2

LESS

37
Q

FELINE WEIGHT GAIN can be associated with WHAT 2 BIOCHEMICAL PROCESSES?

if the body returns to a NORMAL weight, then…

why is it HARDER to get CATS to LOSE WEIGHT?

A

WEIGHT GAIN…
1. HYPERGLYCEMIA
2. INCREASED INSULIN SECRETION

if body returns to a NORMAL weight, then BOTH CAN BE REVERSIBLE

harder for CATS to lose weight because IF THEY DON’T EAT ENOUGH, then CAN GET HEPATIC LIPIDOSIS

38
Q

AMYLOID DEPOSITION…

can be a CAUSE for ___ ___ DIABETES MELLITUS, but ONLY IN ____ and NOT ____

can be a ___ finding, but MOST have ____

synthesized from ___ ____ ___

after amyloid deposition, causes WHAT 3 PATHOLOGIC CHANGES?

A

TYPE 2, DOGS, CATS

can be a NORMAL finding in CATS, but MOST have DIABETES

synthesized from ISLET AMYLOID POLYPEPTIDE

after amyloid deposition, causes…
1. BETA CELL DESTRUCTION
2. DECREASED INSULIN SECRETION
3. INCREASED INSULIN RESISTANCE

39
Q

AMYLOID can BEHAVE DIFFERENTLY depending on…

DO NOT see ANY AMYLOID ACCUMULATION if… & this is true in WHAT species?

A

depending on AMINO ACID SEQUENCE

DO NOT see ANY AMYLOID ACCUMULATION if SERINE in position 28 is SUBSTITUTED for PROLINE & this is true in RODENTS

40
Q

dogs will ONLY develop PANCREATIC AMYLOID DEPOSITION when associated with WHAT disease?

A

INSULINOMA

41
Q

4 CAT breeds associated with DEVELOPMENT OF DIABETES MELLITUS?

A
  1. NORWEGIAN FOREST
  2. BURMESE
  3. RUSSIAN BLUE
  4. ABYSSINIAN
42
Q

SECONDARY DIABETES MELLITUS…

this is SEPARATE from WHAT OTHER TWO DISEASES?

can develop in DOGS due to.. (2)

can develop in CATS due to…

in ALL of these cases, EXCESS ___ causes INCREASED ____ ____ which causes ____ ____

A

SEPARATE from TYPE 1/TYPE 2 DIABETES

DOGS
1. DIESTRUS
2. PREGNANCY

CATS
1. given MEGESTROL ACETATE (for CONTRACEPTION, not in US)

in ALL of these cases, EXCESS PROGESTERONE causes INCREASED GROWTH HORMONE which causes INSULIN RESISTANCE

43
Q

TRANSIENT diabetes mellitus…

commonality in DOGS/CATS?

why is this CHALLENGING/DANGEROUS?

A

RARE in DOGS, UNCOMMON in CATS

CHALLENGING/DANGEROUS because if we’re giving INSULIN when the patient doesn’t need it, can be LETHAL (HYPOGLYCEMIC)

44
Q

2 MAIN reasons for TRANSIENT DIABETES MELLITUS?

A
  1. SUBCLINICAL DIABETES that’s STIMULATED by CONCURRENT DZ that causes STRESS or ADMINISTRATION of EXOGENOUS COUNTER-REGULATORY HORMONE
  2. GLUCOSE DESENSITIZATION
45
Q

GLUCOSE TOXICITY/DESENSITIZATION…

commonly associated with WHAT kind of diabetes mellitus?

= how does it work? & GIVE A SPECIFIC NUMERICAL PARAMETER

A

commonly associated with TRANSIENT DIABETES MELLITUS

= at HIGH concentrations of GLUCOSE (>540 mg/dL) can INHIBIT INSULIN SECRETION from the PANCREAS when it should NORMALLY BE SECRETED

46
Q

SUBCLINICAL diabetes mellitus…

usually presents as WHAT kind of diabetes mellitus?

pathogenesis? (4)

A

usually presents as TRANSIENT DIABETES MELLITUS

pathogenesis?
1. patient likely has SUBCLINICAL DIABETES

  1. then has CONCURRENT DZ that causes STRESS & release of COUNTER-REGULATORY HORMONES or we’ve GIVEN IT a COUNTER-REGULATORY HORMONE via STEROID
  2. this pushes cat INTO DIABETES (–> NOT ENOUGH INSULIN and BLOOD SUGAR TOO HIGH)
  3. but, if we TREAT DISORDER or TAKE OFF OF DRUG, then PANCREAS can PRODUCE NORMAL INSULIN, and combined with EXOGENOUS insulin –> HYPOGLYCEMIA
47
Q

TRUE/FALSE

insulin treatment is needed in VIRTUALLY ALL DOGS with DM

A

TRUE

48
Q

TRUE/FALSE

TRANSIENT diabetes mellitus is COMMON in cats

A

FALSE, STILL UNCOMMON

49
Q

UNCOMPLICATED diabetes mellitus in DOGS…
1. age range?

  1. 3 breeds at INCREASED risk?
  2. 3 breeds at DECREASED risk?
  3. what breed tends to have CONGENITAL form of diabetes?
  4. SEX at increased risk?
A
  1. 7-9 YEARS OLD
  2. INCREASED RISK = SAMOYEDS, TOY POODLES, PUGS
  3. DECREASED RISK = GERMAN SHEPHERDS, GOLDEN RETRIEVER, PITBULLS
  4. CONGENITAL FORM = KEESHUND
  5. FEMALES at increased risk
50
Q

2 forms of COMPLICATED diabetes mellitus?

A
  1. DIABETIC KETOACIDOSIS
  2. HYPEROSMOLAR NONKETOTIC DIABETES MELLITUS
51
Q

what is the MOST COMMON presentation of DIABETES MELLITUS in SMALL ANIMALS?

A

UNCOMPLICATED!

52
Q

UNCOMPLICATED diabetes mellitus in CATS…

  1. MEAN age?
  2. SEX at increased risk? intact or not?
A
  1. 10 YEARS
  2. NEUTERED MALES
53
Q

why does PU/PD occur in DIABETES? (2)

what is the RENAL THRESHOLD?
–> parameters for DOGS & CATS?

A
  1. GLUCOSE EXCEEDS capacity of SGLT2 to REABSORB GLUCOSE from URINE
  2. glucose SPILLS INTO URINE & acts as an OSMOTIC AGENT = POLYURIA

RENAL THRESHOLD = the CONCENTRATION of GLUCOSE that, if EXCEEDED, will cause glucose to SPILL INTO THE URINE
–> DOGS = 180 mg/dL
–> CATS = 280 mg/dL

54
Q

why do animals have WEIGHT LOSS in DIABETES? (2)

A
  1. ANABOLIC hormone INSULIN is NOT WORKING, so the body is in a CATABOLIC STATE
  2. that means BREAKING DOWN MUSCLE & FAT
55
Q

why do animals have POLYPHAGIA in DM? (2)

A
  1. because GLUCOSE is NOT BEING PUSHED INTO CELLS = STARVING
  2. also SATIETY signal is NOT BEING SENT
56
Q

____ with diabetes can sometimes present with a ____ STANCE

___ with diabetes can present with BLINDNESS

A

CATS, PLANTIGRADE

DOGS –> BLINDNESS

57
Q

TRUE/FALSE

on PE, diabetes patients can be NORMAL and the BODY WEIGHT can be NORMAL, OBESE, or UNDERWEIGHT

A

TRUE

58
Q

if diabetes is caught EARLY-ON, patients can appear…

A

UNDERWEIGHT

59
Q

GLUCOSURIA DIFFERENTIALS… (2)

A
  1. DIABETES
  2. TUBULAR DEFECT
60
Q

DIABETIC PERIPHERAL NEUROPATHY is more common in DOGS/CATS

A

CATS

61
Q

we would expect HYPO/HYPERCHOLESTEROLEMIA in DIABETES

A

HYPOCHOLESTEROLEMIA

Year 1/2 (139 decks)

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